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AuthorTitleYearJournal/ProceedingsReftypeDOI/URL
Alanazi, I.O., Shehri, Z.S.A., Ebrahimie, E., Giahi, H. and Mohammadi-Dehcheshmeh, M. Non-coding and coding and genomic variants distinguish prostate cancer, castration-resistant prostate cancer, familial prostate cancer, and metastatic castration-resistant prostate cancer from each other 2019 Molecular Carcinogenesis  article DOI URL 
BibTeX:
@article{Alanazi2019,
  author = {Alanazi, Ibrahim O and Shehri, Zafer Saad Al and Ebrahimie, Esmaeil and Giahi, Hassan and Mohammadi-Dehcheshmeh, Manijeh},
  title = {Non-coding and coding and genomic variants distinguish prostate cancer, castration-resistant prostate cancer, familial prostate cancer, and metastatic castration-resistant prostate cancer from each other},
  journal = {Molecular Carcinogenesis},
  publisher = {John Wiley & Sons, Ltd},
  year = {2019},
  url = {http://doi.wiley.com/10.1002/mc.22975},
  doi = {http://doi.org/10.1002/mc.22975}
}
Jung, Y.-d., Cho, J., Park, S., Kang, M., Park, S.-j., Choi, D., Jeong, M., Park, K., Yeom, Y., Lee, D., Jung, Y.-d., Cho, J.H., Park, S., Kang, M., Park, S.-j., Choi, D.H., Jeong, M., Park, K.C., Yeom, Y.I. and Lee, D.C. Lactate Activates the E2F Pathway to Promote Cell Motility by Up-Regulating Microtubule Modulating Genes 2019 Cancers
Vol. 11(3), pp. 274 
article DOI URL 
Abstract: textlessptextgreaterExcess lactate production due to enhanced aerobic glycolysis is characteristic of malignant cancers, which is also intimately associated with poor cancer prognoses. Although tumor-associated lactate contributes to all major steps in carcinogenesis, its action mechanism remains obscure. To understand the molecular mechanism of the lactate-induced tumor metastatic process, we identified an array of lactate-responsive genes via transcriptome analysis of a metformin-induced hyper-glycolytic liver cancer model. Gene set enrichment analysis suggested E2F-RB pathway as the dominant regulator of the lactate-induced gene expression. We experimentally verified that lactate indeed activates E2F-mediated transcription by promoting E2F1 protein accumulation through a posttranscriptional mechanism. Literature-based analysis of target pathways potentially modulated by 136 top-ranked genes indicated that genes functioning in cell-cell or cell-matrix communications dominate the lactate-induced gene expression. Especially, those regulating microtubule functions, including a group of kinesin family members, were significantly up-regulated in lactate- and E2F1-dependent manners. Depletion of E2F1 or kinesins (KIF2C, KIF18B, KIF20A) led to deformation of microtubule structures, impairing cell motility as much as the deficit in lactate production. These results indicate that E2F pathway activation by tumor-associated lactate and subsequent transcriptional activation of microtubule functions play crucial roles in tumor metastasis, providing mechanistic clues to cell motility-directed anti-cancer strategies.textless/ptextgreater
BibTeX:
@article{Jung2019,
  author = {Jung, Yi-deun and Cho, Jung and Park, Seulki and Kang, Minho and Park, Seung-jin and Choi, Dong and Jeong, Moonkyung and Park, Kyung and Yeom, Young and Lee, Dong and Jung, Yi-deun and Cho, Jung Hee and Park, Seulki and Kang, Minho and Park, Seung-jin and Choi, Dong Hee and Jeong, Moonkyung and Park, Kyung Chan and Yeom, Young Il and Lee, Dong Chul},
  title = {Lactate Activates the E2F Pathway to Promote Cell Motility by Up-Regulating Microtubule Modulating Genes},
  journal = {Cancers},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2019},
  volume = {11},
  number = {3},
  pages = {274},
  url = {http://www.mdpi.com/2072-6694/11/3/274},
  doi = {http://doi.org/10.3390/cancers11030274}
}
Lehmann, S.G., Seve, M., Vanwonterghem, L., Michelland, S., Cunin, V., Coll, J.-L., Hurbin, A. and Bourgoin-Voillard, S. A large scale proteome analysis of the gefitinib primary resistance overcome by KDAC inhibition in KRAS mutated adenocarcinoma cells overexpressing amphiregulin 2019 Journal of Proteomics  article DOI URL 
Abstract: KDAC inhibitors (KDACi) overcome gefitinib primary resistance in non-small cell lung cancer (NSCLC) including mutant-KRAS lung adenocarcinoma. To identify which proteins are involved in the restoration of this sensitivity and to provide new therapeutic targets for mutant-KRAS lung adenocarcinoma, we performed an iTRAQ quantitative proteomic analysis after subcellular fractionation of H358-NSCLC treated with gefitinib and KDACi (TSA/NAM) versus gefitinib alone. The 86 proteins found to have been significantly dysregulated between the two conditions, were mainly involved in cellular metabolism and cell transcription processes. As expected, the pathway related to histone modifications was affected by the KDACi. Pathways known for controlling tumor development and (chemo)-resistance (miRNA biogenesis/glutathione metabolism) were affected by the KDACi/gefitinib treatment. Moreover, 57 dysregulated proteins were upstream of apoptosis (such as eEF1A2 and STAT1) and hence provide potential therapeutic targets. The inhibition by siRNA of eEF1A2 expression resulted in a slight decrease in H358-NSCLC viability. In addition, eEF1A2 and STAT1 siRNA transfections suggested that both STAT1 and eEF1A2 prevent AKT phosphorylation known for enhancing gefitinib resistance in NSCLC. Therefore, altogether our data provide new insights into proteome regulations in the context of overcoming the NSCLC resistance to gefitinib through KDACi in H358 KRAS mutated and amphiregulin-overexpressing NSCLC cells.
BibTeX:
@article{Lehmann2019,
  author = {Lehmann, Sylvia G. and Seve, Michel and Vanwonterghem, Laetitia and Michelland, Sylvie and Cunin, Valérie and Coll, Jean-Luc and Hurbin, Amandine and Bourgoin-Voillard, Sandrine},
  title = {A large scale proteome analysis of the gefitinib primary resistance overcome by KDAC inhibition in KRAS mutated adenocarcinoma cells overexpressing amphiregulin},
  journal = {Journal of Proteomics},
  publisher = {Elsevier},
  year = {2019},
  url = {https://www.sciencedirect.com/science/article/pii/S187439191930017X},
  doi = {http://doi.org/10.1016/J.JPROT.2019.01.009}
}
Nehme, A., Kobeissy, F., Zhao, J., Zhu, R., Feugier, P., Mechref, Y. and Zibara, K. Functional pathways associated with human carotid atheroma: a proteomics analysis 2019 Hypertension Research, pp. 1  article DOI URL 
Abstract: Advances in large-scale analysis are becoming very useful in understanding health and disease. Here, we used high-throughput mass spectrometry to identify differentially expressed proteins between early and advanced lesions. Carotid endarterectomy samples were collected and dissected into early and advanced atherosclerotic lesion portions. Proteins were extracted and subjected to liquid chromatography–tandem mass spectrometry (LC–MS/MS) analysis. Differentially expressed proteins were identified and verified using multiple reaction monitoring (MRM), on which advanced systems biology and enrichment analyses were performed. The identified proteins were further compared to the transcriptomic data of 32 paired samples obtained from early and advanced atherosclerotic lesions. A total of 95 proteins were upregulated, and 117 proteins were downregulated in advanced lesions compared to early atherosclerotic lesions (p textless 0.05). The upregulated proteins were associated with proatherogenic processes, whereas downregulated proteins were involved in extracellular matrix organization and vascular smooth muscle cytoskeleton. Many of the identified proteins were linked to various “upstream regulators”, among which TGFβ had the highest connections. Specifically, a total of 19 genes were commonly upregulated, and 30 genes were downregulated at the mRNA and protein levels. These genes were involved in vascular smooth muscle cell activity, for which enriched transcription factors were identified. This study deciphers altered pathways in atherosclerosis and identifies upstream regulators that could be candidate targets for treatment.
BibTeX:
@article{Nehme2019,
  author = {Nehme, Ali and Kobeissy, Firas and Zhao, Jingfu and Zhu, Rui and Feugier, Patrick and Mechref, Yehia and Zibara, Kazem},
  title = {Functional pathways associated with human carotid atheroma: a proteomics analysis},
  journal = {Hypertension Research},
  publisher = {Nature Publishing Group},
  year = {2019},
  pages = {1},
  url = {http://www.nature.com/articles/s41440-018-0192-4},
  doi = {http://doi.org/10.1038/s41440-018-0192-4}
}
Pawłowski, K., Pires, J.A., Faulconnier, Y., Chambon, C., Germon, P., Boby, C., Leroux, C., Pawłowski, K., Pires, J.A.A., Faulconnier, Y., Chambon, C., Germon, P., Boby, C. and Leroux, C. Mammary Gland Transcriptome and Proteome Modifications by Nutrient Restriction in Early Lactation Holstein Cows Challenged with Intra-Mammary Lipopolysaccharide 2019 International Journal of Molecular Sciences
Vol. 20(5), pp. 1156 
article DOI URL 
Abstract: textlessptextgreater: The objective is to study the effects of nutrient restrictions, which induce a metabolic imbalance on the inflammatory response of the mammary gland in early lactation cows. The aim is to decipher the molecular mechanisms involved, by comparing a control, with a restriction group, a transcriptome and proteome, after an intra-mammary lipopolysaccharide challenge. Multi-parous cows were either allowed ad libitum intake of a lactation diet (n = 8), or a ration containing low nutrient density (n = 8; 48% barley straw and dry matter basis) for four days starting at 24 ± 3 days in milk. Three days after the initiation of their treatments, one healthy rear mammary quarter of 12 lactating cows was challenged with 50 µg of lipopolysaccharide (LPS). Transcriptomic and proteomic analyses were performed on mammary biopsies obtained 24 h after the LPS challenge, using bovine 44K microarrays, and nano-LC-MS/MS, respectively. Restriction-induced deficits in energy, led to a marked negative energy balance (41 versus 97 ± 15% of Net Energy for Lactation (NEL) requirements) and metabolic imbalance. A microarray analyses identified 25 differentially expressed genes in response to restriction, suggesting that restriction had modified mammary metabolism, specifically β-oxidation process. Proteomic analyses identified 53 differentially expressed proteins, which suggests that the modification of protein synthesis from mRNA splicing to folding. Under-nutrition influenced mammary gland expression of the genes involved in metabolism, thereby increasing β-oxidation and altering protein synthesis, which may affect the response to inflammation.textless/ptextgreater
BibTeX:
@article{Pawowski2019,
  author = {Pawłowski, Karol and Pires, José A.A. and Faulconnier, Yannick and Chambon, Christophe and Germon, Pierre and Boby, Céline and Leroux, Christine and Pawłowski, Karol and Pires, José A. A. and Faulconnier, Yannick and Chambon, Christophe and Germon, Pierre and Boby, Céline and Leroux, Christine},
  title = {Mammary Gland Transcriptome and Proteome Modifications by Nutrient Restriction in Early Lactation Holstein Cows Challenged with Intra-Mammary Lipopolysaccharide},
  journal = {International Journal of Molecular Sciences},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2019},
  volume = {20},
  number = {5},
  pages = {1156},
  url = {https://www.mdpi.com/1422-0067/20/5/1156},
  doi = {http://doi.org/10.3390/ijms20051156}
}
Ruan, C.-M., Wang, J., Yang, Y.-X., Hu, J.-J., Ma, Y.-J., Zhang, Y. and Zhao, X.-X. Proteomic analysis of Tianzhu White Yak ( textlessitextgreaterBos grunnienstextless/itextgreater ) testis at different sexual developmental stages 2019 Animal Science Journal  article DOI URL 
BibTeX:
@article{Ruan2019,
  author = {Ruan, Chong-Mei and Wang, Jing and Yang, Yong-Xin and Hu, Jun-Jie and Ma, You-Ji and Zhang, Yong and Zhao, Xing-Xu},
  title = {Proteomic analysis of Tianzhu White Yak ( textlessitextgreaterBos grunnienstextless/itextgreater ) testis at different sexual developmental stages},
  journal = {Animal Science Journal},
  publisher = {John Wiley & Sons, Ltd (10.1111)},
  year = {2019},
  url = {http://doi.wiley.com/10.1111/asj.13157},
  doi = {http://doi.org/10.1111/asj.13157}
}
Udvari, E.B., Völgyi, K., Kékesi, K.A., Simon, D., Hunyadi-Gulyás, É. and Dobolyi, A. Proteomic Analysis of the Maternal Preoptic Area in Rats 2019 Neurochemical Research, pp. 1-11  article DOI URL 
BibTeX:
@article{Udvari2019,
  author = {Udvari, Edina Brigitta and Völgyi, Katalin and Kékesi, Katalin Adrienna and Simon, Dorina and Hunyadi-Gulyás, Éva and Dobolyi, Arpád},
  title = {Proteomic Analysis of the Maternal Preoptic Area in Rats},
  journal = {Neurochemical Research},
  publisher = {Springer US},
  year = {2019},
  pages = {1--11},
  url = {http://link.springer.com/10.1007/s11064-019-02755-y},
  doi = {http://doi.org/10.1007/s11064-019-02755-y}
}
Zali, H., Golchin, A., Farahani, M., Yazdani, M., Ranjbar, M.M. and Dabbagh, A. FDA Approved Drugs Repurposing Of Toll-Like Receptor4 (TLR4) Candidate for Neuropathy 2019   techreport URL 
BibTeX:
@techreport{Zali2019,
  author = {Zali, Hakimeh and Golchin, Ali and Farahani, Masoumeh and Yazdani, Mohsen and Ranjbar, Mohammad Mehdi and Dabbagh, Ali},
  title = {FDA Approved Drugs Repurposing Of Toll-Like Receptor4 (TLR4) Candidate for Neuropathy},
  year = {2019},
  url = {http://ijpr.sbmu.ac.ir/article2394959c1a4d593e33041fc86fa674122266.pdf}
}
Zhu, X., Liao, J., Xia, X., Xiong, F., Li, Y., Shen, J., Wen, B., Ma, Y., Wang, Y. and Fang, W. Physiological and iTRAQ-based proteomic analyses reveal the function of exogenous γ-aminobutyric acid (GABA) in improving tea plant (Camellia sinensis L.) tolerance at cold temperature 2019 BMC Plant Biology
Vol. 19(1), pp. 43 
article DOI URL 
BibTeX:
@article{Zhu2019,
  author = {Zhu, Xujun and Liao, Jieren and Xia, Xingli and Xiong, Fei and Li, Yue and Shen, Jiazhi and Wen, Bo and Ma, Yuanchun and Wang, Yuhua and Fang, Wanping},
  title = {Physiological and iTRAQ-based proteomic analyses reveal the function of exogenous γ-aminobutyric acid (GABA) in improving tea plant (Camellia sinensis L.) tolerance at cold temperature},
  journal = {BMC Plant Biology},
  publisher = {BioMed Central},
  year = {2019},
  volume = {19},
  number = {1},
  pages = {43},
  url = {https://bmcplantbiol.biomedcentral.com/articles/10.1186/s12870-019-1646-9},
  doi = {http://doi.org/10.1186/s12870-019-1646-9}
}
Ali, M. and del Sol, A. Modeling of Cellular Systems: Application in Stem Cell Research and Computational Disease Modeling 2018 , pp. 129-138  incollection DOI URL 
BibTeX:
@incollection{Ali2018,
  author = {Ali, Muhammad and del Sol, Antonio},
  title = {Modeling of Cellular Systems: Application in Stem Cell Research and Computational Disease Modeling},
  publisher = {Springer, Cham},
  year = {2018},
  pages = {129--138},
  url = {http://link.springer.com/10.1007/978-3-319-74974-77},
  doi = {http://doi.org/10.1007/978-3-319-74974-7_7}
}
Alieva, A., Zyrin, V., Rudenok, M., Kolacheva, A., Shulskaya, M., Ugryumov, M., Slominsky, P. and Shadrina, M. Whole-Transcriptome Analysis of Mouse Models with MPTP-Induced Early Stages of Parkinson's Disease Reveals Stage-Specific Response of Transcriptome and a Possible Role of Myelin-Linked Genes in Neurodegeneration 2018 Molecular Neurobiology, pp. 1-13  article DOI URL 
BibTeX:
@article{Alieva2018,
  author = {Alieva, A.Kh. and Zyrin, V.S. and Rudenok, M.M. and Kolacheva, A.A. and Shulskaya, M.V. and Ugryumov, M.V. and Slominsky, P.A. and Shadrina, M.I.},
  title = {Whole-Transcriptome Analysis of Mouse Models with MPTP-Induced Early Stages of Parkinson's Disease Reveals Stage-Specific Response of Transcriptome and a Possible Role of Myelin-Linked Genes in Neurodegeneration},
  journal = {Molecular Neurobiology},
  publisher = {Springer US},
  year = {2018},
  pages = {1--13},
  url = {http://link.springer.com/10.1007/s12035-018-0907-1},
  doi = {http://doi.org/10.1007/s12035-018-0907-1}
}
Amiri, M., Nourian, A., Khoshkam, M. and Ramazani, A. Apigenin inhibits growth of the textlessitextgreaterPlasmodium bergheitextless/itextgreater and disrupts some metabolic pathways in mice 2018 Phytotherapy Research  article DOI URL 
BibTeX:
@article{Amiri2018,
  author = {Amiri, Mahdi and Nourian, Abbasali and Khoshkam, Maryam and Ramazani, Ali},
  title = {Apigenin inhibits growth of the textlessitextgreaterPlasmodium bergheitextless/itextgreater and disrupts some metabolic pathways in mice},
  journal = {Phytotherapy Research},
  publisher = {Wiley-Blackwell},
  year = {2018},
  url = {http://doi.wiley.com/10.1002/ptr.6113},
  doi = {http://doi.org/10.1002/ptr.6113}
}
Ayubov, M.S., Abdurakhmonov, I.Y., Sripathi, V.R., Saha, S., Norov, T.M., Buriev, Z.T., Shermatov, S.E., Ubaydullaeva, K.A., Mccarty, J.C., Deng, D.D. and Jenkins, J.N. Recent Developments in Fiber Genomics of Tetraploid Cotton Species 2018   article DOI URL 
Abstract: Cotton (Gossypium spp.) produces naturally soft, single-celled trichomes as fiber on the seed coat supplying the main source of natural raw material for the textile industry. It is economically considered as one of the most leading cash crops in the world and evolutionarily very important as a model system for detailed scientific investigations. Cotton production is going through a big transition stage such as losing the market share in competition with the synthetic fibers, high popularity of Bt and herbicide resistance genes in cotton cultivars, and the recent shift of fiber demands to meet the standard fiber quality due to change of textile technologies to produce high superior quality of fibers in the global market. Recently, next-generation sequencing technologies through high-throughput sequencing at greatly reduced costs provided opportunities to sequence the diploid and tetraploid cotton genomes. With the availability of large volume of literatures on molecular mapping, new genomic resources, characterization of cotton genomes, dis-coveries of many novel genes, regulatory elements including small and microRNAs and new genetic tools such as gene silencing or gene editing technique for genome manipula-tion, this report attempted to provide the readers a comprehensive review on the recent advances of cotton fiber genomics research.
BibTeX:
@article{Ayubov2018,
  author = {Ayubov, Mirzakamol S and Abdurakhmonov, Ibrokhim Y and Sripathi, Venkateswara R and Saha, Sukumar and Norov, Tokhir M and Buriev, Zabardast T and Shermatov, Shukhrat E and Ubaydullaeva, Khurshida A and Mccarty, Jack C and Deng, Dewayne D and Jenkins, Johnie N},
  title = {Recent Developments in Fiber Genomics of Tetraploid Cotton Species},
  year = {2018},
  url = {http://dx.doi.org/10.5772/intechopen.72922},
  doi = {http://doi.org/10.5772/intechopen.72922}
}
Burkhard, R., Keller, I., Arambasic, M., Juskevicius, D., Tzankov, A., Lundberg, P., Bruggman, R., Dirnhofer, S., Radpour, R. and Novak, U. TIRAP p.R81C is a novel lymphoma risk variant which enhances cell proliferation via NF-κB mediated signaling in B-cells. 2018 Haematologica, pp. haematol.2018.201590  article DOI URL 
Abstract: Diffuse large B-cell lymphoma is the most common malignant lymphoma in adults. By gene-expression profiling, this lymphoma is divided in three cell-of-origin subtypes with distinct molecular and clinical features. Most lymphomas arise sporadically, yet familial clustering is known, suggesting a genetic contribution to disease risk. Familial lymphoma cases are a valuable tool to investigate risk genes. We studied a Swiss/Japanese family with two sisters affected by a primary mediastinal B-cell lymphoma and a non-germinal center diffuse large B-cell lymphoma not otherwise specified, respectively. The somatic landscape of both lym-phomas was marked by alterations affecting multiple components of the JAK-STAT pathway. Consequently, this pathway was constitutively activated as evidenced by high pJAK2 as well as increased nuclear pSTAT3 and pSTAT6 in malignant cells. Potential lymphoma risk vari-ants were identified by whole-exome sequencing of the germline DNA derived from siblings and unaffected family members. This analysis revealed a pathogenic variant in TIRAP, an upstream regulator of NF-κB, in both affected siblings and their mother. We observed in-creased B-cell proliferation in family members harboring the TIRAP p.R81C variant. B-cell proliferation correlated with TIRAP and NF-κB target gene expression, suggesting enhanced NF-κB pathway activity in TIRAP p.R81C individuals. TIRAP knockdown reduced B-cell sur-vival and NF-κB target gene expression, particularly in individuals with TIRAP p.R81C. Func-tional studies revealed significantly increased NF-κB activity and resistance to stress-induced cell-death by TIRAP p.R81C. The identification of an inherited TIRAP variant pro-vides evidence for a novel link between genetic alterations affecting the NF-κB pathway and lymphomagenesis.
BibTeX:
@article{Burkhard2018,
  author = {Burkhard, Regula and Keller, Irene and Arambasic, Miroslav and Juskevicius, Darius and Tzankov, Alexandar and Lundberg, Pontus and Bruggman, Rémy and Dirnhofer, Stephan and Radpour, Ramin and Novak, Urban},
  title = {TIRAP p.R81C is a novel lymphoma risk variant which enhances cell proliferation via NF-κB mediated signaling in B-cells.},
  journal = {Haematologica},
  publisher = {Haematologica},
  year = {2018},
  pages = {haematol.2018.201590},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/30381301},
  doi = {http://doi.org/10.3324/haematol.2018.201590}
}
Cao, F., Souders Ii, C.L., Perez-Rodriguez, V. and Martyniuk, C.J. Elucidating Conserved Transcriptional Networks Underlying Pesticide Exposure and Parkinson's Disease: A Focus on Chemicals of Epidemiological Relevance. 2018 Frontiers in genetics
Vol. 9, pp. 701 
article DOI URL 
Abstract: While a number of genetic mutations are associated with Parkinson's disease (PD), it is also widely acknowledged that the environment plays a significant role in the etiology of neurodegenerative diseases. Epidemiological evidence suggests that occupational exposure to pesticides (e.g., dieldrin, paraquat, rotenone, maneb, and ziram) is associated with a higher risk of developing PD in susceptible populations. Within dopaminergic neurons, environmental chemicals can have an array of adverse effects resulting in cell death, such as aberrant redox cycling and oxidative damage, mitochondrial dysfunction, unfolded protein response, ubiquitin-proteome system dysfunction, neuroinflammation, and metabolic disruption. More recently, our understanding of how pesticides affect cells of the central nervous system has been strengthened by computational biology. New insight has been gained about transcriptional and proteomic networks, and the metabolic pathways perturbed by pesticides. These networks and cell signaling pathways constitute potential therapeutic targets for intervention to slow or mitigate neurodegenerative diseases. Here we review the epidemiological evidence that supports a role for specific pesticides in the etiology of PD and identify molecular profiles amongst these pesticides that may contribute to the disease. Using the Comparative Toxicogenomics Database, these transcripts were compared to those regulated by the PD-associated neurotoxicant MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). While many transcripts are already established as those related to PD (alpha-synuclein, caspases, leucine rich repeat kinase 2, and parkin2), lesser studied targets have emerged as "pesticide/PD-associated transcripts" [e.g., phosphatidylinositol glycan anchor biosynthesis class C (Pigc), allograft inflammatory factor 1 (Aif1), TIMP metallopeptidase inhibitor 3, and DNA damage inducible transcript 4]. We also compared pesticide-regulated genes to a recent meta-analysis of genome-wide association studies in PD which revealed new genetic mutant alleles; the pesticides under review regulated the expression of many of these genes (e.g., ELOVL fatty acid elongase 7, ATPase H+ transporting V0 subunit a1, and bridging integrator 3). The significance is that these proteins may contribute to pesticide-related increases in PD risk. This review collates information on transcriptome responses to PD-associated pesticides to develop a mechanistic framework for quantifying PD risk with exposures.
BibTeX:
@article{Cao2018,
  author = {Cao, Fangjie and Souders Ii, Christopher L and Perez-Rodriguez, Veronica and Martyniuk, Christopher J},
  title = {Elucidating Conserved Transcriptional Networks Underlying Pesticide Exposure and Parkinson's Disease: A Focus on Chemicals of Epidemiological Relevance.},
  journal = {Frontiers in genetics},
  publisher = {Frontiers Media SA},
  year = {2018},
  volume = {9},
  pages = {701},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/30740124 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC6355689},
  doi = {http://doi.org/10.3389/fgene.2018.00701}
}
Carvalho, L.J.C.B., Anderson, J.V., Chen, S., Mba, C. and Doğramaci, M. Domestication Syndrome in Cassava (Manihot esculenta Crantz): Assessing Morphological Traits and Differentially Expressed Genes Associated with Genetic Diversity of Storage Root 2018 Cassava  incollection DOI URL 
BibTeX:
@incollection{Carvalho2018,
  author = {Carvalho, Luiz Joaquim Castelo Branco and Anderson, James V. and Chen, Songbi and Mba, Chikelu and Doğramaci, Münevver},
  title = {Domestication Syndrome in Cassava (Manihot esculenta Crantz): Assessing Morphological Traits and Differentially Expressed Genes Associated with Genetic Diversity of Storage Root},
  booktitle = {Cassava},
  publisher = {InTech},
  year = {2018},
  url = {http://www.intechopen.com/books/cassava/domestication-syndrome-in-cassava-manihot-esculenta-crantz-assessing-morphological-traits-and-differ},
  doi = {http://doi.org/10.5772/intechopen.71348}
}
Chiha, W., LeVaillant, C.J., Bartlett, C.A., Hewitt, A.W., Melton, P.E., Fitzgerald, M. and Harvey, A.R. Retinal genes are differentially expressed in areas of primary versus secondary degeneration following partial optic nerve injury 2018 PLOS ONE
Vol. 13(2), pp. e0192348 
article DOI URL 
BibTeX:
@article{Chiha2018,
  author = {Chiha, Wissam and LeVaillant, Chrisna J. and Bartlett, Carole A. and Hewitt, Alex W. and Melton, Phillip E. and Fitzgerald, Melinda and Harvey, Alan R.},
  title = {Retinal genes are differentially expressed in areas of primary versus secondary degeneration following partial optic nerve injury},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2018},
  volume = {13},
  number = {2},
  pages = {e0192348},
  url = {http://dx.plos.org/10.1371/journal.pone.0192348},
  doi = {http://doi.org/10.1371/journal.pone.0192348}
}
Dong, Y., Cao, H. and Liang, Z. A Curated Target Gene Pool Assisting Early Disease Prediction and Patient-Specific Treatment for Small Cell Lung Cancer 2018 Journal of Computational Biology, pp. cmb.2017.0071  article DOI URL 
Abstract: Abstract Hundreds of genes have been linked to small cell lung cancer (SCLC), presenting multiple levels of connections with the disease. The question is whether these genes are sufficient as genetic biomarkers for the early diagnosis and personalized treatment of SCLC. An SCLC genetic database was developed through comprehensive ResNet relationship data analysis, where 557 SCLC target genes were curated. Multiple levels of associations between these genes and SCLC were studied. Then, a sparse representation-based variable selection (SRVS) was employed for gene selection for four SCLC gene expression data sets, followed by a case–control classification. Results were compared with that of analysis of variance (ANOVA)-based gene selection approaches. Using SRVS, a gene vector was selected for each data set, leading to significant higher classification accuracy compared with randomly selected genes (100%, 77.12%, 100%, and 100%; permutation p values: 0.017, 0.00060, 0.012, and 0.0066). The SRVS method outper...
BibTeX:
@article{Dong2018,
  author = {Dong, Yan and Cao, Hongbao and Liang, Zhigang},
  title = {A Curated Target Gene Pool Assisting Early Disease Prediction and Patient-Specific Treatment for Small Cell Lung Cancer},
  journal = {Journal of Computational Biology},
  publisher = { Mary Ann Liebert, Inc. 140 Huguenot Street, 3rd Floor New Rochelle, NY 10801 USA },
  year = {2018},
  pages = {cmb.2017.0071},
  url = {http://www.liebertpub.com/doi/10.1089/cmb.2017.0071},
  doi = {http://doi.org/10.1089/cmb.2017.0071}
}
Donma, M.M. and Donma, O. Asprosin: Possible target in connection with ghrelin and cytokine network expression in the post-burn treatment 2018 Medical Hypotheses  article DOI URL 
Abstract: Burn injury is a severe form of trauma associated with pain, metabolic abnormalities, susceptibility to infections, muscle loss, mental and emotional distress. Conventional therapies as well as some recent approaches for the treatment of burned patients are currently in use. Nutritional therapy is also suggested as a supplementary option in major burns. Within this context, hormones involved in the regulation of appetite will have a paramount importance. The aim is to evaluate the interactions among ghrelin, some inflammatory parameters and the burn injury. Asprosin is also involved into this discussion due to its ghrelin-like actions. Aside from the consideration of insulin as well as stress hormones (cortisol, epinephrine, norepinephrine), an orexigenic, anti-inflammatory hormone, ghrelin affecting both metabolic and inflammatory systems is also involved in the protocols designed for burn treatment. Ghrelin's actions exerted by way of growth-hormone secretagogue receptor, neuropeptide Y, agouti-related protein, proopiomelanocortin and gamma amino butyric acid are being investigated. Asprosin, one of the remarkably few hormones identified as appetite stimulator, acts as another orexigenic hormone by using almost the same signalling pathways as those of ghrelin. Interleukin-6 should also be evaluated both as a reliable biomarker of inflammation and also with its inhibitory effects on TNF-α within the scope of burn injury. In conclusion, treatment protocols during burn injury may be designed to raise decreased concentrations of ghrelin and to repress increased levels of inflammatory agents such as TNF-α. IL-6 may be evaluated from an entirely different aspect. The potential therapeutic use of asprosin may be considered within an integrative approach with a focus on cachexia-anorexia developed in severe burn trauma.
BibTeX:
@article{Donma2018,
  author = {Donma, Mustafa Metin and Donma, Orkide},
  title = {Asprosin: Possible target in connection with ghrelin and cytokine network expression in the post-burn treatment},
  journal = {Medical Hypotheses},
  publisher = {Churchill Livingstone},
  year = {2018},
  url = {https://www.sciencedirect.com/science/article/pii/S0306987718303232},
  doi = {http://doi.org/10.1016/J.MEHY.2018.07.008}
}
Ernst, A.-K., Putscher, A., Samatov, T.R., Suling, A., Galatenko, V.V., Shkurnikov, M.Y., Knyazev, E.N., Tonevitsky, A.G., Haalck, T., Lange, T., Maar, H., Schröder- Schwarz, J., Riecken, K., Schumacher, U. and Wicklein, D. Knockdown of L1CAM significantly reduces metastasis in a xenograft model of human melanoma: L1CAM is a potential target for anti-melanoma therapy 2018 PLOS ONE
Vol. 13(2), pp. e0192525 
article DOI URL 
Abstract: Finding additional functional targets for combination therapy could improve the outcome for melanoma patients. In a spontaneous metastasis xenograft model of human melanoma a shRNA mediated knockdown of L1CAM more than sevenfold reduced the number of lung metastases after the induction of subcutaneous tumors for two human melanoma cell lines (MeWo, MV3). Whole genome expression arrays of the initially L1CAM high MeWo subcutaneous tumors revealed unchanged or downregulated genes involved in epithelial to mesenchymal transition (EMT) except an upregulation of Jagged 1, indicating a compensatory change in Notch signaling especially as Jagged 1 expression showed an increase in MeWo L1CAM metastases and Jagged 1 was expressed in metastases of the initially L1CAM low MV3 cells as well. Expression of 17 genes showed concordant regulation for L1CAM knockdown tumors of both cell lines. The changes in gene expression indicated changes in the EMT network of the melanoma cells and an increase in p53/p21 and p38 activity contributing to the reduced metastatic potential of the L1CAM knockdowns. Taken together, these data make L1CAM a highly interesting therapeutic target to prevent further metastatic spread in melanoma patients.
BibTeX:
@article{Ernst2018,
  author = {Ernst, Ann-Kathrin and Putscher, Annika and Samatov, Timur R. and Suling, Anna and Galatenko, Vladimir V. and Shkurnikov, Maxim Yu and Knyazev, Evgeny N. and Tonevitsky, Alexander G. and Haalck, Thomas and Lange, Tobias and Maar, Hanna and Schröder- Schwarz, Jennifer and Riecken, Kristoffer and Schumacher, Udo and Wicklein, Daniel},
  title = {Knockdown of L1CAM significantly reduces metastasis in a xenograft model of human melanoma: L1CAM is a potential target for anti-melanoma therapy},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2018},
  volume = {13},
  number = {2},
  pages = {e0192525},
  url = {http://dx.plos.org/10.1371/journal.pone.0192525},
  doi = {http://doi.org/10.1371/journal.pone.0192525}
}
Grünblatt, E., Bartl, J. and Walitza, S. Methylphenidate enhances neuronal differentiation and reduces proliferation concomitant to activation of Wnt signal transduction pathways 2018 Translational Psychiatry
Vol. 8(1), pp. 51 
article DOI URL 
Abstract: Methylphenidate (Ritalin) is the most commonly prescribed drug in the treatment of attention-deficit hyperactivity disorder. It is suggested that in vivo, methylphenidate treatment supports cortical maturation, however, the molecular and cellular mechanisms are not well understood. This study aimed to explore the potential effect of methylphenidate on cell proliferation and maturation in various cellular models, hypothesizing its interaction with the Wnt-signaling. The termination of cell proliferation concomitant to neuronal maturation following methylphenidate treatment was observed in all of the cell-models tested: murine neural stem-, rat PC12- and the human SH-SY5Y-cells. Inhibition of Wnt-signaling in SH-SY5Y cells with Dkk1 30 min before methylphenidate treatment suppressed neuronal differentiation but enhanced proliferation. The possible involvement of the dopamine-transporter in cell differentiation was discounted following the observation of opposing results after GBR-12909 treatment. Moreover, Wnt-activation via methylphenidate was confirmed in Wnt-luciferase-reporter assay. These findings reveal a new mechanism of action of methylphenidate that might explain long-term effects.
BibTeX:
@article{Grunblatt2018,
  author = {Grünblatt, Edna and Bartl, Jasmin and Walitza, Susanne},
  title = {Methylphenidate enhances neuronal differentiation and reduces proliferation concomitant to activation of Wnt signal transduction pathways},
  journal = {Translational Psychiatry},
  publisher = {Nature Publishing Group},
  year = {2018},
  volume = {8},
  number = {1},
  pages = {51},
  url = {http://www.nature.com/articles/s41398-018-0096-8},
  doi = {http://doi.org/10.1038/s41398-018-0096-8}
}
Günel, T., Gumusoglu, E., Dogan, B., Ertem, F.B., Hosseini, M.K., Cevik, N., Senol, T., Topuz, S. and Aydinli, K. Potential biomarker of circulating hsa-miR-1273g-3p level for detection of recurrent epithelial ovarian cancer 2018 Archives of Gynecology and Obstetrics, pp. 1-8  article DOI URL 
BibTeX:
@article{Gunel2018,
  author = {Günel, Tuba and Gumusoglu, Ece and Dogan, Berkcan and Ertem, Fatma Betül and Hosseini, Mohammad Kazem and Cevik, Nazife and Senol, Taylan and Topuz, Samet and Aydinli, Kilic},
  title = {Potential biomarker of circulating hsa-miR-1273g-3p level for detection of recurrent epithelial ovarian cancer},
  journal = {Archives of Gynecology and Obstetrics},
  publisher = {Springer Berlin Heidelberg},
  year = {2018},
  pages = {1--8},
  url = {http://link.springer.com/10.1007/s00404-018-4913-3},
  doi = {http://doi.org/10.1007/s00404-018-4913-3}
}
Horvath, D.P., Bruggeman, S., Moriles-Miller, J., Anderson, J.V., Dogramaci, M., Scheffler, B.E., Hernandez, A.G., Foley, M.E. and Clay, S. Weed presence altered biotic stress and light signaling in maize even when weeds were removed early in the critical weed-free period 2018 Plant Direct
Vol. 2(4), pp. e00057 
article DOI URL 
BibTeX:
@article{Horvath2018,
  author = {Horvath, David P. and Bruggeman, Stephanie and Moriles-Miller, Janet and Anderson, James V. and Dogramaci, Munevver and Scheffler, Brian E. and Hernandez, Alvaro G. and Foley, Michael E. and Clay, Sharon},
  title = {Weed presence altered biotic stress and light signaling in maize even when weeds were removed early in the critical weed-free period},
  journal = {Plant Direct},
  publisher = {Wiley-Blackwell},
  year = {2018},
  volume = {2},
  number = {4},
  pages = {e00057},
  url = {http://doi.wiley.com/10.1002/pld3.57},
  doi = {http://doi.org/10.1002/pld3.57}
}
Hottel, J., Yin, C., Lian, Y., Siegel, R., Tan, X. and Fu, S.W. BP1 Regulates PI3K/Akt Pathway by Targeting Vascular Endothelial Growth Factor (VEGF) in Breast Cancer 2018 Oncomedicine
Vol. 3, pp. 67-73 
article DOI URL 
BibTeX:
@article{Hottel2018,
  author = {Hottel, Jenny and Yin, Caiqiao and Lian, Yi and Siegel, Robert and Tan, Xiaohui and Fu, Sidney W},
  title = {BP1 Regulates PI3K/Akt Pathway by Targeting Vascular Endothelial Growth Factor (VEGF) in Breast Cancer},
  journal = {Oncomedicine},
  year = {2018},
  volume = {3},
  pages = {67--73},
  url = {http://www.oncm.org},
  doi = {http://doi.org/10.7150/oncm.25500}
}
Huang, B., Zhong, N., Cao, H. and Yu, G. A curated target gene pool assisting disease prediction and patient‑specific biomarker selection for lung squamous cell carcinoma 2018 Oncology Letters  article DOI URL 
BibTeX:
@article{Huang2018,
  author = {Huang, Bin and Zhong, Ning and Cao, Hongbao and Yu, Guiping},
  title = {A curated target gene pool assisting disease prediction and patient‑specific biomarker selection for lung squamous cell carcinoma},
  journal = {Oncology Letters},
  publisher = {Spandidos Publications},
  year = {2018},
  url = {http://www.spandidos-publications.com/10.3892/ol.2018.9241},
  doi = {http://doi.org/10.3892/ol.2018.9241}
}
Huang, B., Zhong, N., Xia, L., Yu, G. and Cao, H. Sparse Representation-Based Patient-Specific Diagnosis and Treatment for Esophageal Squamous Cell Carcinoma 2018 Bulletin of Mathematical Biology, pp. 1-13  article DOI URL 
BibTeX:
@article{Huang2018a,
  author = {Huang, Bin and Zhong, Ning and Xia, Lili and Yu, Guiping and Cao, Hongbao},
  title = {Sparse Representation-Based Patient-Specific Diagnosis and Treatment for Esophageal Squamous Cell Carcinoma},
  journal = {Bulletin of Mathematical Biology},
  publisher = {Springer US},
  year = {2018},
  pages = {1--13},
  url = {http://link.springer.com/10.1007/s11538-018-0449-8},
  doi = {http://doi.org/10.1007/s11538-018-0449-8}
}
Kara, S., Pirela-Morillo, G.A., Gilliam, C.T. and Wilson, G.D. Identification of novel susceptibility genes associated with seven autoimmune disorders using whole genome molecular interaction networks 2018 Journal of Autoimmunity  article DOI URL 
Abstract: Convergent evidence from multiple and independent genetics studies implicate a small number of genes that predispose individuals to multiple autoimmune disorders (AuD). These intersecting loci reinforced the hypothesis that disorders with overlapping etiology group into a cluster of closely related genes within a whole genome molecular interaction network. We tested the hypothesis that “biological network proximity” within a whole genome molecular interaction network can be used to inform the search for multigene inheritance. Using a set of nine previously published genome wide association studies (GWAS) of AuD genes, we generated AuD-specific molecular interaction networks to identify networks of associated genes. We show that all nine “seed genes” can be connected within a 35-member network via interactions with 26 connecting genes. We show that this network is more connected than expected by chance, and 13 of the connecting genes showed association with multiple AuD upon GWAS reanalysis. Furthermore, we report association of SNPs in five new genes (IL10RA, DGKA, GRB2, STAT5A, and NFATC2) which were not previously considered as AuD candidates, and show significant association in novel disease samples of Crohn's disease and systemic lupus erythematosus. Furthermore, we show that the connecting genes show no association in four non-AuD GWAS. Finally, we test the connecting genes in psoriasis GWAS, and show association to previously identified loci and report new loci. These findings support the hypothesis that molecular interaction networks can be used to inform the search for multigene disease etiology, especially for disorders with overlapping etiology.
BibTeX:
@article{Kara2018,
  author = {Kara, Sam and Pirela-Morillo, Gerardo A. and Gilliam, Conrad T. and Wilson, George D.},
  title = {Identification of novel susceptibility genes associated with seven autoimmune disorders using whole genome molecular interaction networks},
  journal = {Journal of Autoimmunity},
  publisher = {Academic Press},
  year = {2018},
  url = {https://www.sciencedirect.com/science/article/pii/S0896841118305080},
  doi = {http://doi.org/10.1016/J.JAUT.2018.10.002}
}
Karmakar, P.C., Cho, Y.-J., Kim, Y.-H., Jung, S.-E., Jin, J.-H., Kim, B.-J., Kwon, W.-S., Kim, Y.-H., Pang, M.-G. and Ryu, B.-Y. Chemotherapeutic Drugs Alter Functional Properties and Proteome of Mouse Testicular Germ Cells in vitro 2018 Toxicological Sciences  article DOI URL 
BibTeX:
@article{Karmakar2018,
  author = {Karmakar, Polash Chandra and Cho, Yeon-Jin and Kim, Yong-Hee and Jung, Sang-Eun and Jin, Ju-Hee and Kim, Bang-Jin and Kwon, Woo-Sung and Kim, Young-Hyun and Pang, Myung-Geol and Ryu, Buom-Yong},
  title = {Chemotherapeutic Drugs Alter Functional Properties and Proteome of Mouse Testicular Germ Cells in vitro},
  journal = {Toxicological Sciences},
  year = {2018},
  url = {https://academic.oup.com/toxsci/advance-article/doi/10.1093/toxsci/kfy098/4992531},
  doi = {http://doi.org/10.1093/toxsci/kfy098}
}
Khalid ABDOUN1,*, E.S., Aly OKAB1, 2, M.A.-B., Mohamed EL-ZAREI3, Ali AL-SEAF3 and Ahmed AL-HAIDARY1 Correlation of blood triiodothyronine (T3) level with some production traits in male goat kids 2018   article URL 
Abstract: Abstract: Thyroid hormones are known for their stimulation of feed efficiency and growth performance in different farm animals. More interestingly, the level of thyroid hormones is influenced by selection for growth in some animal species. Therefore, it was the aim of the current study to investigate whether a correlation exists between the blood triiodothyronine (T3 ) level and some production traits (daily feed intake, average daily gain, and feed conversion ratio). To test this hypothesis, six male goat kids (21.9 ± 2.4 kg; 5 months old) belonging to Aardi, Damascus, and their cross breed (two kids from each genotype) were used in the current study. The obtained results revealed a positive linear correlation of plasma T3 level with both average daily feed intake and average daily gain with correlation coefficients of 99% and 97%, respectively (P ≤ 0.001). On the other hand, feed conversion ratio was negatively correlated to the plasma T3 level with a correlation coefficient of 81% (P = 0.05). The obtained results indicate the possible use of blood T3 level for the prediction of feed intake, daily body weight gain, and feed conversion ratio in addition to the possible use of blood T3 level as a criterion of breeding selection for growth performance in the future.
BibTeX:
@article{KhalidABDOUN1*2018,
  author = {Khalid ABDOUN1,*, Emad SAMARA1 and Aly OKAB1, 2, Mohamed AL-BADWI1 and Mohamed EL-ZAREI3 and Ali AL-SEAF3 and Ahmed AL-HAIDARY1},
  title = {Correlation of blood triiodothyronine (T3) level with some production traits in male goat kids},
  year = {2018},
  url = {file:///C:/Users/caoho/Desktop/vet-1705-6.pdf}
}
Khatun, A., Kang, K.-H., Ryu, D.-Y., Rahman, M.S., Kwon, W.-S. and Pang, M.-G. Effect of Aminopeptidase N on functions and fertility of mouse spermatozoa in vitro 2018 Theriogenology
Vol. 118, pp. 182-189 
article DOI URL 
Abstract: Aminopeptidase N (APN) is defined as a multifunctional enzyme, which regulate cellular physiology of a wide variety of cells in human. Earlier studies reported that mammalian semen shares this common enzyme as a major protein of seminal plasma that has correlation with male fertility, while the regulatory mechanisms of APN in spermatozoa are still far from being well understood. Present study was designed to investigate the role of APN in biological and chemical functions of spermatozoa using an in vitro antagonistic approach. Results showed that lower APN activity in sperm culture medium significantly increased sperm motility and the percentage of high speed spermatozoa and decreased the percentage of slow speed spermatozoa after a dose dependent inhibitor treatment (10, 100, and 1000 μM leuhistin) on epididymal mouse spermatozoa in a capacitating media for 90 min. Both 100 μM and 1000 μM decreased APN activity, while only 1000 μM decreased cell viability and increased PKA activity significantly compared to control. Nonetheless capacitation status, acrosome reaction status, and lactate dehydrogenase activity were not affected. Intriguingly, the treatment affected embryonic development through decreasing tyrosine phosphorylation of proteins and increasing reactive oxygen species levels. Further in silico analysis revealed associated regulatory proteins, which have critical functional role for male fertility.
BibTeX:
@article{Khatun2018,
  author = {Khatun, Amena and Kang, Kyu-Ho and Ryu, Do-Yeal and Rahman, Md Saidur and Kwon, Woo-Sung and Pang, Myung-Geol},
  title = {Effect of Aminopeptidase N on functions and fertility of mouse spermatozoa in vitro},
  journal = {Theriogenology},
  year = {2018},
  volume = {118},
  pages = {182--189},
  url = {https://linkinghub.elsevier.com/retrieve/pii/S0093691X1830342X},
  doi = {http://doi.org/10.1016/j.theriogenology.2018.06.005}
}
Kholghi Oskooei V., G.-F.S.O.M. A Combined Bioinformatics and Literature Based Approach for Identification of Long Non-cod ing RNAs That Modulate Vitamin D Receptor Signal ing in Breast 2018 Klinicka onkologie Journal  article DOI URL 
BibTeX:
@article{KholghiOskooeiV.2018,
  author = {Kholghi Oskooei V., Ghafouri-Fard S. Omrani MD},
  title = {A Combined Bioinformatics and Literature Based Approach for Identification of Long Non-cod ing RNAs That Modulate Vitamin D Receptor Signal ing in Breast},
  journal = {Klinicka onkologie Journal},
  year = {2018},
  url = {http://dx.doi.org/10.14735/amko2018264},
  doi = {http://doi.org/10.1093/annoc/mdw611}
}
Khudoshin, A. and Yuryev, A. Application of bioinformatics for biomarkers research, drug R&D and clinical practice 2018 Meta Gene
Vol. 17, pp. S15 
article DOI URL 
Abstract: Liver toxicity is a key reason why new drugs fail in clinical trials, or once they are in broader use. Drug-induced cholestasis is a common form of liver toxicity. Yet currently there is no model or test to predict which drugs may induce cholestasis in patients. This report demonstrate how bioinformatics approach on the example of using Elsevier's Pathway Studio® pathway analysis software can be used to create complex, predictive mechanistic models of biological processes, providing novel insights to researchers and helping them direct the course of their studies. The report will highlight application of bioinformatics and mechanistic models approach to biomarkers research. Presented examples include following: prediction of biomarkers based on reconstructed liver toxicity model, identification of new potential candidates for drug targets, identification of drug efficacy biomarkers or safety biomarkers and assessment of clinical biomarker specificity.
BibTeX:
@article{Khudoshin2018,
  author = {Khudoshin, Andrey and Yuryev, Anton},
  title = {Application of bioinformatics for biomarkers research, drug R&D and clinical practice},
  journal = {Meta Gene},
  publisher = {Elsevier},
  year = {2018},
  volume = {17},
  pages = {S15},
  url = {https://www.sciencedirect.com/science/article/pii/S2214540018301117},
  doi = {http://doi.org/10.1016/J.MGENE.2018.05.061}
}
Kopp, S., Sahana, J., Islam, T., Petersen, A.G., Bauer, J., Corydon, T.J., Schulz, H., Saar, K., Huebner, N., Slumstrup, L., Riwaldt, S., Wehland, M., Infanger, M., Luetzenberg, R. and Grimm, D. The role of NFκB in spheroid formation of human breast cancer cells cultured on the Random Positioning Machine 2018 Scientific Reports
Vol. 8(1), pp. 921 
article DOI URL 
Abstract: Human MCF-7 breast cancer cells were exposed to a Random Positioning Machine (RPM). After 24 hours (h) the cells grew either adherently within a monolayer (AD) or within multicellular spheroids (MCS). AD and MCS populations were separately harvested, their cellular differences were determined performing qPCR on genes, which were differently expressed in AD and MCS cells. Gene array technology was applied to detect RPM-sensitive genes in MCF-7 cells after 24 h. Furthermore, the capability to form multicellular spheroids in vitro was compared with the intracellular distribution of NF-kappaB (NFκB) p65. NFκB was equally distributed in static control cells, but predominantly localized in the cytoplasm in AD cells and nucleus in MCS cells exposed to the RPM. Gene array analyses revealed a more than 2-fold change of only 23 genes including some whose products are affected by oxygen levels or regulate glycolysis. Significant upregulations of the mRNAs of enzymes degrading heme, of ANXA1, ANXA2, CTGF, CAV2 and ICAM1, as well as of FAS, Casp8, BAX, p53, CYC1 and PARP1 were observed in MCS cells as compared with 1g-control and AD cells. An interaction analysis of 47 investigated genes suggested that HMOX-1 and NFκB variants are activated, when multicellular spheroids are formed.
BibTeX:
@article{Kopp2018,
  author = {Kopp, Sascha and Sahana, Jayashree and Islam, Tawhidul and Petersen, Asbjørn Graver and Bauer, Johann and Corydon, Thomas J. and Schulz, Herbert and Saar, Kathrin and Huebner, Norbert and Slumstrup, Lasse and Riwaldt, Stefan and Wehland, Markus and Infanger, Manfred and Luetzenberg, Ronald and Grimm, Daniela},
  title = {The role of NFκB in spheroid formation of human breast cancer cells cultured on the Random Positioning Machine},
  journal = {Scientific Reports},
  publisher = {Nature Publishing Group},
  year = {2018},
  volume = {8},
  number = {1},
  pages = {921},
  url = {http://www.nature.com/articles/s41598-017-18556-8},
  doi = {http://doi.org/10.1038/s41598-017-18556-8}
}
Laulederkind, S.J.F., Hayman, G.T., Wang, S.-J., Smith, J.R., Petri, V., Hoffman, M.J., De Pons, J., Tutaj, M.A., Ghiasvand, O., Tutaj, M., Thota, J., Dwinell, M.R. and Shimoyama, M. A Primer for the Rat Genome Database (RGD) 2018 , pp. 163-209  incollection DOI URL 
BibTeX:
@incollection{Laulederkind2018,
  author = {Laulederkind, Stanley J. F. and Hayman, G. Thomas and Wang, Shur-Jen and Smith, Jennifer R. and Petri, Victoria and Hoffman, Matthew J. and De Pons, Jeff and Tutaj, Marek A. and Ghiasvand, Omid and Tutaj, Monika and Thota, Jyothi and Dwinell, Melinda R. and Shimoyama, Mary},
  title = {A Primer for the Rat Genome Database (RGD)},
  publisher = {Humana Press, New York, NY},
  year = {2018},
  pages = {163--209},
  url = {http://link.springer.com/10.1007/978-1-4939-7737-68},
  doi = {http://doi.org/10.1007/978-1-4939-7737-6_8}
}
Lee, W., Lee, H.J., Jang, H.B., Kim, H.-J., Ban, H.-J., Kim, K.Y., Nam, M.S., Choi, J.S., Lee, K.-T., Cho, S.B., Park, S.I. and Lee, H.-J. Asymmetric dimethylarginine (ADMA) is identified as a potential biomarker of insulin resistance in skeletal muscle 2018 Scientific Reports
Vol. 8(1), pp. 2133 
article DOI URL 
Abstract: To unravel metabolic determinats of insulin resistance, we performed a targeted metabolomics analysis in Korean Children-Adolescent Cohort Study (KoCAS, n = 430). Sixty-seven metabolites were associated with insulin resistance in adolescents and the association also found in an adult population (KoGES, n = 2,485). Functional interactions of metabolites with gene/proteins using biological pathway with insulin resistance were not identified biological significance and regulatory effects of asymmetric dimethylarginine (ADMA). However, ADMA showed a higher association with adolescent obesity (P textless 0.001) and adult diabetes (P = 0.007) and decreased after obesity intervention program. Functional studies in cellular and mouse models demonstrated that an accumulation of ADMA is associated with the regulation of obesity-induced insulin resistance in skeletal muscle. ADMA treatment inhibited dimethylarginine-dimethylaminohydrolase (DDAH) activity and mRNA expression in insulin resistance muscle cell. Moreover, the treatment led to decrease of phosphorylation of insulin receptor (IR), AKT, and GLUT4 but increase of protein-tyrosine phosphatase 1B (PTP1B). Accordingly, increased ADMA significantly inhibited glucose uptake in myotube cell. We suggest that accumulation of ADMA is associated with modulation of insulin signaling and insulin resistance. ADMA might expand the possibilities of new therapeutic target for functional and clinical implications in the control of energy and metabolic homeostasis in humans.
BibTeX:
@article{Lee2018,
  author = {Lee, Woojung and Lee, Hyo Jung and Jang, Han Byul and Kim, Hyo-Jin and Ban, Hyo-Jeong and Kim, Kwang Youl and Nam, Moon Suk and Choi, Joo Sun and Lee, Kyung-Tae and Cho, Seong Beom and Park, Sang Ick and Lee, Hye-Ja},
  title = {Asymmetric dimethylarginine (ADMA) is identified as a potential biomarker of insulin resistance in skeletal muscle},
  journal = {Scientific Reports},
  publisher = {Nature Publishing Group},
  year = {2018},
  volume = {8},
  number = {1},
  pages = {2133},
  url = {http://www.nature.com/articles/s41598-018-20549-0},
  doi = {http://doi.org/10.1038/s41598-018-20549-0}
}
Li, Z., Li, W., Zha, J., Chen, H., Martyniuk, C.J. and Liang, X. Transcriptome analysis reveals benzotriazole ultraviolet stabilizers regulate networks related to inflammation in juvenile zebrafish ( textlessitextgreaterDanio reriotextless/itextgreater ) brain 2018 Environmental Toxicology  article DOI URL 
BibTeX:
@article{Li2018,
  author = {Li, Zhitong and Li, Wenjing and Zha, Jinmiao and Chen, Huihui and Martyniuk, Christopher J. and Liang, Xuefang},
  title = {Transcriptome analysis reveals benzotriazole ultraviolet stabilizers regulate networks related to inflammation in juvenile zebrafish ( textlessitextgreaterDanio reriotextless/itextgreater ) brain},
  journal = {Environmental Toxicology},
  publisher = {Wiley-Blackwell},
  year = {2018},
  url = {http://doi.wiley.com/10.1002/tox.22663},
  doi = {http://doi.org/10.1002/tox.22663}
}
Li, Z., Xiong, Z., Manor, L.C., Cao, H. and Li, T. Integrative computational evaluation of genetic markers for Alzheimer's disease 2018 Saudi Journal of Biological Sciences  article DOI URL 
Abstract: Recent studies have reported hundreds of genes linked to Alzheimer's Disease (AD). However, many of these candidate genes may be not identified in different studies when analyses were replicated. Moreover, results could be controversial. Here, we proposed a computational workflow to curate and evaluate AD related genes. The method integrates large scale literature knowledge data and gene expression data that were acquired from postmortem human brain regions (AD case/control: 31/32 and 22/8). Pathway Enrichment, Sub-Network Enrichment, and Gene-Gene Interaction analysis were conducted to study the pathogenic profile of the candidate genes, with 4 metrics proposed and validated for each gene. By using our approach, a scalable AD genetic database was developed, including AD related genes, pathways, diseases and info of supporting references. The AD case/control classification supported the effectiveness of the 4 proposed metrics, which successfully identified 21 well-studied AD genes (i.g. TGFB1, CTNNB1, APP, IL1B, PSEN1, PTGS2, IL6, VEGFA, SOD1, AKT1, CDK5, TNF, GSK3B, TP53, CCL2, BDNF, NGF, IGF1, SIRT1, AGER and TLR) and highlighted one recently reported AD gene (i.g. ITGB1). The computational biology approach and the AD database developed in this study provide a valuable resource which may facilitate the understanding of the AD genetic profile.
BibTeX:
@article{Li2018a,
  author = {Li, Zhe and Xiong, ZhenZhen and Manor, Lydia C. and Cao, Hongbao and Li, Tao},
  title = {Integrative computational evaluation of genetic markers for Alzheimer's disease},
  journal = {Saudi Journal of Biological Sciences},
  year = {2018},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S1319562X1830130X},
  doi = {http://doi.org/10.1016/j.sjbs.2018.05.019}
}
Liang, X., Feswick, A., Simmons, D. and Martyniuk, C.J. Reprint of: Environmental toxicology and omics: A question of sex 2018 Journal of Proteomics  article DOI URL 
Abstract: Molecular initiating events and downstream transcriptional/proteomic responses provide valuable information for adverse outcome pathways, which can be used predict the effects of chemicals on physiological systems. There has been a paucity of research that addresses sex-specific expression profiling in toxicology and due to cost, time, and logistic considerations, sex as a variable has not been widely considered. In response to this deficiency, federal agencies in the United States, Canada, and Europe have highlighted the importance of including sex as a variable in scientific investigations. Using case studies from both aquatic and mammalian toxicology, we report that there can be less than ˜20–25% consensus in how the transcriptome and proteome of each sex responds to chemicals. Chemicals that have been shown to elicit sex-specific responses in the transcriptome or proteome include pharmaceuticals, anti-fouling agents, anticorrosive agents, and fungicides, among others. Sex-specific responses in the transcriptome and proteome are not isolated to whole animals, as investigations demonstrate that primary cell cultures isolated from each sex responds differently to toxicants. This signifies that sex is important, even in cell lines. Sex has significant implications for predictive toxicology, and both male and female data are required to improve robustness of adverse outcome pathways.

BIOLOGICAL SIGNIFICANCE
Clinical toxicology recognizes that sex is an important variable, as pharmacokinetics (ADME; absorption, distribution, metabolism, and excretion) can differ between females and males. However, few studies in toxicology have explored the implication of sex in relation to the transcriptome and proteome of whole organisms. High-throughput molecular approaches are becoming more frequently applied in toxicity screens (e.g. pre-clinical experiments, fish embryos, cell lines, synthetic tissues) and such data are expected to build upon reporter-based cell assays (e.g. receptor activation, enzyme inhibition) used in toxicant screening programs (i.e. Tox21, ToxCast, REACH). Thus, computational models can more accurately predict the diversity of adverse effects that can occur from chemical exposure within the biological system. Our studies and those synthesized from the literature suggest that the transcriptome and proteome of females and males respond quite differentially to chemicals. This has significant implications for predicting adverse effects in one sex when using molecular data generated in the other sex. While molecular initiating events are not expected to differ dramatically between females and males (i.e. an estrogen binds estrogen receptors in both sexes), it is important to acknowledge that the downstream transcriptomic and proteomic responses can differ based upon the presence/absence of co-regulators and inherent sex-specific variability in regulation of transcriptional and translational machinery. Transcriptomic and proteomic studies also reveal that cell processes affected by chemicals can differ due to sex, and this can undoubtedly lead to sex-specific physiological responses.
BibTeX:
@article{Liang2018,
  author = {Liang, Xuefang and Feswick, April and Simmons, Denina and Martyniuk, Christopher J.},
  title = {Reprint of: Environmental toxicology and omics: A question of sex},
  journal = {Journal of Proteomics},
  publisher = {Elsevier},
  year = {2018},
  url = {https://www.sciencedirect.com/science/article/pii/S1874391918301131?via%3Dihub},
  doi = {http://doi.org/10.1016/J.JPROT.2018.03.018}
}
Liu, Y., Tong, J., Tong, Y., Li, P., Cui, X. and Cao, H. In vitro anti-influenza virus effect of total flavonoid from Trollius ledebouri Reichb 2018 Journal of International Medical Research, pp. 030006051775028  article DOI URL 
Abstract: ObjectiveTo investigate the in vitro antivirus effect of total flavonoid from Trollius ledebouri Reichb (TFTLR).MethodsMadin-Darby canine kidney (MDCK) and Human epithelial type 2 (HEp-2) cell lines were used to test the antivirus effect of TFTLR on nine virus subtypes: four H1N1, one H3N2, and four other subtypes prevalent in North China. Tamiflu, Ribavirin and Lianhua Qingwen were used as active comparators. Comprehensive molecular pathway analyses of TFTLR-H1N1 and TFTLR-H3N2 relationships were also conducted.ResultsTFTLR inhibited MDCK cell lesions induced by H1N1 subtypes (A/FM1/1/47, A/Puerto Rico/8/1934 H1N1, A1/Tianjin Jinnan/15/2009, and A/Brisbane/59/2007) and by the H3N2 Brisbane/10/2009 strain. TFTLR inhibitory concentration (IC)50 values against these viruses were 0.13, 0.07, 0.06, 0.14, and 0.07 mg/ml, respectively; and therapeutic index (TI) values were 8.62, 16.0, 18.67, 8.0, and 16.0, respectively. TFTLR showed no effect on parainfluenza virus type 1, herpes simplex virus type 1, respirat...
BibTeX:
@article{Liu2018,
  author = {Liu, Yongping and Tong, Jiming and Tong, Ying and Li, Ping and Cui, Xiaolan and Cao, Hongbao},
  title = {In vitro anti-influenza virus effect of total flavonoid from Trollius ledebouri Reichb},
  journal = {Journal of International Medical Research},
  publisher = {SAGE PublicationsSage UK: London, England},
  year = {2018},
  pages = {030006051775028},
  url = {http://journals.sagepub.com/doi/10.1177/0300060517750284},
  doi = {http://doi.org/10.1177/0300060517750284}
}
Lützenberg, R., Solano, K., Buken, C., Sahana, J., Riwaldt, S., Kopp, S., Krüger, M., Schulz, H., Saar, K., Huebner, N., Hemmersbach, R., Bauer, J., Infanger, M., Grimm, D. and Wehland, M. Pathway Analysis Hints Towards Beneficial Effects of Long-Term Vibration on Human Chondrocytes. 2018 Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Vol. 47(4), pp. 1729-1741 
article DOI URL 
Abstract: BACKGROUND/AIMS Spaceflight negatively influences the function of cartilage tissue in vivo. In vitro human chondrocytes exhibit an altered gene expression of inflammation markers after a two-hour exposure to vibration. Little is known about the impact of long-term vibration on chondrocytes. METHODS Human cartilage cells were exposed for up to 24 h (VIB) on a specialised vibration platform (Vibraplex) simulating the vibration profile which occurs during parabolic flights and compared to static control conditions (CON). Afterwards, they were investigated by phase-contrast microscopy, rhodamine phalloidin staining, microarray analysis, qPCR and western blot analysis. RESULTS Morphological investigations revealed no changes between CON and VIB chondrocytes. F-Actin staining showed no alterations of the cytoskeleton in VIB compared with CON cells. DAPI and TUNEL staining did not identify apoptotic cells. ICAM-1 was elevated and vimentin, beta-tubulin and osteopontin proteins were significantly reduced in VIB compared to CON cells. qPCR of cytoskeletal genes, ITGB1, SOX3, SOX5, SOX9 did not reveal differential regulations. Microarray analysis detected 13 differentially expressed genes, mostly indicating unspecific stimulations. Pathway analyses demonstrated interactions of PSMD4 and CNOT7 with ICAM. CONCLUSIONS Long-term vibration did not damage human chondrocytes in vitro. The reduction of osteopontin protein and the down-regulation of PSMD4 and TBX15 gene expression suggest that in vitro long-term vibration might even positively influence cultured chondrocytes.
BibTeX:
@article{Lutzenberg2018,
  author = {Lützenberg, Ronald and Solano, Kendrick and Buken, Christoph and Sahana, Jayashree and Riwaldt, Stefan and Kopp, Sascha and Krüger, Marcus and Schulz, Herbert and Saar, Kathrin and Huebner, Norbert and Hemmersbach, Ruth and Bauer, Johann and Infanger, Manfred and Grimm, Daniela and Wehland, Markus},
  title = {Pathway Analysis Hints Towards Beneficial Effects of Long-Term Vibration on Human Chondrocytes.},
  journal = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology},
  publisher = {Karger Publishers},
  year = {2018},
  volume = {47},
  number = {4},
  pages = {1729--1741},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/29949789},
  doi = {http://doi.org/10.1159/000491006}
}
McKee, C., Beeravolu, N., Bakshi, S., Thibodeau, B., Wilson, G., Perez-Cruet, M. and Rasul Chaudhry, G. Cytotoxicity of radiocontrast dyes in human umbilical cord mesenchymal stem cells 2018 Toxicology and Applied Pharmacology  article DOI URL 
Abstract: Radiocontrast dyes are used for a wide range of diagnostic procedures for enhancing the image of anatomical structures, pain targets, and vascular uptake. While some of these dyes show toxicity to primary cells, their effect on stem cells, particularly mesenchymal stem cells (MSCs), is unknown. This study investigates the cytotoxic effects of two clinically used radiocontrast dyes, iohexol and iopamidol, on bone marrow and human umbilical cord MSCs. Exposure to these dyes significantly affected morphology of MSCs from both sources, as treated cells appeared transparent and no longer fibroblastoid. Cell viability decreased as determined by trypan blue and Annexin-V/PI staining, in a dose dependent manner with simultaneous loss of CD90 and CD105 concurrent with spontaneous differentiation in MSCs treated with iohexol and iopamidol. In addition, significantly higher cell death was observed in MSCs exposed to iopamidol than iohexol. At a concentration of 1:1, iohexol and iopamidol induced apoptosis in 19% and 92% (textless.01) of MSCs, respectively. Global transcriptome analysis of treated MSCs revealed 139 and 384 differentially expressed genes in iohexol vs control and iopamidol vs control at p ≤ .01 and 1.5-fold, respectively. This suggested that iopamidol had more significant effect on the transcription of MSCs. Based on these results a molecular mechanism of radiocontast dye induced cell death via intrinsic apoptosis pathway mediated by p53 was proposed. Since iopamidol was significantly more toxic than iohexol in human MSCs, a more careful examination of safety of radiocontrast dyes for clinical use is warranted.
BibTeX:
@article{McKee2018,
  author = {McKee, Christina and Beeravolu, Naimisha and Bakshi, Shreeya and Thibodeau, Bryan and Wilson, George and Perez-Cruet, Mick and Rasul Chaudhry, G.},
  title = {Cytotoxicity of radiocontrast dyes in human umbilical cord mesenchymal stem cells},
  journal = {Toxicology and Applied Pharmacology},
  publisher = {Academic Press},
  year = {2018},
  url = {https://www.sciencedirect.com/science/article/pii/S0041008X18301765},
  doi = {http://doi.org/10.1016/J.TAAP.2018.04.032}
}
Mehta, A. and Hasija, Y. Bioinformatics Approaches for Genomics and Post Genomics Applications of Anticancer Plants 2018 Anticancer Plants: Mechanisms and Molecular Interactions, pp. 283-317  incollection DOI URL 
BibTeX:
@incollection{Mehta2018,
  author = {Mehta, Avni and Hasija, Yasha},
  title = {Bioinformatics Approaches for Genomics and Post Genomics Applications of Anticancer Plants},
  booktitle = {Anticancer Plants: Mechanisms and Molecular Interactions},
  publisher = {Springer Singapore},
  year = {2018},
  pages = {283--317},
  url = {http://link.springer.com/10.1007/978-981-10-8417-112},
  doi = {http://doi.org/10.1007/978-981-10-8417-1_12}
}
Mel'nik, N., Komarov, N. and Tambovtseva О.М., C.S.A.L.M.(R.F. Digital technologies in the service of biological science 2018 Vestnik of the Russian Agricultural Science  article URL 
BibTeX:
@article{Melnik2018,
  author = {Mel'nik, N.N. and Komarov, N.G. and Tambovtseva, О.М., Central Scientific Agricultural Library, Moscow (Russian Federation)},
  title = {Digital technologies in the service of biological science},
  journal = {Vestnik of the Russian Agricultural Science},
  year = {2018},
  url = {http://agris.fao.org/agris-search/search.do?recordID=RU2018001277}
}
Oh, J.-H., Lee, Y.-J., Byeon, E.-J., Kang, B.-C., Kyeoung, D.-S. and Kim, C.-K. Whole-genome resequencing and transcriptomic analysis of genes regulating anthocyanin biosynthesis in black rice plants 2018 3 Biotech
Vol. 8(2), pp. 115 
article DOI URL 
BibTeX:
@article{Oh2018,
  author = {Oh, Jae-Hyeon and Lee, Ye-Ji and Byeon, Eun-Ju and Kang, Byeong-Chul and Kyeoung, Dong-Soo and Kim, Chang-Kug},
  title = {Whole-genome resequencing and transcriptomic analysis of genes regulating anthocyanin biosynthesis in black rice plants},
  journal = {3 Biotech},
  publisher = {Springer Berlin Heidelberg},
  year = {2018},
  volume = {8},
  number = {2},
  pages = {115},
  url = {http://link.springer.com/10.1007/s13205-018-1140-3},
  doi = {http://doi.org/10.1007/s13205-018-1140-3}
}
Onishi, M., Yamanaka, K., Miyamoto, Y., Waki, H. and Gouraud, S.S. Trpv4 involvement in the gender differences in blood pressure regulation in spontaneously hypertensive rats. 2018 Physiological Genomics, pp. physiolgenomics.00096.2017  article DOI URL 
Abstract: Arterial pressure (AP) is lower in pre-menopausal women than in men of a similar age. Pre-menopausal women exhibit a lower sympathetic outflow and a greater baroreceptor reflex; however, mechanisms for the gender differences in blood pressure regulation are still not well understood. We hypothesized that different neuronal functions in the cardiovascular centers in the brains of men and women could contribute to the gender difference in cardiovascular homeostasis. Our previous studies on male spontaneously hypertensive rats (SHRs) and their normotensive counterparts, Wistar Kyoto (WKY) rats, revealed that the gene expression profile of the nucleus tractus solitarius (NTS), a pivotal region of the medulla oblongata for regulating the set-point of AP, is strongly associated with the AP level. Thus, we hypothesized that gene expression profiles in the rat NTS are related to gender differences in AP regulation. Since female SHRs clearly exhibit lower AP levels than their male counterparts at a similar age, we...
BibTeX:
@article{Onishi2018,
  author = {Onishi, Makiko and Yamanaka, Ko and Miyamoto, Yasunori and Waki, Hidefumi and Gouraud, Sabine S},
  title = {Trpv4 involvement in the gender differences in blood pressure regulation in spontaneously hypertensive rats.},
  journal = {Physiological Genomics},
  publisher = { American Physiological Society Bethesda, MD },
  year = {2018},
  pages = {physiolgenomics.00096.2017},
  url = {http://www.physiology.org/doi/10.1152/physiolgenomics.00096.2017},
  doi = {http://doi.org/10.1152/physiolgenomics.00096.2017}
}
Reznik, A., Plotnikova, O., Skvortsov, A., Skoblov, M., Reznik, O. and Baranova, A. Reperfusion Activates AP-1 and Heat Shock Response in Donor Kidney Parenchyma after Warm Ischemia 2018 BioMed Research International
Vol. 2018, pp. 1-9 
article DOI URL 
Abstract: textlessptextgreater Utilization of kidneys from extended criteria donors leads to an increase in average warm ischemia time (WIT), which is associated with larger degrees of ischemia-reperfusion injury (IRI). Kidney resuscitation by extracorporeal perfusion in situ allows up to 60 minutes of asystole after the circulatory death. Molecular studies of kidney grafts from human donors with critically expanded WIT are warranted. Transcriptomes of two human kidneys from two different donors were profiled after 35-45 minutes of WIT and after 120 minutes of normothermic perfusion and compared. Baseline gene expression patterns in ischemic grafts display substantial intrinsic differences. IRI does not lead to substantial change in overall transcription landscape but activates a highly connected protein network with hubs centered on Jun/Fos/ATF transcription factors and HSP1A/HSPA5 heat shock proteins. This response is regulated by positive feedback. IRI networks are enriched in soluble proteins and biofluids assayable substances, thus, indicating feasibility of the longitudinal, minimally invasive assessment textlessitalictextgreaterin vivotextless/italictextgreater . Mapping of IRI related molecules in ischemic and reperfused kidneys provides a rationale for possible organ conditioning during machine assisted ex vivo normothermic perfusion. A study of natural diversity of the transcriptional landscapes in presumably normal, transplantation-suitable human organs is warranted. textless/ptextgreater
BibTeX:
@article{Reznik2018,
  author = {Reznik, Alexandr and Plotnikova, Olga and Skvortsov, Andrey and Skoblov, Mikhail and Reznik, Oleg and Baranova, Ancha},
  title = {Reperfusion Activates AP-1 and Heat Shock Response in Donor Kidney Parenchyma after Warm Ischemia},
  journal = {BioMed Research International},
  publisher = {Hindawi},
  year = {2018},
  volume = {2018},
  pages = {1--9},
  url = {https://www.hindawi.com/journals/bmri/2018/5717913/},
  doi = {http://doi.org/10.1155/2018/5717913}
}
Sadkowski, T., Ciecierska, A., Oprzadek, J. and Balcerek, E. Breed-dependent microRNA expression in the primary culture of skeletal muscle cells subjected to myogenic differentiation 2018 BMC Genomics
Vol. 19(1), pp. 109 
article DOI URL 
Abstract: Skeletal muscle in livestock develops into meat, an important source of protein and other nutrients for human consumption. The muscle is largely composed of a fixed number of multinucleated myofibers determined during late gestation and remains constant postnatally. A population of postnatal muscle stem cells, called satellite cells, gives rise to myoblast cells that can fuse with the existing myofibers, thus increasing their size. This requires a delicate balance of transcription and growth factors and specific microRNA (miRNA) expressed by satellite cells and their supporting cells from the muscle stem cell niche. The role of transcription and growth factors in bovine myogenesis is well-characterized; however, very little is known about the miRNA activity during this process. We have hypothesized that the expression of miRNA can vary between primary cultures of skeletal muscle cells isolated from the semitendinosus muscles of different cattle breeds and subjected to myogenic differentiation. After a 6-day myogenic differentiation of cells isolated from the muscles of the examined cattle breeds, we found statistically significant differences in the number of myotubes between Hereford (HER)/Limousine (LIM) beef breeds and the Holstein-Friesian (HF) dairy breed (p ≤ 0.001). The microarray analysis revealed differences in the expression of 23 miRNA among the aforementioned primary cultures. On the basis of a functional analysis, we assigned 9 miRNA as molecules responsible for differentiation progression (miR-1, -128a, -133a, -133b, -139, -206, -222, -486, and -503). The target gene prediction and functional analysis revealed 59 miRNA-related genes belonging to the muscle organ development process. The number of myotubes and the miRNA expression in the primary cultures of skeletal muscle cells derived from the semitendinosus muscles of the HER/LIM beef cattle breeds and the HF dairy breed vary when cells are subjected to myogenic differentiation. The net effect of the identified miRNA and their target gene action should be considered the result of the breed-dependent activity of satellite cells and muscle stem cell niche cells and their mutual interactions, which putatively can be engaged in the formation of a larger number of myotubes in beef cattle-related cells (HER/LIM) during in vitro myogenesis.
BibTeX:
@article{Sadkowski2018,
  author = {Sadkowski, Tomasz and Ciecierska, Anna and Oprzadek, Jolanta and Balcerek, Edyta},
  title = {Breed-dependent microRNA expression in the primary culture of skeletal muscle cells subjected to myogenic differentiation},
  journal = {BMC Genomics},
  publisher = {BioMed Central},
  year = {2018},
  volume = {19},
  number = {1},
  pages = {109},
  url = {https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-018-4492-5},
  doi = {http://doi.org/10.1186/s12864-018-4492-5}
}
Samuel I. Anyanwu1, Akins Doherty1, Michael D. Powell1, Chamberlain Obialo2, Ming B. Huang1, Alexander, Quarshie3, Claudette Mitchell1, Khalid Bashir2 and and Gale W. Newman1 Detection of HIV-1 and human proteins in urinary extracellular vesicles from HIV+ patients 2018 Advances in Virology  article URL 
Abstract: Background: Extracellular vesicles (EVs) are membrane bound, secreted by cells, detected in bodily fluids, including urine, and contain proteins, RNA, and DNA. Our goal was to identify HIV and human proteins (HP) in urinary EVs from HIV+ patients and compare them to HIV- samples. Methods: Urine samples were collected from HIV+ (n=35) and HIV- individuals (n=12). EVs were isolated by ultrafiltration, characterized using transmission electron microscopy, tandem mass spectrometry (LC/MS/MS), and nanoparticle tracking analysis (NTA). Western blots confirmed the presence of HIV proteins. Gene ontology (GO) analysis was performed using FunRich and HIV Human Interaction database (HHID). Results: EVs from urine were 30-400 nm in size. More EVs were in HIV+ patients, Ptextless0.05, by NTA. HIV+ samples had 14,475, HPs using LC/MS/MS while only 111 were in HIV-. HPs in the EVs were of exosomal origin. LC/MS/MS showed all HIV+ samples contained at least one HIV protein. GO analysis showed differences in proteins between HIV+ and HIV- samples and more than 50% of the published HPs in the HHID interacted with EV HIV proteins. Conclusion: Differences in the proteomic profile of EVs from HIV+ versus HIV- samples were found. HIV and HPs in EVs could be used to detect infection and/or diagnose HIV disease syndromes
BibTeX:
@article{SamuelI.Anyanwu1,
  author = {Samuel I. Anyanwu1 and Akins Doherty1 and Michael D. Powell1 and Chamberlain Obialo2 and Ming B. Huang1 and Alexander and Quarshie3 and Claudette Mitchell1 and Khalid Bashir2 and and Gale W. Newman1},
  title = {Detection of HIV-1 and human proteins in urinary extracellular vesicles from HIV+ patients},
  journal = {Advances in Virology},
  year = {2018},
  url = {https://doi.org/10.1155/2018/7863412}
}
Sani, N.F.A., Damanhuri, M.H.A., Hamzah, A.I.Z.A., Bakar, Z.H.A., Kit, T.J., Aripin, K.N.N., Rani, M.D.M., Noh, N.A., Shamaan, N.A., Razali, R., Mazlan, M., Yusof, Y.A.M., Makpol, S. and Ngah, a.Z.W. Peripheral Blood Gene Microarray Reveals Inflammation and Signal Transduction Pathway is Associated with Cognitive Decline in Normal Ageing 2018 PROSIDING SEMINAR NASIONAL & INTERNASIONAL
Vol. 1(1) 
article URL 
Abstract: Background Declined cognitive function during ageing is multi-factorial and gene expression changes are one of the factors influencing this trajectory event in the absence of neurodegenerative disease. Identifying these genes and biological processes involved in this study would explain certain individuals resilient to the age-related cognitive decline. Methods A cross sectional study was carried out on 160 Malay healthy subjects aged between 28 – 68 years old who were recruited after screening 1768 volunteers around Selangor and Klang Valley. Out of that, 72 subjects were included for microarray study who were divided into four groups according to their age. They were further divided into normal cognitive (NC) (scoretextgreater24) and impaired cognitive (IC) (score textless24) groups based on Montreal Cognitive Assessment (MoCA). Blood samples for total RNA extraction were collected and gene expression analysis was performed by using Illumina HT-12 Bead Chips. Partek Genomic software was used to perform gene expression profiling analysis and the overrepresentation of genes expression was analysed further to identify altered pathway by using Pathway Studio.  Results Transcriptomic data revealed that gene expression pattern in subjects with cognitive impairment have a unique molecular state from normal cognitive aging at early age of 30. Most of the top differentially expressed genes in group G30IC vs G30N were upregulated while most of the top genes in group G60IC vs G60N were downregulated. Subjects with cognitive impairment exhibited prominent upregulation in the expression of genes associated with inflammation, ion channel activity, ion utilization and oxidative stress while decreased expression of several genes involved in DNA repair, signal transduction and synaptic transmission. Conclusion In conclusion, our data revealed that there is an incidence of about 21.88% of the Malay population with cognitive decline as corresponding molecular alteration that classifies normal cognitive and cognitive impairment subjects. Keywords Peripheral blood, microarray, inflammation, signalling pathway, cognitive decline
BibTeX:
@article{Sani2018,
  author = {Sani, Nur Fathiah Abdul and Damanhuri, Mohd Hanafi Ahmad and Hamzah, Ahmad Imran Zaydi Amir and Bakar, Zulzikry Hafiz Abu and Kit, Tan Jen and Aripin, Khairun Nain Nor and Rani, Mohd Dzulkhairi Mohd and Noh, Nor Azila and Shamaan, Nor Aripin and Razali, Rosdinom and Mazlan, Musalmah and Yusof, Yasmin Anum Mohd and Makpol, Suzana and Ngah, an Zurinah Wan},
  title = {Peripheral Blood Gene Microarray Reveals Inflammation and Signal Transduction Pathway is Associated with Cognitive Decline in Normal Ageing},
  journal = {PROSIDING SEMINAR NASIONAL & INTERNASIONAL},
  year = {2018},
  volume = {1},
  number = {1},
  url = {https://jurnal.unimus.ac.id/index.php/psn12012010/article/view/3796}
}
Shamloo-Dashtpagerdi, R., Razi, H., Ebrahimie, E. and Niazi, A. Molecular characterization of Brassica napus stress related transcription factors, BnMYB44 and BnVIP1, selected based on comparative analysis of Arabidopsis thaliana and Eutrema salsugineum transcriptomes 2018 Molecular Biology Reports, pp. 1-14  article DOI URL 
BibTeX:
@article{Shamloo-Dashtpagerdi2018,
  author = {Shamloo-Dashtpagerdi, Roohollah and Razi, Hooman and Ebrahimie, Esmaeil and Niazi, Ali},
  title = {Molecular characterization of Brassica napus stress related transcription factors, BnMYB44 and BnVIP1, selected based on comparative analysis of Arabidopsis thaliana and Eutrema salsugineum transcriptomes},
  journal = {Molecular Biology Reports},
  publisher = {Springer Netherlands},
  year = {2018},
  pages = {1--14},
  url = {http://link.springer.com/10.1007/s11033-018-4262-0},
  doi = {http://doi.org/10.1007/s11033-018-4262-0}
}
Shiri, Y., Solouki, M., Ebrahimie, E., Emamjomeh, A. and Zahiri, J. Unraveling the Transcriptional Complexity of Compactness in Sistan Grape Cluster 2018 Plant Science  article DOI URL 
Abstract: Yaghooti grape of Sistan is the earliest ripening grape in Iran, harvested every May annually. It is adapted to dry conditions in Sistan region and its water requirement is less than the other grape cultivars. The transcriptional complexity of this grape was studied in three stages of cluster development. Totally, 24121 genes were expressed in different cluster development steps (step 1: cluster formation, step 2: berry formation, step 3: final size of cluster) of which 3040 genes in the first stage, 2381 genes in the second stage and 2400 genes in the third stage showed a significant increase in expression. GO analysis showed that when the clusters are ripening, the activity of the nucleus, cytoplasmic, cytosol, membrane and chloroplast genes in the cluster architecture cells decreases. In contrast, the activity of the endoplasmic reticulum, vacuole and extracellular region genes enhances. When Yaghooti grape is growing and developing, some of metabolic pathways were activated in the response to biotic and abiotic stresses. Gene co-expression network reconstruction showed that AGAMOUS is a key gene in compactness of Sistan grape cluster, because it influences on expression of GA gene which leads to increase cluster length and berries size.
BibTeX:
@article{Shiri2018,
  author = {Shiri, Yasoub and Solouki, Mahmood and Ebrahimie, Esmaeil and Emamjomeh, Abbasali and Zahiri, Javad},
  title = {Unraveling the Transcriptional Complexity of Compactness in Sistan Grape Cluster},
  journal = {Plant Science},
  year = {2018},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S0168945217309469},
  doi = {http://doi.org/10.1016/j.plantsci.2018.02.011}
}
Smith, L.C., Lavelle, C.M., Silva-Sanchez, C., Denslow, N.D. and Sabo-Attwood, T. Early phosphoproteomic changes for adverse outcome pathway development in the fathead minnow (Pimephales promelas) brain 2018 Scientific Reports
Vol. 8(1), pp. 10212 
article DOI URL 
Abstract: Adverse outcome pathways (AOPs) are conceptual frameworks that organize and link contaminant-induced mechanistic molecular changes to adverse biological responses at the individual and population level. AOPs leverage molecular and high content mechanistic information for regulatory decision-making, but most current AOPs for hormonally active agents (HAAs) focus on nuclear receptor-mediated effects only despite the overwhelming evidence that HAAs also activate membrane receptors. Activation of membrane receptors triggers non-genomic signaling cascades often transduced by protein phosphorylation leading to phenotypic changes. We utilized label-free LC-MS/MS to identify proteins differentially phosphorylated in the brain of fathead minnows (Pimephales promelas) aqueously exposed for 30 minutes to two HAAs, 17α-ethinylestradiol (EE2), a strong estrogenic substance, and levonorgestrel (LNG), a progestin, both components of the birth control pill. EE2 promoted differential phosphorylation of proteins involved in neuronal processes such as nervous system development, synaptic transmission, and neuroprotection, while LNG induced differential phosphorylation of proteins involved in axon cargo transport and calcium ion homeostasis. EE2 and LNG caused similar enrichment of synaptic plasticity and neurogenesis. This study is the first to identify molecular changes in vivo in fish after short-term exposure and highlights transduction of rapid signaling mechanisms as targets of HAAs, in addition to nuclear receptor-mediated pathways.
BibTeX:
@article{Smith2018,
  author = {Smith, L. C. and Lavelle, C. M. and Silva-Sanchez, C. and Denslow, N. D. and Sabo-Attwood, T.},
  title = {Early phosphoproteomic changes for adverse outcome pathway development in the fathead minnow (Pimephales promelas) brain},
  journal = {Scientific Reports},
  publisher = {Nature Publishing Group},
  year = {2018},
  volume = {8},
  number = {1},
  pages = {10212},
  url = {http://www.nature.com/articles/s41598-018-28395-w},
  doi = {http://doi.org/10.1038/s41598-018-28395-w}
}
Sproll, P., Eid, W., Gomes, C.R., Mendonca, B.B., Gomes, N.L., M-F Costa, E., Biason-Lauber, A. and Paulo, S. Assembling the jigsaw puzzle: CBX2 isoform 2 and its targets in disorders/differences of sex development 2018   article DOI URL 
Abstract: Background: One of the defining moments of human life occurs early during embryonic development, when individuals sexually differentiate into either male or female. Perturbation of this process can lead to disorders/differences of sex
BibTeX:
@article{Sproll2018,
  author = {Sproll, Patrick and Eid, Wassim and Gomes, Camila R and Mendonca, Berenice B and Gomes, Nathalia L and M-F Costa, Elaine and Biason-Lauber, Anna and Paulo, Sao},
  title = {Assembling the jigsaw puzzle: CBX2 isoform 2 and its targets in disorders/differences of sex development},
  year = {2018},
  url = {https://onlinelibrary.wiley.com/doi/pdf/10.1002/mgg3.445},
  doi = {http://doi.org/10.1002/mgg3.445}
}
Sternlicht, M.D., Wirkner, U., Bickelhaupt, S., Lopez Perez, R., Tietz, A., Lipson, K.E., Seeley, T.W. and Huber, P.E. Radiation-induced pulmonary gene expression changes are attenuated by the CTGF antibody Pamrevlumab 2018 Respiratory Research
Vol. 19(1), pp. 14 
article DOI URL 
Abstract: Fibrosis is a delayed side effect of radiation therapy (RT). Connective tissue growth factor (CTGF) promotes the development of fibrosis in multiple settings, including pulmonary radiation injury. To better understand the cellular interactions involved in RT-induced lung injury and the role of CTGF in these responses, microarray expression profiling was performed on lungs of irradiated and non-irradiated mice, including mice treated with the anti-CTGF antibody pamrevlumab (FG-3019). Between group comparisons (Welch's t-tests) and principal components analyses were performed in Genespring. At the mRNA level, the ability of pamrevlumab to prolong survival and ameliorate RT-induced radiologic, histologic and functional lung deficits was correlated with the reversal of a clear enrichment in mast cell, macrophage, dendritic cell and mesenchymal gene signatures. Cytokine, growth factor and matrix remodeling genes that are likely to contribute to RT pneumonitis and fibrosis were elevated by RT and attenuated by pamrevlumab, and likely contribute to the cross-talk between enriched cell-types in injured lung. CTGF inhibition had a normalizing effect on select cell-types, including immune cells not typically regarded as being regulated by CTGF. These results suggest that interactions between RT-recruited cell-types are critical to maintaining the injured state; that CTGF plays a key role in this process; and that pamrevlumab can ameliorate RT-induced lung injury in mice and may provide therapeutic benefit in other immune and fibrotic disorders.
BibTeX:
@article{Sternlicht2018,
  author = {Sternlicht, Mark D. and Wirkner, Ute and Bickelhaupt, Sebastian and Lopez Perez, Ramon and Tietz, Alexandra and Lipson, Kenneth E. and Seeley, Todd W. and Huber, Peter E.},
  title = {Radiation-induced pulmonary gene expression changes are attenuated by the CTGF antibody Pamrevlumab},
  journal = {Respiratory Research},
  publisher = {BioMed Central},
  year = {2018},
  volume = {19},
  number = {1},
  pages = {14},
  url = {https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-018-0720-4},
  doi = {http://doi.org/10.1186/s12931-018-0720-4}
}
Terawaki, K., Kashiwase, Y., Uzu, M., Nonaka, M., Sawada, Y., Miyano, K., Higami, Y., Yanagihara, K., Yamamoto, M. and Uezono, Y. Leukemia inhibitory factor via the Toll-like receptor 5 signaling pathway involves aggravation of cachexia induced by human gastric cancer-derived 85As2 cells in rats. 2018 Oncotarget
Vol. 9(78), pp. 34748-34764 
article DOI URL 
Abstract: Cancer cachexia is highly prevalent in gastric cancer patients and characterized by decreased food consumption and body weight. We previously created a rat model of cancer cachexia using MKN45cl85 and 85As2 cells derived from human gastric cancer. The 85As2 cells induced cachexia more potently compared to MKN45cl85 cells. To clarify the mechanism underlying the difference in the cachexia-inducing ability of these cells, we conducted DNA microarray analysis, focusing on cell proliferation and the production of leukemia inhibitory factor (LIF), a cachexia-inducing factor. The plasma human LIF levels of 85As2-induced cachexic rats increased as symptoms worsened, whereas the plasma levels of MKNcl85 were low. 85As2 cells displayed more genetic changes compared to MKN45cl85 cells, which were related to Toll-like receptor (TLR) 4/5 signaling. Stimulation of both cells with TLR4 (lipopolysaccharide) or TLR5 (flagellin) agonists did not affect proliferation. However, in 82As2 cells, LIF production was significantly increased by stimulation with TLR5, which was suppressed by an inhibitor of interleukin-1 receptor-associated kinase-1/4, which are important factors in the TLR5 signaling pathway. The increase in LIF production resulting from activation of the TLR5 signaling pathway may contribute to the cachexia-inducing ability of 85As2 cells.
BibTeX:
@article{Terawaki2018,
  author = {Terawaki, Kiyoshi and Kashiwase, Yohei and Uzu, Miaki and Nonaka, Miki and Sawada, Yumi and Miyano, Kanako and Higami, Yoshikazu and Yanagihara, Kazuyoshi and Yamamoto, Masahiro and Uezono, Yasuhito},
  title = {Leukemia inhibitory factor via the Toll-like receptor 5 signaling pathway involves aggravation of cachexia induced by human gastric cancer-derived 85As2 cells in rats.},
  journal = {Oncotarget},
  publisher = {Impact Journals, LLC},
  year = {2018},
  volume = {9},
  number = {78},
  pages = {34748--34764},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/30410674 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC6205166},
  doi = {http://doi.org/10.18632/oncotarget.26190}
}
Tiys, E.S., Ivanisenko, T.V., Demenkov, P.S. and Ivanisenko, V.A. FunGeneNet: a web tool to estimate enrichment of functional interactions in experimental gene sets 2018 BMC Genomics
Vol. 19(S3), pp. 76 
article DOI URL 
Abstract: Estimation of functional connectivity in gene sets derived from genome-wide or other biological experiments is one of the essential tasks of bioinformatics. A promising approach for solving this problem is to compare gene networks built using experimental gene sets with random networks. One of the resources that make such an analysis possible is CrossTalkZ, which uses the FunCoup database. However, existing methods, including CrossTalkZ, do not take into account individual types of interactions, such as protein/protein interactions, expression regulation, transport regulation, catalytic reactions, etc., but rather work with generalized types characterizing the existence of any connection between network members. We developed the online tool FunGeneNet, which utilizes the ANDSystem and STRING to reconstruct gene networks using experimental gene sets and to estimate their difference from random networks. To compare the reconstructed networks with random ones, the node permutation algorithm implemented in CrossTalkZ was taken as a basis. To study the FunGeneNet applicability, the functional connectivity analysis of networks constructed for gene sets involved in the Gene Ontology biological processes was conducted. We showed that the method sensitivity exceeds 0.8 at a specificity of 0.95. We found that the significance level of the difference between gene networks of biological processes and random networks is determined by the type of connections considered between objects. At the same time, the highest reliability is achieved for the generalized form of connections that takes into account all the individual types of connections. By taking examples of the thyroid cancer networks and the apoptosis network, it is demonstrated that key participants in these processes are involved in the interactions of those types by which these networks differ from random ones. FunGeneNet is a web tool aimed at proving the functionality of networks in a wide range of sizes of experimental gene sets, both for different global networks and for different types of interactions. Using examples of thyroid cancer and apoptosis networks, we have shown that the links over-represented in the analyzed network in comparison with the random ones make possible a biological interpretation of the original gene/protein sets. The FunGeneNet web tool for assessment of the functional enrichment of networks is available at
http://www-bionet.sscc.ru/fungenenet/

.
BibTeX:
@article{Tiys2018,
  author = {Tiys, Evgeny S. and Ivanisenko, Timofey V. and Demenkov, Pavel S. and Ivanisenko, Vladimir A.},
  title = {FunGeneNet: a web tool to estimate enrichment of functional interactions in experimental gene sets},
  journal = {BMC Genomics},
  publisher = {BioMed Central},
  year = {2018},
  volume = {19},
  number = {S3},
  pages = {76},
  url = {https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-018-4474-7},
  doi = {http://doi.org/10.1186/s12864-018-4474-7}
}
Völgyi, K., Badics, K., Sialana, F.J., Gulyássy, P., Udvari, E.B., Kis, V., Drahos, L., Lubec, G., Kékesi, K.A. and Juhász, G. Early Presymptomatic Changes in the Proteome of Mitochondria-Associated Membrane in the APP/PS1 Mouse Model of Alzheimer's Disease 2018 Molecular Neurobiology, pp. 1-19  article DOI URL 
BibTeX:
@article{Volgyi2018,
  author = {Völgyi, Katalin and Badics, Kata and Sialana, Fernando J. and Gulyássy, Péter and Udvari, Edina Brigitta and Kis, Viktor and Drahos, László and Lubec, Gert and Kékesi, Katalin Adrienna and Juhász, Gábor},
  title = {Early Presymptomatic Changes in the Proteome of Mitochondria-Associated Membrane in the APP/PS1 Mouse Model of Alzheimer's Disease},
  journal = {Molecular Neurobiology},
  publisher = {Springer US},
  year = {2018},
  pages = {1--19},
  url = {http://link.springer.com/10.1007/s12035-018-0955-6},
  doi = {http://doi.org/10.1007/s12035-018-0955-6}
}
Wang, C.-C., Ying, L., Barnes, E.A., Adams, E.S., Kim, F.Y., Engel, K.W., Alvira, C.M. and Cornfield, D.N. Pulmonary artery smooth muscle cell HIF-1α regulates endothelin expression via microRNA-543 2018 American Journal of Physiology-Lung Cellular and Molecular Physiology, pp. ajplung.00475.2017  article DOI URL 
Abstract: Pulmonary artery smooth muscle cells (PASMC) express endothelin (ET-1) which modulates the pulmonary vascular response to hypoxia. Although cross-talk between hypoxia-inducible factor-1α (HIF-1α), an O2-sensitive transcription factor, and ET-1 is established, the cell-specific relationship between HIF-1α and ET-1 expression remains incompletely understood. We tested the hypotheses that in PASMC: (i) HIF-1α expression constrains ET-1 expression; and (ii) a specific microRNA (miRNA) links HIF-1α and ET-1 expression. In human PASMC (hPASMC), depletion of HIF-1α with siRNA, increased ET-1 expression at both the mRNA and protein level (ptextless0.01). In HIF-1α-/- murine (m)PASMC, ET-1 gene and protein expression was increased (ptextless0.0001) compared to HIF-1α+/+ cells. miRNA profiles were screened in hPASMC transfected with siRNA-HIF-1α and RNA hybridization performed on the Agilent human miRNA microarray. With HIF-1α depletion, miRNA-543 increased by 2.4 fold (ptextless0.01). In hPASMC, miRNA-543 overexpression increased ET-1...
BibTeX:
@article{Wang2018,
  author = {Wang, Ching-Chia and Ying, Lihua and Barnes, Elizabeth A. and Adams, Eloa S. and Kim, Francis Y. and Engel, Karl W. and Alvira, Cristina M. and Cornfield, David N.},
  title = {Pulmonary artery smooth muscle cell HIF-1α regulates endothelin expression via microRNA-543},
  journal = {American Journal of Physiology-Lung Cellular and Molecular Physiology},
  publisher = { American Physiological Society Bethesda, MD },
  year = {2018},
  pages = {ajplung.00475.2017},
  url = {http://www.physiology.org/doi/10.1152/ajplung.00475.2017},
  doi = {http://doi.org/10.1152/ajplung.00475.2017}
}
Yang, J.H., Kim, H.S., Koo, B.K., Lee, C.M., Jung, J.-H. and Seo, Y.R. Considerations of Human Health Risk Assessment in Chemical Accident: Suggestions from a Toxicogenomic Approach 2018 Toxicology and Environmental Health Sciences
Vol. 10(2), pp. 79-89 
article DOI URL 
BibTeX:
@article{Yang2018,
  author = {Yang, Jun Hyuek and Kim, Hyun Soo and Koo, Bon Kon and Lee, Cheol Min and Jung, Jong-Hyeon and Seo, Young Rok},
  title = {Considerations of Human Health Risk Assessment in Chemical Accident: Suggestions from a Toxicogenomic Approach},
  journal = {Toxicology and Environmental Health Sciences},
  publisher = {Korean Society of Environmental Risk Assessment and Health Science},
  year = {2018},
  volume = {10},
  number = {2},
  pages = {79--89},
  url = {http://link.springer.com/10.1007/s13530-018-0350-8},
  doi = {http://doi.org/10.1007/s13530-018-0350-8}
}
Yuan, H., Wang, X., Lu, J., Zhang, Q., Brandina, I., Alexandrov, I. and Glazer, R.I. MMTV-NeuT/ATTAC mice: a new model for studying the stromal tumor microenvironment. 2018 Oncotarget
Vol. 9(8), pp. 8042-8053 
article DOI URL 
Abstract: One of the central challenges in cancer prevention is the identification of factors in the tumor microenvironment (TME) that increase susceptibility to tumorigenesis. One such factor is stromal fibrosis, a histopathologic negative prognostic criterion for invasive breast cancer. Since the stromal composition of the breast is largely adipose and fibroblast tissue, it is important to understand how alterations in these tissues affect cancer progression. To address this question, a novel transgenic animal model was developed by crossing MMTV-NeuT mice containing a constitutively active ErbB2 gene into the FAT-ATTAC (fat apoptosis through targeted activation of caspase 8) background, which expresses an inducible caspase 8 fusion protein targeted to mammary adipose tissue. Upon caspase 8 activation, lipoatrophy of the mammary gland results in stromal fibrosis and acceleration of mammary tumor development with an increase in tumor multiplicity. Fibrosis was accompanied by an increase in collagen deposition, α-smooth muscle actin and CD31 expression in the tumor stroma as well as an increase in PD-L1-positive tumor cells, and infiltration by regulatory T cells, myeloid-derived suppressor cells and tumor-associated macrophages. Gene expression and signal transduction profiling indicated upregulation of pathways associated with cytokine signaling, inflammation and proliferation. This model should be useful for evaluating new therapies that target desmoplasia in the TME associated with invasive cancer.
BibTeX:
@article{Yuan2018,
  author = {Yuan, Hongyan and Wang, Xiaoyi and Lu, Jin and Zhang, Qiongsi and Brandina, Irina and Alexandrov, Ilya and Glazer, Robert I},
  title = {MMTV-NeuT/ATTAC mice: a new model for studying the stromal tumor microenvironment.},
  journal = {Oncotarget},
  publisher = {Impact Journals, LLC},
  year = {2018},
  volume = {9},
  number = {8},
  pages = {8042--8053},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/29487713 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5814280},
  doi = {http://doi.org/10.18632/oncotarget.24233}
}
Zheng, Y., Wang, Y., Cao, H., Chen, Q. and Zhang, X. Integrated computational biology analysis to evaluate target genes for chronic myelogenous leukemia 2018 Molecular Medicine Reports  article DOI URL 
BibTeX:
@article{Zheng2018,
  author = {Zheng, Yu and Wang, Yu‑Ping and Cao, Hongbao and Chen, Qiusheng and Zhang, Xi},
  title = {Integrated computational biology analysis to evaluate target genes for chronic myelogenous leukemia},
  journal = {Molecular Medicine Reports},
  publisher = {Spandidos Publications},
  year = {2018},
  url = {http://www.spandidos-publications.com/10.3892/mmr.2018.9125},
  doi = {http://doi.org/10.3892/mmr.2018.9125}
}
Aghagolzadeh, P., Radpour, R., Bachtler, M., van Goor, H., Smith, E.R., Lister, A., Odermatt, A., Feelisch, M. and Pasch, A. Hydrogen sulfide attenuates calcification of vascular smooth muscle cells via KEAP1/NRF2/NQO1 activation 2017 Atherosclerosis  article DOI URL 
Abstract: BACKGROUND AND AIMS
Vascular calcification is a common health problem related to oxidative stress, inflammation, and circulating calciprotein particles (CPP). Hydrogen sulfide is an endogenous signaling molecule with antioxidant properties and potential for drug development targeting redox signaling. Yet, its molecular mechanisms of action in vascular smooth muscle cell (VSMC) calcification have not been delineated. We therefore sought to identify key pathways involved in the calcification-inhibitory properties of sulfide employing our recently developed CPP-induced VSMC calcification model.

METHODS
Using next-generation sequencing, we investigated the transcriptomic changes of sodium hydrosulfide-treated versus non-treated calcifying VSMCs. The potential role of candidate genes and/or regulatory pathways in prevention of calcification was investigated by small interfering RNA (siRNA).

RESULTS
CPP led to a pronounced accumulation of cell-associated calcium, which was decreased by sulfide in a concentration-dependent manner. Both, CPP-induced hydrogen peroxide production and enhanced pro-inflammatory/oxidative stress-related gene expression signatures were attenuated by sulfide-treatment. Gene ontology enrichment and in silico pathway analysis of our transcriptome data suggested NAD(P)H dehydrogenase [quinone] 1 (NQO1) as potential mediator. Corroborating these findings, silencing of Kelch-like ECH-associated protein 1 (KEAP1), an inhibitor of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) nuclear activity, enhanced NQO1 expression, whereas NRF2 silencing reduced the expression of NQO1 and abrogated the calcification-suppressing activity of sulfide. Moreover, immunofluorescence microscopy confirmed nuclear translocation of NRF2 by sulfide in VSMC.

CONCLUSIONS
Sulfide attenuates CPP-induced VSMC calcification in vitro via the KEAP1-NRF2 redox sensing/stress response system by enhancing NQO1 expression.
BibTeX:
@article{Aghagolzadeh2017,
  author = {Aghagolzadeh, Parisa and Radpour, Ramin and Bachtler, Matthias and van Goor, Harry and Smith, Edward R. and Lister, Adam and Odermatt, Alex and Feelisch, Martin and Pasch, Andreas},
  title = {Hydrogen sulfide attenuates calcification of vascular smooth muscle cells via KEAP1/NRF2/NQO1 activation},
  journal = {Atherosclerosis},
  year = {2017},
  url = {http://www.sciencedirect.com/science/article/pii/S0021915017312340},
  doi = {http://doi.org/10.1016/j.atherosclerosis.2017.08.012}
}
Ahn, J., Park, Y.-J., Chen, P., Lee, T.J., Jeon, Y.-J., Croce, C.M., Suh, Y., Hwang, S., Kwon, W.-S., Pang, M.-G., Kim, C.-H., Lee, S.S. and Lee, K. Comparative expression profiling of testis-enriched genes regulated during the development of spermatogonial cells 2017 PLOS ONE
Vol. 12(4), pp. e0175787 
article DOI URL 
BibTeX:
@article{Ahn2017,
  author = {Ahn, Jinsoo and Park, Yoo-Jin and Chen, Paula and Lee, Tae Jin and Jeon, Young-Jun and Croce, Carlo M. and Suh, Yeunsu and Hwang, Seongsoo and Kwon, Woo-Sung and Pang, Myung-Geol and Kim, Cheorl-Ho and Lee, Sang Suk and Lee, Kichoon},
  title = {Comparative expression profiling of testis-enriched genes regulated during the development of spermatogonial cells},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2017},
  volume = {12},
  number = {4},
  pages = {e0175787},
  url = {http://dx.plos.org/10.1371/journal.pone.0175787},
  doi = {http://doi.org/10.1371/journal.pone.0175787}
}
Albalat, A., Mullen, W., Husi, H. and Mischak, H. Tissue Proteomics in Vascular Disease. 2017 Methods in molecular biology (Clifton, N.J.)
Vol. 1527, pp. 53-60 
article URL 
Abstract: In vascular diseases, as in many other pathophysiological conditions, tissue proteins are subjected to a number of different changes such as protein expression, posttranslational modifications, and proteolytic cleavage. For this reason, the study of the tissue proteome is becoming an increasingly important tool in biological and clinical research. In this chapter, we describe in detail the methodology for the analysis of tryptic digested peptides from aortic tissue extracts from mice with the aim to elucidate differences in the proteome between control and case or vascular diseased tissue samples. The method encompasses the analysis of these complex extracts in a single chromatographic run allowing for increased reproducibility. We also outline the main workflow for the processing of the generated data by statistical and bioinformatic analysis.
BibTeX:
@article{Albalat2017,
  author = {Albalat, Amaya and Mullen, William and Husi, Holger and Mischak, Harald},
  title = {Tissue Proteomics in Vascular Disease.},
  journal = {Methods in molecular biology (Clifton, N.J.)},
  year = {2017},
  volume = {1527},
  pages = {53--60},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28116706}
}
Anastasia P. Nesterova, Eugene A. Klimov, Maria Zharkova, V.S. Pathways Analysis in Brain Aging 2017   inproceedings URL 
Abstract: Aging is initiated in each and every cell of an organism, but has its characteristic features specific to every differentiated tissue. The “Elsevier Aging Pathways” collection (42 pathways) which is the interactive catalog of currently known facts about molecular bases of aging-related processes in human brain, is a valid source for bioinformatic analysis of gene expression experiments.
BibTeX:
@inproceedings{AnastasiaP.NesterovaEugeneA.KlimovMariaZharkova,
  author = {Anastasia P. Nesterova, Eugene A. Klimov, Maria Zharkova, Vladimir Sobolev},
  title = {Pathways Analysis in Brain Aging},
  publisher = {Precision Medicine 2017 Virtual Event, Labroots},
  year = {2017},
  url = {http://www.eposters.net/poster/pathways-analysis-in-brain-aging https://cdn.technologynetworks.com/ep/pdfs/pathways-analysis-in-brain-aging.pdf}
}
Angeline S. Andrew, John A. Baron, L.F.B., Arief A. Suriawinata 1, Gregory J. Tsongalis 1 and Christina M. Robinson 1 and Christopher I. Amos 1 Hyper-Methylated Loci Persisting from Sessile Serrated Polyps to Serrated Cancers 2017 International Journal of Molecular Sciences  article URL 
Abstract: Abstract: Although serrated polyps were historically considered to pose little risk, it is now
understood that progression down the serrated pathway could account for as many as 15%–35% of
colorectal cancers. The sessile serrated adenoma/polyp (SSA/P) is the most prevalent pre-invasive
serrated lesion. Our objective was to identify the CpG loci that are persistently hyper-methylated
during serrated carcinogenesis, from the early SSA/P lesion through the later cancer phases
of neoplasia development. We queried the loci hyper-methylated in serrated cancers within
our right-sided SSA/Ps from the New Hampshire Colonoscopy Registry, using the Illumina
Infinium Human Methylation 450 k panel to comprehensively assess the DNA methylation
status. We identified CpG loci and regions consistently hyper-methylated throughout the serrated
carcinogenesis spectrum, in both our SSA/P specimens and in serrated cancers. Hyper-methylated
CpG loci included the known the tumor suppressor gene RET (p = 5.72 × 10−10), as well as loci in
differentially methylated regions for GSG1L, MIR4493, NTNG1, MCIDAS, ZNF568, and RERG. The
hyper-methylated loci that we identified help characterize the biology of SSA/P development, and
could be useful as therapeutic targets, or for future identification of patients who may benefit from
shorter surveillance intervals.
BibTeX:
@article{AngelineS.AndrewJohnA.Baron2017,
  author = {Angeline S. Andrew, John A. Baron, Lynn F. Butterly and Arief A. Suriawinata 1 and Gregory J. Tsongalis 1 and Christina M. Robinson 1 and Christopher I. Amos 1},
  title = {Hyper-Methylated Loci Persisting from Sessile Serrated Polyps to Serrated Cancers},
  journal = {International Journal of Molecular Sciences},
  year = {2017},
  url = {file:///C:/Users/caoho/Desktop/ijms-18-00535-v2 (1).pdf}
}
Anirban Bhar & Sumanti Gupta & Moniya Chatterjee &, Senjuti Sen & Sampa Das, Bhar, A., Gupta, S., Chatterjee, M., Sen, S. and Das, S. Differential expressions of photosynthetic genes provide clues to the resistance mechanism during Fusarium oxysporum f.sp. ciceri race 1 (Foc1) infection in chickpea (Cicer arietinum L.) 2017 European Journal of Plant Pathology, pp. 1-17  article URL 
Abstract: t Fusarium oxysporum f.sp. ciceri race 1 (Foc1), a root-invading pathogen causes vascular wilt in chickpea (Cicer arietinum L.). Foc1 is known to induce reactive oxygen species (ROS) mediated localized defense responses at the site of colonization in roots. However, the effect of this localized infection on distant shoot tissues is still unknown. In the present study, the effect of Foc1 on shoot tissues of both susceptible and resistant chickpea plants was studied. Total pigment content and fluorescence of chlorophyll was measured. Occurrence of oxidative damage in shoots was confirmed by both biochemical and lipid peroxidation assays. Expression pattern of some redox responsive transcripts were also analyzed. Additionally, transcriptional accumulations of some key genes related to light reaction, carbon reduction and photosystem II (PSII) of photosynthesis were analyzed at different time points post infection. Expressional status of stress induced sugar metabolism related genes (sucrose synthase, β amylase and invertase) were also investigated. Finally, gene networks were constructed showing interconnection of the photosynthetic genes, sugar metabolism-related genes and redox responsive transcripts with other metabolic and stress related pathways. The results demonstrate that the infection in root tissues of chickpea by Foc1 dramatically increases the ROS levels in shoot tissues of susceptible plants. The oxidative outburst in shoot tissues of susceptible plants also hampers the photosynthetic stability by down-regulating the key photosynthetic genes. On the contrary, resistant chickpea lines are grossly devoid of such instances with few behavioral irregularities at later time points.
BibTeX:
@article{AnirbanBhar&SumantiGupta&MoniyaChatterjee&,
  author = {Anirban Bhar & Sumanti Gupta & Moniya Chatterjee & and Senjuti Sen & Sampa Das and Bhar, Anirban and Gupta, Sumanti and Chatterjee, Moniya and Sen, Senjuti and Das, Sampa},
  title = {Differential expressions of photosynthetic genes provide clues to the resistance mechanism during Fusarium oxysporum f.sp. ciceri race 1 (Foc1) infection in chickpea (Cicer arietinum L.)},
  journal = {European Journal of Plant Pathology},
  publisher = {Springer Netherlands},
  year = {2017},
  pages = {1--17},
  url = {https://link.springer.com/article/10.1007/s10658-016-1109-1}
}
Assidi, M., Abu-Elmagd, M., Gauthaman, K., Gari, M., Chaudhary, A., Abuzenadah, A., Pushparaj, P.N. and Al-Qahtani, M. The potential of immunogenomics in personalized healthcare 2017   article URL 
Abstract: Background Immunogenomics is an expanding field which will allow expanding basic knowledge about the contribution of the genomic immunology and its interaction with the environment including the microbiome of both human health and disease [1]. It helps us to understand the immune mechanisms in both health and disease and provides critical clues to foster the medical transition towards precision medicine through the provision of individualized diagnostics and therapeutics [2, 3]. In this study, we provide an overview of the recent developments in Immunogenomics and their potent role to develop novel preventive and therapeutic strategies for the wellbeing of humans. Materials and methods High throughput data, obtained from individual patients, using advanced technological platforms such as microarrays, next generation sequencing (NGS) methodologies were examined using freewares like R and commercial platforms like Genespring GX13.1 (Agilent, USA), Partek Genomics Suite (Partek Inc., USA), JMP Genomics Software (SAS, USA) etc., The differential expression patterns of immune genes has been analysed using the Database for Annotation and Visualization and Integrated Discovery (DAVID), and commercial knowledge bases like Pathway Analysis (IPA) (Ingenuity Systems, Qiagen USA), Pathway Studio (Elsevier, Netherlands) etc., to decipher biomarkers and novel immune-regulatory pathways. Results The screening of available high throughput data and further analysis of molecular using computational and comparative genomics tools provide us key biomarkers and/or pathways driving human immunogenomic behaviour at both physiological and pathological contexts.
BibTeX:
@article{Assidi,
  author = {Assidi, Mourad and Abu-Elmagd, Muhammad and Gauthaman, Kalamegam and Gari, Mamdooh and Chaudhary, Adeel and Abuzenadah, Adel and Pushparaj, Peter Natesan and Al-Qahtani, Mohammed},
  title = {The potential of immunogenomics in personalized healthcare},
  year = {2017},
  url = {https://www.researchgate.net/profile/MuhammadAbu-Elmagd2/publication/305584918Thepotentialofimmunogenomicsinpersonalizedhealthcare/links/580b41cb08aeef1bfee7ee8f/The-potential-of-immunogenomics-in-personalized-healthcare.pdf}
}
Bartsch, D.K., Hans Scherübl, M. and Lumpur, K. Visceral Medicine 2017
Vol. 33(5) 
book URL 
BibTeX:
@book{Bartsch2017,
  author = {Bartsch, Detlef K and Hans Scherübl, Marburg and Lumpur, Kuala},
  title = {Visceral Medicine},
  year = {2017},
  volume = {33},
  number = {5},
  url = {https://www.karger.com/Article/PDF/484148}
}
Buzdin, A.A., Prassolov, V., Zhavoronkov, A.A. and Borisov, N.M. Bioinformatics Meets Biomedicine: OncoFinder, a Quantitative Approach for Interrogating Molecular Pathways Using Gene Expression Data 2017 , pp. 53-83  incollection DOI URL 
BibTeX:
@incollection{Buzdin2017,
  author = {Buzdin, Anton A. and Prassolov, Vladimir and Zhavoronkov, Alex A. and Borisov, Nikolay M.},
  title = {Bioinformatics Meets Biomedicine: OncoFinder, a Quantitative Approach for Interrogating Molecular Pathways Using Gene Expression Data},
  publisher = {Humana Press, New York, NY},
  year = {2017},
  pages = {53--83},
  url = {http://link.springer.com/10.1007/978-1-4939-7027-84},
  doi = {http://doi.org/10.1007/978-1-4939-7027-8_4}
}
Chao, W.S., Doğramacı, M., Horvath, D.P., Anderson, J.V. and Foley, M.E. Comparison of phytohormone levels and transcript profiles during seasonal dormancy transitions in underground adventitious buds of leafy spurge 2017 Plant Molecular Biology, pp. 1-22  article DOI URL 
BibTeX:
@article{Chao2017,
  author = {Chao, Wun S. and Doğramacı, Münevver and Horvath, David P. and Anderson, James V. and Foley, Michael E.},
  title = {Comparison of phytohormone levels and transcript profiles during seasonal dormancy transitions in underground adventitious buds of leafy spurge},
  journal = {Plant Molecular Biology},
  publisher = {Springer Netherlands},
  year = {2017},
  pages = {1--22},
  url = {http://link.springer.com/10.1007/s11103-017-0607-7},
  doi = {http://doi.org/10.1007/s11103-017-0607-7}
}
Choi, Y.-J., Kim, E., Musa, A., Reza, M.T., Hong, K., Song, H., Park, C., Cho, S.-K., Lee, K., Prather, R.S. and Kim, J.-H. Recombination activating gene-2 null severe combined immunodeficient pigs and mice engraft human induced pluripotent stem cells differently 2017   article URL 
Abstract: This study comparatively investigated the transcriptional, physiological, and phenotypic differences of the immune disorder between severe combined immunodeficient (SCID) mouse and pig models. We discovered that the recombination activating gene-2 (Rag-2) SCID mice, but not RAG-2 SCID pigs, showed intense, infrequent, and mild cluster of CD3 + -, CD4 + -, and CD8 + signals respectively, suggesting that distinct species-specific effects exist. Furthermore, the expression of six relevant genes (NFATC1, CD79B, CD2, BLNK, FOXO1, and CD40) was more downregulated than that in the Rag-2 SCID mice, which provides a partial rationale for the death of T/B cells in the lymphoid organs of RAG-2 SCID pigs but not in Rag-2 SCID mice. Further, NK cell maturation-related gene expression was significantly lower in RAG-2 SCID pigs than in Rag-2 SCID mice. Consistently, the RAG-2 SCID pigs, but not Rag-2 SCID mice, developed human induced pluripotent stem cell-derived teratomas that were the same as those of perforin/Rag-2 SCID mice. Therefore, these unexpected findings indicate the superiority of RAG-2 SCID pigs over Rag-2 SCID mice as a suitable model for investigating human diseases.
BibTeX:
@article{Choi2017,
  author = {Choi, Yun-Jung and Kim, Eunsu and Musa, Abu and Reza, Md Talimur and Hong, Kwonho and Song, Hyuk and Park, Chankyu and Cho, Seong-Keun and Lee, Kiho and Prather, Randall S and Kim, Jin-Hoi},
  title = {Recombination activating gene-2 null severe combined immunodeficient pigs and mice engraft human induced pluripotent stem cells differently},
  year = {2017},
  url = {https://www.researchgate.net/profile/Jin-HoiKim/publication/319455171Recombinationactivatinggene-2nullseverecombinedimmunodeficientpigsandmiceengrafthumaninducedpluripotentstemcellsdifferently/links/59ac776e458515d09cd8a0cf/Recombination-}
}
Cowie, A.M., Sarty, K.I., Mercer, A., Koh, J., Kidd, K.A. and Martyniuk, C.J. The pesticide dieldrin disrupts proteins related to oxidative respiration and mitochondrial stress in the central nervous system 2017 Data in Brief  article DOI URL 
BibTeX:
@article{Cowie2017,
  author = {Cowie, Andrew M. and Sarty, Kathleena I. and Mercer, Angella and Koh, Jin and Kidd, Karen A. and Martyniuk, Christopher J.},
  title = {The pesticide dieldrin disrupts proteins related to oxidative respiration and mitochondrial stress in the central nervous system},
  journal = {Data in Brief},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S2352340917300847},
  doi = {http://doi.org/10.1016/j.dib.2017.03.008}
}
Darabi, S.A.S., Almodares, A. and Ebrahimi, M. In silico study shows arsenic induces P1B ATPase gene family as cation transporter by abscisic acid signaling pathway in seedling of Sorghum bicolor 2017 Acta Physiologiae Plantarum
Vol. 39(8), pp. 172 
article DOI URL 
BibTeX:
@article{Darabi2017,
  author = {Darabi, Seyed Ahmad Shafiei and Almodares, Abbas and Ebrahimi, Mansour},
  title = {In silico study shows arsenic induces P1B ATPase gene family as cation transporter by abscisic acid signaling pathway in seedling of Sorghum bicolor},
  journal = {Acta Physiologiae Plantarum},
  publisher = {Springer Berlin Heidelberg},
  year = {2017},
  volume = {39},
  number = {8},
  pages = {172},
  url = {http://link.springer.com/10.1007/s11738-017-2472-z},
  doi = {http://doi.org/10.1007/s11738-017-2472-z}
}
Delcourt, V., Franck, J., Leblanc, E., Narducci, F., Robin, Y.-M., Gimeno, J.-P., Quanico, J., Wisztorski, M., Kobeissy, F., Jacques, J.-F., Roucou, X., Salzet, M. and Fournier, I. Combined Mass Spectrometry Imaging and Top-down Microproteomics Reveals Evidence of a Hidden Proteome in Ovarian Cancer 2017 EBioMedicine  article DOI URL 
Abstract: BACKGROUND
Recently, it was demonstrated that proteins can be translated from alternative open reading frames (altORFs), increasing the size of the actual proteome. Top-down mass spectrometry-based proteomics allows the identification of intact proteins containing post-translational modifications (PTMs) as well as truncated forms translated from reference ORFs or altORFs.

METHODS
Top-down tissue microproteomics was applied on benign, tumor and necrotic-fibrotic regions of serous ovarian cancer biopsies, identifying proteins exhibiting region-specific cellular localization and PTMs. The regions of interest (ROIs) were determined by MALDI mass spectrometry imaging and spatial segmentation.

FINDINGS
Analysis with a customized protein sequence database containing reference and alternative proteins (altprots) identified 15 altprots, including alternative G protein nucleolar 1 (AltGNL1) found in the tumor, and translated from an altORF nested within the GNL1 canonical coding sequence. Co-expression of GNL1 and altGNL1 was validated by transfection in HEK293 and HeLa cells with an expression plasmid containing a GNL1-FLAG(V5) construct. Western blot and immunofluorescence experiments confirmed constitutive co-expression of altGNL1-V5 with GNL1-FLAG.

CONCLUSIONS
Taken together, our approach provides means to evaluate protein changes in the case of serous ovarian cancer, allowing the detection of potential markers that have never been considered.
BibTeX:
@article{Delcourt2017,
  author = {Delcourt, Vivian and Franck, Julien and Leblanc, Eric and Narducci, Fabrice and Robin, Yves-Marie and Gimeno, Jean-Pascal and Quanico, Jusal and Wisztorski, Maxence and Kobeissy, Firas and Jacques, Jean-François and Roucou, Xavier and Salzet, Michel and Fournier, Isabelle},
  title = {Combined Mass Spectrometry Imaging and Top-down Microproteomics Reveals Evidence of a Hidden Proteome in Ovarian Cancer},
  journal = {EBioMedicine},
  year = {2017},
  url = {http://www.sciencedirect.com/science/article/pii/S2352396417302293},
  doi = {http://doi.org/10.1016/j.ebiom.2017.06.001}
}
Devaux, S., Cizkova, D., Mallah, K., Karnoub, M.-A., Laouby, Z., Kobeissy, F., Blasko, J., Nataf, S., Pays, L., Meriaux, C., Fournier, I. and Salzet, M. RhoA inhibitor treatment at acute phase of spinal cord injury may induce neurite outgrowth and synaptogenesis. 2017 Molecular & cellular proteomics : MCP, pp. mcp.M116.064881  article DOI URL 
Abstract: The therapeutic use of RhoA inhibitors (RhoAi) has been experimentally tested in spinal cord injury (SCI). In order to decipher the underlying molecular mechanisms involved in such a process, an in vitro neuroproteomic-systems biology platform was developed in which the pan-proteomic profile of the dorsal root ganglia (DRG) cell line ND7/23 DRG was assessed in a large array of culture conditions using RhoAi and/or conditioned media obtained from SCI ex-vivo derived spinal cord slices. A fine mapping of the spatio-temporal molecular events of the RhoAi treatment in SCI was performed. The data obtained allow a better understanding of regeneration/degeneration induced above and below the lesion site. Results notably showed a time-dependent alteration of the transcription factors profile along with the synthesis of growth cone-related factors (receptors, ligands, and signaling pathways) in RhoAi treated DRG cells. Furthermore, we assessed in a rat SCI model the in vivo impact of RhoAi treatment administered in situ via alginate scaffold that was combined with FK506 delivery. The improved recovery of locomotion was detected only at the early post-injury time points, while after overall survival a dramatic increase of synaptic contacts on outgrowing neurites in affected segments was observed. We validate these results by an in vivo proteomic studies along the spinal cord segments from tissue and secreted media analyses, confirming the increase of the synaptogenesis expression factors under RhoAi treatment. Taken together, we demonstrate that RhoAi treatment seems to be useful to stimulate neurite outgrowth in both in vitro as well in vivo environments. However, for in vivo experiments there is a need for sustained delivery regiment to facilitate axon regeneration and promote synaptic reconnections with appropriate target neurons also at chronic phase, which in turn may lead to higher assumption for functional improvement.
BibTeX:
@article{Devaux2017,
  author = {Devaux, Stephanie and Cizkova, Dasa and Mallah, Khalil and Karnoub, Melodie-Anne and Laouby, Zahra and Kobeissy, Firas and Blasko, Juraj and Nataf, Serge and Pays, Laurent and Meriaux, Celine and Fournier, Isabelle and Salzet, Michel},
  title = {RhoA inhibitor treatment at acute phase of spinal cord injury may induce neurite outgrowth and synaptogenesis.},
  journal = {Molecular & cellular proteomics : MCP},
  publisher = {American Society for Biochemistry and Molecular Biology},
  year = {2017},
  pages = {mcp.M116.064881},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28659490},
  doi = {http://doi.org/10.1074/mcp.M116.064881}
}
Djabou, A.S.M., Carvalho, L.J.C.B., Li, Q.X., Niemenak, N. and Chen, S. Cassava postharvest physiological deterioration: a complex phenomenon involving calcium signaling, reactive oxygen species and programmed cell death 2017 Acta Physiologiae Plantarum
Vol. 39(4), pp. 91 
article DOI URL 
BibTeX:
@article{Djabou2017,
  author = {Djabou, Astride S. M. and Carvalho, Luiz J. C. B. and Li, Qing X. and Niemenak, Nicolas and Chen, Songbi},
  title = {Cassava postharvest physiological deterioration: a complex phenomenon involving calcium signaling, reactive oxygen species and programmed cell death},
  journal = {Acta Physiologiae Plantarum},
  publisher = {Springer Berlin Heidelberg},
  year = {2017},
  volume = {39},
  number = {4},
  pages = {91},
  url = {http://link.springer.com/10.1007/s11738-017-2382-0},
  doi = {http://doi.org/10.1007/s11738-017-2382-0}
}
Dongbai.Liu, Z. Identification and Validation Novel Risk Genes for Autism Spectrum Disorder – A Meta-Analysis 2017 Journal of Psychiatry and Brain Science  article URL 
Abstract: Abstract: Background: Autism spectrum disorders (ASD) are classified as neurodevelopmental disorders. The aim of this study was to investigate the genetic risk of ASD by systematically reviewing the published literature and performing a meta-analysis. Method: A comprehensive search of electronic databases was completed using Illumina BaseSpace Correlation Engine. Seven ASD case/control bio-sets from three different studies were selected, including 61 ASD cases and 83 controls. The top ASD risk genes from meta-analysis were further analyzed with an online open source ASD genetic database. Pathway enrichment analysis (PEA) and network connectivity analysis (NCA) were conducted to identify potential functional association between novel target genes and ASD.
BibTeX:
@article{Dongbai.Liu2017,
  author = {Dongbai.Liu, Zeya.Wang},
  title = {Identification and Validation Novel Risk Genes for Autism Spectrum Disorder – A Meta-Analysis},
  journal = {Journal of Psychiatry and Brain Science},
  year = {2017},
  url = {http://www.qingres.com/JournalsDetail.aspx?id=884&magazineID=15}
}
Dubovenko, A., Nikolsky, Y., Rakhmatulin, E. and Nikolskaya, T. Functional Analysis of OMICs Data and Small Molecule Compounds in an Integrated “Knowledge-Based” Platform 2017 , pp. 101-124  incollection DOI URL 
BibTeX:
@incollection{Dubovenko2017,
  author = {Dubovenko, Alexey and Nikolsky, Yuri and Rakhmatulin, Eugene and Nikolskaya, Tatiana},
  title = {Functional Analysis of OMICs Data and Small Molecule Compounds in an Integrated “Knowledge-Based” Platform},
  publisher = {Humana Press, New York, NY},
  year = {2017},
  pages = {101--124},
  url = {http://link.springer.com/10.1007/978-1-4939-7027-86},
  doi = {http://doi.org/10.1007/978-1-4939-7027-8_6}
}
Edited by Zekayi Kutlubay and Server Serdaroglu Hair and Scalp Disorders | InTechOpen 2017   book URL 
Abstract: This textbook contains the latest advances and scientific knowledge from the leading experts in hair biology, hair disorders, and clinical trichology. The book consists of ten sections in which hair biology, hair genetics, hair diagnostics, hair loss types, pathogenesis, treatment options, and restoration techniques are discussed. This book also emphasizes on various genetic and nongenetic alopecia types, differential diagnosis, and the measurement of hair loss. One chapter of the book is devoted to natural products for hair care and treatment. We believe that this textbook will serve as a comprehensive guide to many physicians dealing with hair disorders in their clinical practice.
BibTeX:
@book{EditedbyZekayiKutlubayandServerSerdaroglu2017,
  author = {Edited by Zekayi Kutlubay and Server Serdaroglu},
  title = {Hair and Scalp Disorders | InTechOpen},
  year = {2017},
  url = {https://www.intechopen.com/books/hair-and-scalp-disorders}
}
Eugene Klimov, Olga Rudko, Elena Naumova, Artemiy Tretiakov, Vladimir Sobolev, Kirill Skorobogatykh, Julia Azimova, Alexey Sergeev, Anna Soboleva, Zarema Kokaeva, G.T. Familial hemiplegic migraine type I: the molecular signaling pathway 2017 Journal of Neurology & Stroke
Vol. 7(5), pp. 00249 
article DOI  
Abstract: Migraine is a multifactorial disease, manifested by intense bouts of recurrent headaches. Molecular mechanisms of migraine attack are not clear. In this study, we carried out the analysis of molecular processes in the pathogenesis of a rare hereditary form of migraine - familial hemiplegic migraine type I. Constructed hypothetical signaling pathways allowed us to understand the causes of a migraine attack and identify key molecules and signaling pathways for further experimental and clinical studies.
BibTeX:
@article{EugeneKlimovOlgaRudkoElenaNaumovaArtemiyTretiakovVladimirSobolevKirillSkorobogatykhJuliaAzimovaAlexeySergeevAnnaSobolevaZaremaKokaeva2017,
  author = {Eugene Klimov, Olga Rudko, Elena Naumova, Artemiy Tretiakov, Vladimir Sobolev, Kirill Skorobogatykh, Julia Azimova, Alexey Sergeev, Anna Soboleva, Zarema Kokaeva, Gyuzyal Tabeeva},
  title = {Familial hemiplegic migraine type I: the molecular signaling pathway},
  journal = {Journal of Neurology & Stroke },
  year = {2017},
  volume = {7},
  number = {5},
  pages = {00249},
  doi = {http://doi.org/10.15406/jnsk.2017.07.00249}
}
Fakhry, M., Skafi, N., Fayyad-Kazan, M., Kobeissy, F., Hamade, E., Mebarek, S., Habib, A., Borghol, N., Zeidan, A., Magne, D., Fayyad-Kazan, H. and Badran, B. Characterization and assessment of potential microRNAs involved in phosphate-induced aortic calcification 2017 Journal of Cellular Physiology  article DOI URL 
BibTeX:
@article{Fakhry2017,
  author = {Fakhry, Maya and Skafi, Najwa and Fayyad-Kazan, Mohammad and Kobeissy, Firas and Hamade, Eva and Mebarek, Saida and Habib, Aida and Borghol, Nada and Zeidan, Asad and Magne, David and Fayyad-Kazan, Hussein and Badran, Bassam},
  title = {Characterization and assessment of potential microRNAs involved in phosphate-induced aortic calcification},
  journal = {Journal of Cellular Physiology},
  year = {2017},
  url = {http://doi.wiley.com/10.1002/jcp.26121},
  doi = {http://doi.org/10.1002/jcp.26121}
}
Feswick, A., Munkittrick, K.R. and Martyniuk, C.J. Estrogen-responsive gene networks in the teleost liver: What are the key molecular indicators? 2017 Environmental Toxicology and Pharmacology  article DOI URL 
Abstract: An overarching goal of environmental genomics is to leverage sensitive suites of markers that are robust and reliable to assess biological responses in a range of species inhabiting variable environments. The objective of this study was to identify core groups of transcripts and molecular signaling pathways that respond to 17alpha-ethylinestadiol (EE2), a ubiquitous estrogenic contaminant, using transcriptome datasets generated from six independent laboratories. We sought to determine which biomarkers and gene networks were those most robust and reliably detected in multiple laboratories. Six laboratories conducted microarray analysis in pieces of the same liver from male fathead minnows exposed to ∼15ng/L EE2 for 96hours. There were common transcriptional networks identified in every dataset. These included a down-regulation of gene networks associated with blood clotting, complement activation, triglyceride storage, and xenobiotic metabolism. Noteworthy was that more than ∼85% of the gene networks were suppressed by EE2. Leveraging both these data and those mined from the Comparative Toxicogenomics Database (CTD), we narrowed in on an EE2-responsive transcriptional network. All transcripts in this network responded ∼±5-fold or more to EE2, increasing reliability of detection. This network included estrogen receptor alpha, transferrin, myeloid cell leukemia 1, insulin like growth factor 1, insulin like growth factor binding protein 2, and methionine adenosyltransferase 2A. This estrogen-responsive interactome has the advantage over single markers (e.g. vitellogenin) in that these entities are directly connected to each other based upon evidence of expression regulation and protein binding. Thus, it represents an interacting functional suite of estrogenic markers. Vitellogenin, the gold standard for estrogenic exposures, can show high individual variability in its response to estrogens, and the use of a multi-gene approach for estrogenic chemicals is expected to improve sensitivity. In our case, the coefficient of variation was significantly lowered by the gene network (∼67%) compared to Vtg alone, supporting the use of this transcriptional network as a sensitive alternative for detecting estrogenic effluents and chemicals. We propose that screening chemicals for estrogenicity using interacting genes within a defined expression network will improve sensitivity, accuracy, and reduce the number of animals required for endocrine disruption assessments.
BibTeX:
@article{Feswick2017,
  author = {Feswick, April and Munkittrick, Kelly R. and Martyniuk, Christopher J.},
  title = {Estrogen-responsive gene networks in the teleost liver: What are the key molecular indicators?},
  journal = {Environmental Toxicology and Pharmacology},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S1382668917302983},
  doi = {http://doi.org/10.1016/j.etap.2017.10.012}
}
Filatova, E., Kasian, A., Kolomin, T., Rybalkina, E., Alieva, A., Andreeva, L., Limborska, S., Myasoedov, N., Pavlova, G., Slominsky, P. and Shadrina, M. GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells 2017 Frontiers in Pharmacology
Vol. 8, pp. 89 
article DOI URL 
Abstract: Clinical studies have shown that Selank had an anxiolytic effect comparable to that of classical benzodiazepine drugs, which can enhance the inhibitory effect of GABA by allosteric modulation of GABAA receptors. These data suggest that the molecular mechanism of the effect of Selank may also be related to its ability to affect the performance of the GABAergic system. To test this hypothesis we studied the changes in expression of 84 genes involved in the functioning of the GABAergic system and in the processes of neurotransmission in the culture of neuroblastoma IMR 32 cells using qPCR metod. As test substances, in addition to Selank, we selected the major GABAA receptor ligand, GABA, the atypical antipsychotic, olanzapine, and combinations of these compounds (Selank and GABA; Selank and olanzapine). We found no changes in the mRNA levels of the genes studied under the effect of Selank. The combined effect of GABA and Selank led to nearly complete suppression of changes in expression of genes in which mRNA levels changed under the effect of GABA. When Selank was used in conjunction with olanzapine, the expression alterations of more genes were observed compared with olanzapine alone. The data obtained indicate that Selank has no direct effect on the mRNA levels of the GABAergic system genes in neuroblastoma IMR-32 cells. At the same time, our results partially confirm the hypothesis that the peptide may affect the interaction of GABA with GABAA receptors. Our data also suggest that Selank may enhance the effect of olanzapine on the expression of the genes studied.
BibTeX:
@article{Filatova2017,
  author = {Filatova, Elena and Kasian, Anastasiya and Kolomin, Timur and Rybalkina, Ekaterina and Alieva, Anelya and Andreeva, Lyudmila and Limborska, Svetlana and Myasoedov, Nikolay and Pavlova, Galina and Slominsky, Petr and Shadrina, Maria},
  title = {GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells},
  journal = {Frontiers in Pharmacology},
  publisher = {Frontiers},
  year = {2017},
  volume = {8},
  pages = {89},
  url = {http://journal.frontiersin.org/article/10.3389/fphar.2017.00089/full},
  doi = {http://doi.org/10.3389/fphar.2017.00089}
}
Hage-Sleiman, R., Bahmad, H., Kobeissy, H., Dakdouk, Z., Kobeissy, F. and Dbaibo, G. Genomic alterations during p53-dependent apoptosis induced by γ-irradiation of Molt-4 leukemia cells 2017   article DOI URL 
Abstract: Molt-4 leukemia cells undergo p53-dependent apoptosis accompanied by accumulation of de novo ceramide after 14 hours of γ-irradiation. In order to identify the potential mediators involved in ceramide accumulation and the cell death response, differentially expressed genes were identified by Affymetrix Microarray Analysis. Molt-4-LXSN cells, expressing wild type p53, and p53-deficient Molt-4-E6 cells were irradiated and harvested at 3 and 8 hours post-irradiation. Human genome U133 plus 2.0 array containing textgreater47,000 transcripts was used for gene expression profiling. From over 10,000 probes, 281 and 12 probes were dif-ferentially expressed in Molt-4-LXSN and Molt-4-E6 cells, respectively. Data analysis re-vealed 63 (upregulated) and 20 (downregulated) genes (textgreater2 fold) in Molt-4-LXSN at 3 hours and 140 (upregulated) and 21 (downregulated) at 8 hours post-irradiation. In Molt-4-E6 cells, 5 (upregulated) genes each were found at 3 hours and 8 hours, respectively. In Molt-4-LXSN cells, a significant fraction of the genes with altered expression at 3 hours were found to be involved in apoptosis signaling pathway (BCL2L11), p53 pathway (PMAIP1, CDKN1A and FAS) and oxidative stress response (FDXR, CROT and JUN). Similarly, at 8 hours the genes with altered expression were involved in the apoptosis signaling pathway (BAX, BIK and JUN), p53 pathway (BAX, CDKN1A and FAS), oxidative stress response (FDXR and CROT) and p53 pathway feedback loops 2 (MDM2 and CDKN1A). A global molecular and biological interaction map analysis showed an association of these altered genes with apoptosis, senescence, DNA damage, oxidative stress, cell cycle arrest and cas-pase activation. In a targeted study, activation of apoptosis correlated with changes in gene expression of some of the above genes and revealed sequential activation of both intrinsic and extrinsic apoptotic pathways that precede ceramide accumulation and subsequent exe-cution of apoptosis. One or more of these altered genes may be involved in p53-dependent ceramide accumulation. PLOS ONE | https://doi.org/10.1371/journal.pone.0190221 December 22, 2017 1 / 17 a1111111111 a1111111111 a1111111111 a1111111111 a1111111111 OPEN ACCESS Citation: Hage-Sleiman R, Bahmad H, Kobeissy H, Dakdouk Z, Kobeissy F, Dbaibo G (2017) Genomic alterations during p53-dependent apoptosis induced by γ-irradiation of Molt-4 leukemia cells. PLoS ONE 12(12):
BibTeX:
@article{Hage-Sleiman2017,
  author = {Hage-Sleiman, Rouba and Bahmad, Hisham and Kobeissy, Hadile and Dakdouk, Zeinab and Kobeissy, Firas and Dbaibo, Ghassan},
  title = {Genomic alterations during p53-dependent apoptosis induced by γ-irradiation of Molt-4 leukemia cells},
  year = {2017},
  url = {https://doi.org/},
  doi = {http://doi.org/10.1371/journal.pone.0190221}
}
Hamid, M.H., Rozano, L., Yeong, W.C., Abdullah, J.O. and Saidi, N.B. Analysis of MAP kinase MPK4/MEKK1/MKK genes of Carica papaya L. comparative to other plant homologues. 2017 Bioinformation
Vol. 13(2), pp. 31-41 
article DOI URL 
Abstract: Mitogen-activated protein kinase 4 (MPK4) interacts with the (Mitogen-activated protein kinase kinase kinase 1) MEKK1/ Mitogenactivated protein kinase kinase 1 (MKK1)/ Mitogen-activated protein kinase kinase 2 (MKK2) complex to affect its function in plant development or against pathogen attacks. The KEGG (Kyoto Encyclopedia of Genes and Genomes) network analysis of Arabidopsis thaliana revealed close interactions between those four genes in the same plant-pathogen interaction pathway, which warrants further study of these genes due to their evolutionary conservation in different plant species. Through targeting the signature sequence in MPK4 of papaya using orthologs from Arabidopsis, the predicted sequence of MPK4 was studied using a comparative in silico approach between different plant species and the MAP cascade complex of MEKK1/MKK1/MKK2. This paper reported that MPK4 was highly conserved in papaya with 93% identical across more than 500 bases compared in each species predicted. Slight variations found in the MEKK1/MKK1/MKK2 complex nevertheless still illustrated sequence similarities between most of the species. Localization of each gene in the cascade network was also predicted, potentiating future functional verification of these genes interactions using knock out or/and gene silencing tactics.
BibTeX:
@article{Hamid2017,
  author = {Hamid, Muhammad Hanam and Rozano, Lina and Yeong, Wee Chien and Abdullah, Janna Ong and Saidi, Noor Baity},
  title = {Analysis of MAP kinase MPK4/MEKK1/MKK genes of Carica papaya L. comparative to other plant homologues.},
  journal = {Bioinformation},
  publisher = {Biomedical Informatics Publishing Group},
  year = {2017},
  volume = {13},
  number = {2},
  pages = {31--41},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28642634 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5463617},
  doi = {http://doi.org/10.6026/97320630013031}
}
Han, A.A., Currie, H.N., Loos, M.S., Scardoni, G., Miller, J.V., Prince, N., Mouch, J.A. and Boyd, J.W. The impact of cytokine responses in the intra- and extracellular signaling network of a traumatic injury 2017 Cytokine  article DOI URL 
BibTeX:
@article{Han2017,
  author = {Han, Alice A. and Currie, Holly N. and Loos, Matthew S. and Scardoni, Giovanni and Miller, Julie V. and Prince, Nicole and Mouch, Julia A. and Boyd, Jonathan W.},
  title = {The impact of cytokine responses in the intra- and extracellular signaling network of a traumatic injury},
  journal = {Cytokine},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S1043466617303411},
  doi = {http://doi.org/10.1016/j.cyto.2017.10.027}
}
Harbeck, N., Thomssen, C., Gnant, M., Foukakis, T., Gulluoglu, B.M., Helbich, T., Janni, W., Kiechle, M., Kiesel, L., Mittlböck, M., Paluch-Shimon, S., Paradiso, A., Steger, G., Tsang, J., Untch, M., Heywang-Köbrunner, S. and Raimund Jakesz, M. Editors-in-Chief Associate Editors 2017
Vol. 12(2) 
article URL 
BibTeX:
@article{Harbeck2017,
  author = {Harbeck, Nadia and Thomssen, Christoph and Gnant, Michael and Foukakis, Theodoros and Gulluoglu, Bahadir M and Helbich, Thomas and Janni, Wolfgang and Kiechle, Marion and Kiesel, Ludwig and Mittlböck, Martina and Paluch-Shimon, Shani and Paradiso, Angelo and Steger, Günther and Tsang, Janice and Untch, Michael and Heywang-Köbrunner, Sylvia and Raimund Jakesz, Munich},
  title = {Editors-in-Chief Associate Editors},
  year = {2017},
  volume = {12},
  number = {2},
  url = {https://www.karger.com/Article/PDF/475829}
}
Harbeck, N., Thomssen, C., Gnant, M., Foukakis, T., Gulluoglu, B.M., Helbich, T., Janni, W., Kiechle, M., Kiesel, L., Mittlböck, M., Paluch-Shimon, S., Paradiso, A., Steger, G., Tsang, J., Untch, M., Heywang-Köbrunner, S. and Raimund Jakesz, M. BreastCare 2017
Vol. 12(3) 
book URL 
BibTeX:
@book{Harbeck2017a,
  author = {Harbeck, Nadia and Thomssen, Christoph and Gnant, Michael and Foukakis, Theodoros and Gulluoglu, Bahadir M and Helbich, Thomas and Janni, Wolfgang and Kiechle, Marion and Kiesel, Ludwig and Mittlböck, Martina and Paluch-Shimon, Shani and Paradiso, Angelo and Steger, Günther and Tsang, Janice and Untch, Michael and Heywang-Köbrunner, Sylvia and Raimund Jakesz, Munich},
  title = {BreastCare},
  year = {2017},
  volume = {12},
  number = {3},
  url = {https://www.karger.com/Article/PDF/478766}
}
Jin, W., Chorath, A. and Cao, S. Three Potential Risk Genes for Bipolar Disorder: MT1E, MT1X and CX3CR1 2017 Bipolar Disorder JPBS
Vol. 2017(2) 
article DOI URL 
Abstract: Background: Bipolar disorder (BP) is one of the most common mental illnesses, with the underlying mechanisms remaining unclear. The aim of this study is to investigate the novel genetic risk of BP by systematically reviewing published literature and performing a meta-analysis.
BibTeX:
@article{Jin2017,
  author = {Jin, Wei and Chorath, Ashley and Cao, Shaolong},
  title = {Three Potential Risk Genes for Bipolar Disorder: MT1E, MT1X and CX3CR1},
  journal = {Bipolar Disorder JPBS},
  year = {2017},
  volume = {2017},
  number = {2},
  url = {http://jpbs.qingres.com/UpLoad/PdfFile/JPBS886.pdf},
  doi = {http://doi.org/10.20900/jpbs.20170004}
}
Karmakar, P.C., Kang, H.-G., Kim, Y.-H., Jung, S.-E., Rahman, M.S., Lee, H.-S., Kim, Y.-H., Pang, M.-G. and Ryu, B.-Y. Bisphenol A Affects on the Functional Properties and Proteome of Testicular Germ Cells and Spermatogonial Stem Cells in vitro Culture Model. 2017 Scientific reports
Vol. 7(1), pp. 11858 
article DOI URL 
Abstract: The endocrine disruptor bisphenol A (BPA) is well known for its adverse effect on male fertility. Growing evidence suggests that BPA may interact with testicular germ cells and cause infertility as a result of its estrogenic activity. Objective of current in vitro study was to investigate the proliferation, survivability and stemness properties of mouse testicular germ cells exposed to BPA, and to evaluate possible expression of cellular proteome. Our results showed that germ cell viability and proliferation were not affected by low concentrations (0.01, 0.1, 1, and 10 µM) although significant reduction observed at 100 µM BPA. Germ cell self-renewal and differentiation related marker proteins expression found unchanged at those concentrations. When BPA-exposed germ cells were transplanted into recipient testes, we observed fewer colonies at higher concentrations (10 and 100 µM). Additionally, a significant frequency of recombination failure during meiosis was observed in 10 µM BPA-exposed germ cell transplanted recipient. Moreover, experiment on continuous BPA-exposed and 100 µM BPA-recovered germ cells suggested that spermatogonial stem cells are more potential to survive in adverse environment. Finally, scrutinizing differentially expressed cellular proteins resulted from our proteomic analysis, we conclude that BPA exposure might be associated with several health risks and infertility.
BibTeX:
@article{Karmakar2017,
  author = {Karmakar, Polash Chandra and Kang, Hyun-Gu and Kim, Yong-Hee and Jung, Sang-Eun and Rahman, Md Saidur and Lee, Hee-Seok and Kim, Young-Hyun and Pang, Myung-Geol and Ryu, Buom-Yong},
  title = {Bisphenol A Affects on the Functional Properties and Proteome of Testicular Germ Cells and Spermatogonial Stem Cells in vitro Culture Model.},
  journal = {Scientific reports},
  publisher = {Nature Publishing Group},
  year = {2017},
  volume = {7},
  number = {1},
  pages = {11858},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28928476 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5605497},
  doi = {http://doi.org/10.1038/s41598-017-12195-9}
}
Keck, T., Herrlinger, K.R., Freiburg, B.textperiodcentered., Paris, textperiodcentered., London, textperiodcentered., York, N., Chennai, textperiodcentered., Delhi, N., Bangkok, textperiodcentered., Beijing, textperiodcentered., Shanghai, textperiodcentered., Tokyo, textperiodcentered., Lumpur, K., Singapore, textperiodcentered. and Sydney, textperiodcentered. Volume and Quality in Visceral Medicine Hamburg (Guest Editors) The Interdisciplinary Approach to Gastrointestinal Disease 2017
Vol. 33(2) 
article URL 
BibTeX:
@article{Keck2017,
  author = {Keck, Tobias and Herrlinger, Klaus R and Freiburg, Basel textperiodcentered and Paris, textperiodcentered and London, textperiodcentered and York, New and Chennai, textperiodcentered and Delhi, New and Bangkok, textperiodcentered and Beijing, textperiodcentered and Shanghai, textperiodcentered and Tokyo, textperiodcentered and Lumpur, Kuala and Singapore, textperiodcentered and Sydney, textperiodcentered},
  title = {Volume and Quality in Visceral Medicine Hamburg (Guest Editors) The Interdisciplinary Approach to Gastrointestinal Disease},
  year = {2017},
  volume = {33},
  number = {2},
  url = {https://www.karger.com/Article/PDF/475720}
}
Khabar, K.S.A. Hallmarks of cancer and AU-rich elements. 2017 Wiley interdisciplinary reviews. RNA
Vol. 8(1) 
article URL 
Abstract: Post-transcriptional control of gene expression is aberrant in cancer cells. Sustained stabilization and enhanced translation of specific mRNAs are features of tumor cells. AU-rich elements (AREs), cis-acting mRNA decay determinants, play a major role in the posttranscriptional regulation of many genes involved in cancer processes. This review discusses the role of aberrant ARE-mediated posttranscriptional processes in each of the hallmarks of cancer, including sustained cellular growth, resistance to apoptosis, angiogenesis, invasion, and metastasis. WIREs RNA 2017, 8:e1368. doi: 10.1002/wrna.1368 For further resources related to this article, please visit the WIREs website.
BibTeX:
@article{Khabar2017,
  author = {Khabar, Khalid S A},
  title = {Hallmarks of cancer and AU-rich elements.},
  journal = {Wiley interdisciplinary reviews. RNA},
  year = {2017},
  volume = {8},
  number = {1},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=5215528&tool=pmcentrez&rendertype=abstract}
}
Kim, H.J., Choi, M.G., Park, M.K. and Seo, Y.R. Predictive and Prognostic Biomarkers of Respiratory Diseases due to Particulate Matter Exposure. 2017 Journal of cancer prevention
Vol. 22(1), pp. 6-15 
article DOI URL 
Abstract: Air pollution is getting severe and concerns about its toxicity effects on airway and lung disease are also increasing. Particulate matter (PM) is major component of air pollutant. It causes respiratory diseases, such as asthma, chronic obstructive pulmonary disease, lung cancer, and so on. PM particles enter the airway and lung by inhalation, causing damages to them. Especially, PM2.5 can penetrate into the alveolus and pass to the systemic circulation. It can affect the cardiopulmonary system and cause cardiopulmonary disorders. In this review, we focused on PM-inducing toxicity mechanisms in the framework of oxidative stress, inflammation, and epigenetic changes. We also reviewed its correlation with respiratory diseases. In addition, we reviewed biomarkers related to PM-induced respiratory diseases. These biomarkers might be used for disease prediction and early diagnosis. With recent trend of using genomic analysis tools in the field of toxicogenomics, respiratory disease biomarkers associated with PM will be continuously investigated. Effective biomarkers derived from earlier studies and further studies might be utilized to reduce respiratory diseases.
BibTeX:
@article{Kim2017,
  author = {Kim, Hyo Jeong and Choi, Min Gi and Park, Moo Kyun and Seo, Young Rok},
  title = {Predictive and Prognostic Biomarkers of Respiratory Diseases due to Particulate Matter Exposure.},
  journal = {Journal of cancer prevention},
  publisher = {Korean Society of Cancer Prevention},
  year = {2017},
  volume = {22},
  number = {1},
  pages = {6--15},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28382281 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5380184},
  doi = {http://doi.org/10.15430/JCP.2017.22.1.6}
}
Kim, H.J., Yang, J.H., Kim, H.S., Kim, Y.J., Jang, W. and Seo, Y.R. Exploring potential biomarker responses to lithium in Daphnia magna from the perspectives of function and signaling networks 2017 Molecular & Cellular Toxicology
Vol. 13(1), pp. 83-94 
article DOI URL 
BibTeX:
@article{Kim2017a,
  author = {Kim, Hyo Jeong and Yang, Jun Hyuek and Kim, Hyun Soo and Kim, Yeo Jin and Jang, Wonhee and Seo, Young Rok},
  title = {Exploring potential biomarker responses to lithium in Daphnia magna from the perspectives of function and signaling networks},
  journal = {Molecular & Cellular Toxicology},
  publisher = {The Korean Society of Toxicogenomics and Toxicoproteomics},
  year = {2017},
  volume = {13},
  number = {1},
  pages = {83--94},
  url = {http://link.springer.com/10.1007/s13273-017-0009-6},
  doi = {http://doi.org/10.1007/s13273-017-0009-6}
}
Klimov, E. Facioscapulohumeral Muscular Dystrophy: The Molecular Signaling Pathway 2017 Journal of Neurology & Stroke
Vol. 6(5), pp. 00216 
article DOI  
Abstract: Facioscapulohumeral muscular dystrophy (FSHD) is the third most common myopathy found in adults. It is a unique genetic disease because the activation of the normally inactive gene leads to the development of pathology. The molecular mechanisms and the signaling pathways remain poorly studied so far. Here the literature data is summarized and the molecular signaling pathway of FSHD is reconstructed.
BibTeX:
@article{Klimov2017,
  author = {Klimov, E.},
  title = {Facioscapulohumeral Muscular Dystrophy: The Molecular Signaling Pathway},
  journal = {Journal of Neurology & Stroke},
  year = {2017},
  volume = {6},
  number = {5},
  pages = {00216},
  doi = {http://doi.org/10.15406/jnsk.2017.06.00216}
}
Klussmann, J.P., Wagner, S., Sharma S, Laban, S.P.J., Doescher, S., Bullinger, J., Hoffmann, L., Ulm, T.K.(., Semrau, R.(. and Cologne Oncology Research and Treatment 2017
Vol. 40(6)Contents 
book URL 
Abstract: Focus: Update in Head and Neck Cancer Editorial 318 Head and Neck Cancer – New Insights into a Heterogeneous Disease 320 Risk Factors for Survival Outcome in Surgically Treated Human Papillomavirus- Negative and Positive Patients with Oropharyngeal Cancer 334 Human Papillomavirus-Related Head and Neck Cancer 342 Novel Treatment Options in Head and Neck Cancer 347 The Role of Radiotherapy in Definitive and Postoperative Treatment of Advanced Head and Neck Cancer
BibTeX:
@book{Klussmann2017,
  author = {Klussmann, J P and Wagner, S and Sharma S and Laban, Schuler P J ; and Doescher, S ; and Bullinger, J ; and Hoffmann, L ; and Ulm, T K ( and Semrau, R ( and Cologne},
  title = {Oncology Research and Treatment},
  booktitle = {Contents},
  year = {2017},
  volume = {40},
  number = {6},
  url = {www.karger.com/ort https://www.karger.com/Article/PDF/477476}
}
Kourtian, S., Soueid, J., Makhoul, N.J., Guisso, D.R., Chahrour, M. and Boustany, R.-M.N. Candidate Genes for Inherited Autism Susceptibility in the Lebanese Population 2017 Scientific Reports
Vol. 7, pp. 45336 
article DOI URL 
BibTeX:
@article{Kourtian2017,
  author = {Kourtian, Silva and Soueid, Jihane and Makhoul, Nadine J. and Guisso, Dikran Richard and Chahrour, Maria and Boustany, Rose-Mary N.},
  title = {Candidate Genes for Inherited Autism Susceptibility in the Lebanese Population},
  journal = {Scientific Reports},
  publisher = {Nature Publishing Group},
  year = {2017},
  volume = {7},
  pages = {45336},
  url = {http://www.nature.com/articles/srep45336},
  doi = {http://doi.org/10.1038/srep45336}
}
Kudin, A., Mawasi, H., Eisenkraft, A., Elger, C., Bialer, M. and Kunz, W. Mitochondrial Liver Toxicity of Valproic Acid and Its Acid Derivatives Is Related to Inhibition of α-Lipoamide Dehydrogenase 2017 International Journal of Molecular Sciences
Vol. 18(9), pp. 1912 
article DOI URL 
Abstract: The liver toxicity of valproic acid (VPA) is an established side effect of this widely used antiepileptic drug, which is extremely problematic for patients with metabolic epilepsy and particularly epilepsy due to mitochondrial dysfunction. In the present report, we investigated the reason for liver mitochondrial toxicity of VPA and several acid and amide VPA analogues. While the pyruvate and 2-oxoglutarate oxidation rates of rat brain mitochondria were nearly unaffected by VPA, rat liver mitochondrial pyruvate and 2-oxoglutarate oxidation was severely impaired by VPA concentrations above 100 µM. Among the reactions involved in pyruvate oxidation, pyruvate transport and dehydrogenation steps were not affected by VPA, while α-lipoamide dehydrogenase was strongly inhibited. Strong inhibition of α-lipoamide dehydrogenase was also noted for the VPA one-carbon homolog sec-butylpropylacetic acid (SPA) and to a lesser extent for the VPA constitutional isomer valnoctic acid (VCA), while the corresponding amides of the above three acids valpromide (VPD), sec-butylpropylacetamide (SPD) and valnoctamide (VCD) showed only small effects. We conclude that the active inhibitors of pyruvate and 2-oxoglutarate oxidation are the CoA conjugates of VPA and its acid analogues affecting selectively α-lipoamide dehydrogenase in liver. Amide analogues of VPA, like VCD, show low inhibitory effects on mitochondrial oxidative phosphorylation in the liver, which might be relevant for treatment of patients with mitochondrial epilepsy.
BibTeX:
@article{Kudin2017,
  author = {Kudin, Alexei and Mawasi, Hafiz and Eisenkraft, Arik and Elger, Christian and Bialer, Meir and Kunz, Wolfram},
  title = {Mitochondrial Liver Toxicity of Valproic Acid and Its Acid Derivatives Is Related to Inhibition of α-Lipoamide Dehydrogenase},
  journal = {International Journal of Molecular Sciences},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2017},
  volume = {18},
  number = {9},
  pages = {1912},
  url = {http://www.mdpi.com/1422-0067/18/9/1912},
  doi = {http://doi.org/10.3390/ijms18091912}
}
Latroche, C., Weiss-Gayet, M., Muller, L., Gitiaux, C., Leblanc, P., Liot, S., Ben-Larbi, S., Abou-Khalil, R., Verger, N., Bardot, P., Magnan, M., Chrétien, F., Mounier, R., Germain, S. and Chazaud, B. Coupling between Myogenesis and Angiogenesis during Skeletal Muscle Regeneration Is Stimulated by Restorative Macrophages 2017 Stem Cell Reports  article DOI URL 
Abstract: In skeletal muscle, new functions for vessels have recently emerged beyond oxygen and nutrient supply, through the interactions that vascular cells establish with muscle stem cells. Here, we demonstrate in human and mouse that endothelial cells (ECs) and myogenic progenitor cells (MPCs) interacted together to couple myogenesis and angiogenesis in vitro and in vivo during skeletal muscle regeneration. Kinetics of gene expression of ECs and MPCs sorted at different time points of regeneration identified three effectors secreted by both ECs and MPCs. Apelin, Oncostatin M, and Periostin were shown to control myogenesis/angiogenesis coupling in vitro and to be required for myogenesis and vessel formation during muscle regeneration in vivo. Furthermore, restorative macrophages, which have been previously shown to support myogenesis in vivo, were shown in a 3D triculture model to stimulate myogenesis/angiogenesis coupling, notably through Oncostatin M production. Our data demonstrate that restorative macrophages orchestrate muscle regeneration by controlling myogenesis/angiogenesis coupling.
BibTeX:
@article{Latroche2017,
  author = {Latroche, Claire and Weiss-Gayet, Michèle and Muller, Laurent and Gitiaux, Cyril and Leblanc, Pascal and Liot, Sophie and Ben-Larbi, Sabrina and Abou-Khalil, Rana and Verger, Nicolas and Bardot, Paul and Magnan, Mélanie and Chrétien, Fabrice and Mounier, Rémi and Germain, Stéphane and Chazaud, Bénédicte},
  title = {Coupling between Myogenesis and Angiogenesis during Skeletal Muscle Regeneration Is Stimulated by Restorative Macrophages},
  journal = {Stem Cell Reports},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S2213671117304824},
  doi = {http://doi.org/10.1016/j.stemcr.2017.10.027}
}
Lee, D., Bigdeli, T.B., Williamson, V.S., Vladimirov, V.I., Riley, B.P., Fanous, A.H., Bacanu, S.-A., van der Harst, P., Moore, J.H. and Asselbergs, F.W. Gene Set Enrichment Analyses: lessons learned from the heart failure phenotype 2017 Bioinformatics
Vol. 31(19), pp. 3099-3104 
article DOI URL 
Abstract: Genetic studies for complex diseases have predominantly discovered main effects at individual loci, but have not focused on genomic and environmental contexts important for a phenotype. Gene Set Enrichment Analysis (GSEA) aims to address this by identifying sets of genes or biological pathways contributing to a phenotype, through gene-gene interactions or other mechanisms, which are not the focus of conventional association methods. Approaches that utilize GSEA can now take input from array chips, either gene-centric or genome-wide, but are highly sensitive to study design, SNP selection and pruning strategies, SNP-to-gene mapping, and pathway definitions. Here, we present lessons learned from our experience with GSEA of heart failure, a particularly challenging phenotype due to its underlying heterogeneous etiology. This case study shows that proper data handling is essential to avoid false-positive results. Well-defined pipelines for quality control are needed to avoid reporting spurious results using GSEA.
BibTeX:
@article{Lee2015a,
  author = {Lee, Donghyung and Bigdeli, T. Bernard and Williamson, Vernell S. and Vladimirov, Vladimir I. and Riley, Brien P. and Fanous, Ayman H. and Bacanu, Silviu-Alin and van der Harst, Pim and Moore, Jason H. and Asselbergs, Folkert W.},
  title = {Gene Set Enrichment Analyses: lessons learned from the heart failure phenotype},
  journal = {Bioinformatics},
  publisher = {BioMed Central},
  year = {2017},
  volume = {31},
  number = {19},
  pages = {3099--3104},
  url = {https://academic.oup.com/bioinformatics/article-lookup/doi/10.1093/bioinformatics/btv348},
  doi = {http://doi.org/10.1093/bioinformatics/btv348}
}
Lee, J.-S., Seo, H., Im, K., Park, S.N., Kim, S.-M., Lee, E.K., Kim, J.-A., Lee, J.-h., Kwon, S., Kim, M., Koh, I., Hwang, S., Park, H.-W., Kang, H.-R., Park, K.S., Kim, J.H. and Lee, D.S. Idiopathic hypereosinophilia is clonal disorder? Clonality identified by targeted sequencing 2017 PLOS ONE
Vol. 12(10), pp. e0185602 
article DOI URL 
BibTeX:
@article{Lee2017,
  author = {Lee, Jee-Soo and Seo, Heewon and Im, Kyongok and Park, Si Nae and Kim, Sung-Min and Lee, Eun Kyoung and Kim, Jung-Ah and Lee, Joon-hee and Kwon, Sunghoon and Kim, Miyoung and Koh, Insong and Hwang, Seungwoo and Park, Heung-Woo and Kang, Hye-Ryun and Park, Kyoung Soo and Kim, Ju Han and Lee, Dong Soon},
  title = {Idiopathic hypereosinophilia is clonal disorder? Clonality identified by targeted sequencing},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2017},
  volume = {12},
  number = {10},
  pages = {e0185602},
  url = {http://dx.plos.org/10.1371/journal.pone.0185602},
  doi = {http://doi.org/10.1371/journal.pone.0185602}
}
Li, Y., He, C., Sheng, J., Jones, P. and Yong Li, G. Med One Possible Linkage Between Osteoporosis and Genes Associated with Type 1 Diabetes Mellitus 2017   article DOI URL 
Abstract: Background: Previous studies suggested that Type 1 diabetes mellitus (T1DM) is related to an increased risk of osteoporosis (OP) with unknown mechanism. Here, we hypothesized that TIDM and OP present shared molecular basis, and that OP related genes may also play roles for TIDM. Method: To identify potential OP risk genes from T1DM-gene group, we conducted an integrated analysis using large scale ResNet relation data and gene expression data for T1DM and OP. Disease-gene relation data were acquired from Pathway Studio ResNet Mammalian database. Gene expression profile were acquired from samples of 40 subjects including 20 OP cases and 20 normal controls. Results: Genes linked to T1DM and OP present significant overlap (183 genes, p-value = 2.84E-128). These genes play roles through multiple genetic pathways (enrichment p-value textless 8.8e-23 for the top 10 pathways) influencing the pathogenesis of both diseases. A genetic network of 16 genes were identified. T1DM may exert influence on OP these genes. Two T1DM genes, ITGAE and RELB, present significant difference (p-value textless 0.0005) between OP cases and controls. Network analysis support the results and reveal strong functional association between OP and these two genes. Conclusion: Results from this study support the hypothesis that complex genetic associations exist between T1DM and OP, and that T1DM related genes should be tested for their potential roles in OP pathogenesis.
BibTeX:
@article{Li2017,
  author = {Li, Yong and He, Chengjun and Sheng, Jinhua and Jones, Paul and Yong Li, Genes},
  title = {Med One Possible Linkage Between Osteoporosis and Genes Associated with Type 1 Diabetes Mellitus},
  year = {2017},
  url = {http://mo.qingres.com},
  doi = {http://doi.org/10.20900/mo.20160026}
}
Liu, D. and Wang, Z. Identification and Validation Novel Risk Genes for Autism Spectrum Disorder – A Meta- Analysis 2017 Autism Spectrum Disorder JPBS
Vol. 12(1) 
article DOI URL 
Abstract: Background: Autism spectrum disorders (ASD) are classified as neurodevelopmental disorders. The aim of this study was to investigate the genetic risk of ASD by systematically reviewing the published literature and performing a meta-analysis.
BibTeX:
@article{Liu2017,
  author = {Liu, Dongbai and Wang, Zeya},
  title = {Identification and Validation Novel Risk Genes for Autism Spectrum Disorder – A Meta- Analysis},
  journal = {Autism Spectrum Disorder JPBS},
  year = {2017},
  volume = {12},
  number = {1},
  url = {http://www.qingres.com/UpLoad/PdfFile/JPBS884.pdf},
  doi = {http://doi.org/10.20900/jpbs.20170002}
}
Liu, Y., Cui, J., Hu, Y., Du, G. and Qin, X. Integrating untargeted metabonomics, partial least square regression analysis and MetPA to explore the targeted pathways involved into Huangqi Jiangzhong Tang against chronic atrophic gastritis rats 2017 Chemometrics and Intelligent Laboratory Systems  article DOI URL 
BibTeX:
@article{Liu2017a,
  author = {Liu, Yuetao and Cui, Jiajia and Hu, Yinghuan and Du, Guanhua and Qin, Xuemei},
  title = {Integrating untargeted metabonomics, partial least square regression analysis and MetPA to explore the targeted pathways involved into Huangqi Jiangzhong Tang against chronic atrophic gastritis rats},
  journal = {Chemometrics and Intelligent Laboratory Systems},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S0169743916304518},
  doi = {http://doi.org/10.1016/j.chemolab.2017.03.005}
}
Liu, Y. and Dey, M. Dietary Phenethyl Isothiocyanate Protects Mice from Colitis Associated Colon Cancer 2017 International Journal of Molecular Sciences
Vol. 18(9), pp. 1908 
article DOI URL 
Abstract: We have previously reported alleviation of dextran sodium sulfate (DSS)-induced ulcerative colitis signs in phenethyl isothiocyanate (PEITC)-treated mice. Here we investigated chemoprotective activities of PEITC in mice with Azoxymethane-DSS induced colitis associated colon carcinogenesis. We also examined the molecular mediators associated with the PEITC effects using relevant cell lines. A 0.12% PEITC-enriched mouse-diet reduced mucosal and submucosal inflammation as well as glandular atypia by 12% and the frequency of adenocarcinoma by 17% with a concomitant improvement in overall disease activity indices compared to the diseased control group. Lipopolysaccharide-induced in vitro up-regulation of key mediators of inflammation, immune response, apoptosis, and cell proliferation were attenuated by 10 μM PEITC. Three of these mediators showed concentration-dependent reduction in respective mRNAs. Furthermore, PEITC inhibited Nuclear factor kappa B1 (NFκB1) proteins in a concentration-dependent manner. The NFκB1 mRNA expression inversely correlated (r = −0.940, p = 0.013) with tri-methylation of lysine 27 on histone 3 near its promoter region in a time-dependent manner. These results indicate that PEITC may slow down the development of colon carcinogenesis in an inflammatory intestinal setting which is potentially associated with epigenetic modulation of NFκB1 signaling.
BibTeX:
@article{Liu2017b,
  author = {Liu, Yi and Dey, Moul},
  title = {Dietary Phenethyl Isothiocyanate Protects Mice from Colitis Associated Colon Cancer},
  journal = {International Journal of Molecular Sciences},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2017},
  volume = {18},
  number = {9},
  pages = {1908},
  url = {http://www.mdpi.com/1422-0067/18/9/1908},
  doi = {http://doi.org/10.3390/ijms18091908}
}
Lo Surdo, P., Calderone, A., Iannuccelli, M., Licata, L., Peluso, D., Castagnoli, L., Cesareni, G. and Perfetto, L. DISNOR: a disease network open resource 2017 Nucleic Acids Research  article DOI URL 
BibTeX:
@article{LoSurdo2017,
  author = {Lo Surdo, Prisca and Calderone, Alberto and Iannuccelli, Marta and Licata, Luana and Peluso, Daniele and Castagnoli, Luisa and Cesareni, Gianni and Perfetto, Livia},
  title = {DISNOR: a disease network open resource},
  journal = {Nucleic Acids Research},
  year = {2017},
  url = {http://academic.oup.com/nar/article/doi/10.1093/nar/gkx876/4282672/DISNOR-a-disease-network-open-resource},
  doi = {http://doi.org/10.1093/nar/gkx876}
}
Lu, Y., Wang, J., Guo, X., Yan, S. and Dai, J. Perfluorooctanoic acid affects endocytosis involving clathrin light chain A and microRNA-133b-3p in mouse testes. 2017 Toxicology and applied pharmacology
Vol. 318, pp. 41-48 
article URL 
Abstract: Perfluorooctanoic acid (PFOA) is an abundant perfluoroalkyl substance widely applied in industrial and consumer products. Among its potential health hazards, testicular toxicity is of major concern. To explore the potential effect of miRNA on post-translational regulation after PFOA exposure, changes in miRNAs were detected via miRNA array. Seventeen miRNAs were differentially expressed (eight upregulated, nine downregulated) in male mouse testes after exposure to 5mg/kg/d of PFOA for 28d (textgreater1.5-fold and Ptextless0.05 compared with the control). Eight of these miRNAs were further selected for TaqMan qPCR analysis. Proteomic profile analysis indicated that many changed proteins after PFOA treatment, including intersectin 1 (ITSN1), serine protease inhibitor A3K (Serpina3k), and apolipoprotein a1 (APOA1), were involved in endocytosis and blood-testis barrier (BTB) processes. These changes were further verified by immunohistochemical and Western blot analyses. Endocytosis-related genes were selected for qPCR analysis, with many found to be significantly changed after PFOA treatment, including epidermal growth factor receptor pathway substrate 8 (Eps8), Eps15, cortactin, cofilin, espin, vinculin, and zyxin. We further predicted the potential interaction between changed miRNAs and proteins, which indicated that miRNAs might play a role in the post-translational regulation of gene expression after PFOA treatment in mouse testes. Among them, miR-133b-3p/clathrin light chain A (CLTA) was selected and verified in vitro by transfection and luciferase activity assay. Results showed that PFOA exposure affects endocytosis in mouse testes and that CLTA is a potential target of miR-133b-3p.
BibTeX:
@article{Lu2017,
  author = {Lu, Yin and Wang, Jianshe and Guo, Xuejiang and Yan, Shengmin and Dai, Jiayin},
  title = {Perfluorooctanoic acid affects endocytosis involving clathrin light chain A and microRNA-133b-3p in mouse testes.},
  journal = {Toxicology and applied pharmacology},
  year = {2017},
  volume = {318},
  pages = {41--48},
  url = {http://www.sciencedirect.com/science/article/pii/S0041008X17300340}
}
Manek, R., Moghieb, A., Yang, Z., Kumar, D., Kobessiy, F., Sarkis, G.A., Raghavan, V. and Wang, K.K. Protein Biomarkers and Neuroproteomics Characterization of Microvesicles/Exosomes from Human Cerebrospinal Fluid Following Traumatic Brain Injury 2017 Molecular Neurobiology, pp. 1-17  article DOI URL 
BibTeX:
@article{Manek2017,
  author = {Manek, Rachna and Moghieb, Ahmed and Yang, Zhihui and Kumar, Dhwani and Kobessiy, Firas and Sarkis, George Anis and Raghavan, Vijaya and Wang, Kevin K.W.},
  title = {Protein Biomarkers and Neuroproteomics Characterization of Microvesicles/Exosomes from Human Cerebrospinal Fluid Following Traumatic Brain Injury},
  journal = {Molecular Neurobiology},
  publisher = {Springer US},
  year = {2017},
  pages = {1--17},
  url = {http://link.springer.com/10.1007/s12035-017-0821-y},
  doi = {http://doi.org/10.1007/s12035-017-0821-y}
}
Marjan, P., Martyniuk, C.J., Fuzzen, M.L.M., MacLatchy, D.L., McMaster, M.E. and Servos, M.R. Returning to normal? Assessing transcriptome recovery over time in male rainbow darter (Etheostoma caeruleum) liver in response to wastewater treatment plant upgrades. 2017 Environmental toxicology and chemistry  article URL 
Abstract: The present study measured hepatic transcriptome responses in male rainbow darter (Etheostoma caeruleum) exposed to 2 municipal wastewater treatment plants (MWWTPs) (Kitchener and Waterloo) over 4 fall seasons (2011 - 2014) in the Grand River Ontario. The overall goal was to determine if upgrades at the Kitchener MWWTP (in 2012) resulted in transcriptome responses indicative of improved effluent quality. The number of differentially expressed probes in fish downstream of the Kitchener outfall (904-1,223), remained comparable to that downstream of Waterloo (767-3,867). Noteworthy was that year, and the interaction of year and site, explained variability in more than twice the number of transcripts than site alone, suggesting that year and the interaction of year and site had a greater effect on the transcriptome than site alone. Gene Set Enrichment Analysis revealed a gradual reduction in the number of gene ontologies over time at exposure sites, which corresponded with lower contaminant load. Sub Network Enrichment Analysis revealed that there were noticeable shifts in the cell pathways differently expressed in the liver pre- and post-upgrade. The dominant pathways altered pre-upgrades were related to genetic modifications and cell division whereas, post-upgrades, they were associated with the immune system, reproduction, and biochemical responses. Molecular pathways were dynamic over time, and following the upgrades, there was little evidence that gene expression profiles in fish collected from high impact sites post-upgrade were more similar to fish collected from reference site. This article is protected by copyright. All rights reserved.
BibTeX:
@article{Marjan2017,
  author = {Marjan, Patricija and Martyniuk, Christopher J and Fuzzen, Meghan L M and MacLatchy, Deborah L and McMaster, Mark E and Servos, Mark R},
  title = {Returning to normal? Assessing transcriptome recovery over time in male rainbow darter (Etheostoma caeruleum) liver in response to wastewater treatment plant upgrades.},
  journal = {Environmental toxicology and chemistry},
  year = {2017},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28106290}
}
Marjan, P., Bragg, L.M., Maclatchy, D.L., Servos, M.R. and Martyniuk, C.J. How does reference site selection influence interpretation of omics data? Evaluating liver transcriptome responses in male rainbow darter (Ethestoma caeruleum) across an urban environment 2017   article URL 
BibTeX:
@article{Marjan2017a,
  author = {Marjan, Patricija and Bragg, Leslie M and Maclatchy, Deborah L and Servos, Mark R and Martyniuk, Christopher J},
  title = {How does reference site selection influence interpretation of omics data? Evaluating liver transcriptome responses in male rainbow darter (Ethestoma caeruleum) across an urban environment},
  year = {2017},
  url = {http://pubs.acs.org/doi/pdf/10.1021/acs.est.7b00894}
}
Middleton, R.P., Lacroix, S., Scott-Boyer, M.-P., Dordevic, N., Kennedy, A.D., Slusky, A.R., Carayol, J., Petzinger-Germain, C., Beloshapka, A. and Kaput, J. Metabolic Differences between Dogs of Different Body Sizes 2017 Journal of Nutrition and Metabolism  article DOI URL 
Abstract: Introduction. Te domesticated dog, Canis lupus familiaris, has been selectively bred to produce extreme diversity in phenotype and
genotype. Dogs have an immense diversity in weight and height. Specifc diferences in metabolism have not been characterized in
small dogs as compared to larger dogs. Objectives.Tis study aims to identify metabolic, clinical, and microbiota diferences between
small and larger dogs. Methods. Gas chromatography/mass spectrometry, liquid chromatography/tandem mass spectrometry,
clinical chemistry analysis, dual-energy X-ray absorptiometry, and 16S pyrosequencing were used to characterize blood metabolic,
clinical, and fecal microbiome systems, respectively. Eighty-three canines from seven diferent breeds, fed the same kibble diet for 5
weeks, were used in the study. Results. 449 metabolites, 16 clinical parameters, and 6 bacteria (at the genus level) were signifcantly
diferent between small and larger dogs. Hierarchical clustering of the metabolites yielded 8 modules associated with small dog size.
Conclusion. Small dogs had a lower antioxidant status and diferences in circulating amino acids. Some of the amino acid diferences
could be attributed to diferences in microfora. Additionally, analysis of small dog metabolites and clinical parameters refected a
network which strongly associates with kidney function.
BibTeX:
@article{Middleton2017,
  author = {Middleton, Rondo P and Lacroix, Sebastien and Scott-Boyer, Marie-Pier and Dordevic, Nikola and Kennedy, Adam D and Slusky, Amanda R and Carayol, Jerome and Petzinger-Germain, Christina and Beloshapka, Alison and Kaput, Jim},
  title = {Metabolic Differences between Dogs of Different Body Sizes},
  journal = {Journal of Nutrition and Metabolism},
  year = {2017},
  url = {https://www.researchgate.net/profile/SebastienLacroix/publication/320634806MetabolicDifferencesbetweenDogsofDifferentBodySizes/links/59f38312a6fdcc075ec34a77/Metabolic-Differences-between-Dogs-of-Different-Body-Sizes.pdf},
  doi = {http://doi.org/10.1155/2017/4535710}
}
Niranjana Murthy, A.S., Veerappa, A.M. and Ramachandra, N.B. Whole exome sequencing of discordant diseases in Monozygotic twins with Down syndrome reveals mutations for Congenital Heart Defect and epileptic seizures 2017 Meta Gene  article DOI URL 
BibTeX:
@article{NiranjanaMurthy2017,
  author = {Niranjana Murthy, Ashitha S. and Veerappa, Avinash M. and Ramachandra, Nallur B.},
  title = {Whole exome sequencing of discordant diseases in Monozygotic twins with Down syndrome reveals mutations for Congenital Heart Defect and epileptic seizures},
  journal = {Meta Gene},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S2214540017300191},
  doi = {http://doi.org/10.1016/j.mgene.2017.03.004}
}
Paiva, C., Rowland, T.A., Sreekantham, B., Godbersen, C., Best, S.R., Kaur, P., Loriaux, M.M., Spurgeon, S.E.F., Danilova, O.V. and Danilov, A.V. SYK inhibition thwarts the BAFF - B-cell receptor crosstalk and thereby antagonizes Mcl-1 in chronic lymphocytic leukemia 2017 Haematologica  article URL 
BibTeX:
@article{Paiva2017,
  author = {Paiva, Cody and Rowland, Taylor A. and Sreekantham, Bhargava and Godbersen, Claire and Best, Scott R. and Kaur, Prabhjot and Loriaux, Marc M. and Spurgeon, Stephen E. F. and Danilova, Olga V. and Danilov, Alexey V.},
  title = {SYK inhibition thwarts the BAFF - B-cell receptor crosstalk and thereby antagonizes Mcl-1 in chronic lymphocytic leukemia},
  journal = {Haematologica},
  year = {2017},
  url = {http://www.haematologica.org/content/early/2017/08/18/haematol.2017.170571}
}
Panach, L., Serna, E., Tarín, J.J., Cano, A. and García-Pérez, M.Á. A translational approach from an animal model identifies CD80 as a candidate gene for the study of bone phenotypes in postmenopausal women 2017 Osteoporosis International, pp. 1-11  article DOI URL 
BibTeX:
@article{Panach2017,
  author = {Panach, L. and Serna, E. and Tarín, J. J. and Cano, A. and García-Pérez, M. Á.},
  title = {A translational approach from an animal model identifies CD80 as a candidate gene for the study of bone phenotypes in postmenopausal women},
  journal = {Osteoporosis International},
  publisher = {Springer London},
  year = {2017},
  pages = {1--11},
  url = {http://link.springer.com/10.1007/s00198-017-4061-9},
  doi = {http://doi.org/10.1007/s00198-017-4061-9}
}
Papaleo, E., Gromova, I. and Gromov, P. Gaining insights into cancer biology through exploration of the cancer secretome using proteomic and bioinformatic tools 2017 Expert Review of Proteomics, pp. 1-15  article DOI URL 
Abstract: ABSTRACTIntroduction: Tumor-associated proteins released by cancer cells and by tumor stroma cells, referred as ‘cancer secretome', represent a valuable resource for discovery of potential cancer biomarkers. The last decade was marked by a great increase in number of studies focused on various aspects of cancer secretome including, composition and identification of components externalized by malignant cells and by the components of tumor microenvironment.Areas covered: Here, we provide an overview of achievements in the proteomic analysis of the cancer secretome, elicited through the tumor-associated interstitial fluid recovered from malignant tissues ex vivo or the protein component of conditioned media obtained from cultured cancer cells in vitro. We summarize various bioinformatic tools and approaches and critically appraise their outcomes, focusing on problems and challenges that arise when applied for the analysis of cancer secretomic databases.Expert commentary: Recent achievements in the omics- ana...
BibTeX:
@article{Papaleo2017,
  author = {Papaleo, Elena and Gromova, Irina and Gromov, Pavel},
  title = {Gaining insights into cancer biology through exploration of the cancer secretome using proteomic and bioinformatic tools},
  journal = {Expert Review of Proteomics},
  publisher = {Taylor & Francis},
  year = {2017},
  pages = {1--15},
  url = {https://www.tandfonline.com/doi/full/10.1080/14789450.2017.1387053},
  doi = {http://doi.org/10.1080/14789450.2017.1387053}
}
Parisien, M., Khoury, S., Chabot-Doré, A.-J., Sotocinal, S.G., Slade, G.D., Smith, S.B., Fillingim, R.B., Ohrbach, R., Greenspan, J.D., Maixner, W., Mogil, J.S., Belfer, I. and Diatchenko, L. Effect of Human Genetic Variability on Gene Expression in Dorsal Root Ganglia and Association with Pain Phenotypes 2017 Cell Reports
Vol. 19(9), pp. 1940-1952 
article DOI URL 
Abstract: Dorsal root ganglia (DRG) relay sensory information to the brain, giving rise to the perception of pain, disorders of which are prevalent and burdensome. Here, we mapped expression quantitative trait loci (eQTLs) in a collection of human DRGs. DRG eQTLs were enriched within untranslated regions of coding genes of low abundance, with some overlapping with other brain regions and blood cell cis-eQTLs. We confirm functionality of identified eQTLs through their significant enrichment within open chromatin and highly deleterious SNPs, particularly at the exon level, suggesting substantial contribution of eQTLs to alternative splicing regulation. We illustrate pain-related genetic association results explained by DRG eQTLs, with the strongest evidence for contribution of the human leukocyte antigen (HLA) locus, confirmed using a mouse inflammatory pain model. Finally, we show that DRG eQTLs are found among hits in numerous genome-wide association studies, suggesting that this dataset will help address pain components of non-pain disorders.
BibTeX:
@article{Parisien2017,
  author = {Parisien, Marc and Khoury, Samar and Chabot-Doré, Anne-Julie and Sotocinal, Susana G. and Slade, Gary D. and Smith, Shad B. and Fillingim, Roger B. and Ohrbach, Richard and Greenspan, Joel D. and Maixner, William and Mogil, Jeffrey S. and Belfer, Inna and Diatchenko, Luda},
  title = {Effect of Human Genetic Variability on Gene Expression in Dorsal Root Ganglia and Association with Pain Phenotypes},
  journal = {Cell Reports},
  year = {2017},
  volume = {19},
  number = {9},
  pages = {1940--1952},
  url = {http://www.sciencedirect.com/science/article/pii/S2211124717306435},
  doi = {http://doi.org/10.1016/j.celrep.2017.05.018}
}
Park, S.K., Jeong, J.Y., Cho, E.S., Jeong, Y.D. and Park, C.S. Short Communication - RNA-Seq Reveals Differentially Expressed Genes of Pig Vaccinated with Modified Live Attenuated Porcine Epidemic Diarrhea 2017 Pakistan Journal of Zoology
Vol. 49(3), pp. 1107-1107 
article URL 
BibTeX:
@article{Park2017,
  author = {Park, Sung Kwon and Jeong, Jin Young and Cho, Eun Seok and Jeong, Yong Dae and Park, Chang Seok},
  title = {Short Communication - RNA-Seq Reveals Differentially Expressed Genes of Pig Vaccinated with Modified Live Attenuated Porcine Epidemic Diarrhea},
  journal = {Pakistan Journal of Zoology},
  publisher = {Asianet-Pakistan},
  year = {2017},
  volume = {49},
  number = {3},
  pages = {1107--1107},
  url = {http://go.galegroup.com/ps/anonymous?id=GALE%7CA493783182&sid=googleScholar&v=2.1&it=r&linkaccess=fulltext&issn=00309923&p=AONE&sw=w&authCount=1&isAnonymousEntry=true}
}
Parodi, D., Greenfield, M., Evans, C., Chichura, A., Alpaugh, A., Williams, J., Cyrus, K. and Martin, M. Alteration of Mammary Gland Development and Gene Expression by In Utero Exposure to Cadmium 2017 International Journal of Molecular Sciences
Vol. 18(9), pp. 1939 
article DOI URL 
Abstract: Environmental exposure to estrogens and estrogen like contaminants during early development is thought to contribute to the risk of developing breast cancer primarily due to an early onset of puberty; however, exposure during key developing windows may also influence the risk of developing the disease. The goal of this study was to ask whether in utero exposure to the metalloestrogen cadmium alters mammary gland development due to acceleration of puberty onset or to an effect on early development of the mammary gland. The results show that, in addition to advancing the onset of puberty, in utero exposure to the metalloestrogen cadmium altered mammary gland development prior to its effect on puberty onset. In utero exposure resulted in an expansion of the number of mammosphere-forming cells in the neonatal mammary gland and an increase in branching, epithelial cells, and density in the prepubertal mammary gland. In the postpubertal mammary gland, there was a further expansion of the mammary stem/progenitor cell population and overexpression of estrogen receptor-alpha (ERα) that was due to the overexpression and altered regulation of the ERα transcripts derived from exons O and OT in response to estradiol. These results suggest that in utero exposure to cadmium increases stem/progenitor cells, cell density, and expression of estrogen receptor-alpha that may contribute to the risk of developing breast cancer.
BibTeX:
@article{Parodi2017,
  author = {Parodi, Daniela and Greenfield, Morgan and Evans, Claire and Chichura, Anna and Alpaugh, Alexandra and Williams, James and Cyrus, Kedra and Martin, Mary},
  title = {Alteration of Mammary Gland Development and Gene Expression by In Utero Exposure to Cadmium},
  journal = {International Journal of Molecular Sciences},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2017},
  volume = {18},
  number = {9},
  pages = {1939},
  url = {http://www.mdpi.com/1422-0067/18/9/1939},
  doi = {http://doi.org/10.3390/ijms18091939}
}
Paullin, T., Powell, C., Menzie, C., Hill, R., Cheng, F., Martyniuk, C.J. and Westerheide, S.D. Spheroid growth in ovarian cancer alters transcriptome responses for stress pathways and epigenetic responses 2017 PLOS ONE
Vol. 12(8), pp. e0182930 
article DOI URL 
BibTeX:
@article{Paullin2017,
  author = {Paullin, Trillitye and Powell, Chase and Menzie, Christopher and Hill, Robert and Cheng, Feng and Martyniuk, Christopher J. and Westerheide, Sandy D.},
  title = {Spheroid growth in ovarian cancer alters transcriptome responses for stress pathways and epigenetic responses},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2017},
  volume = {12},
  number = {8},
  pages = {e0182930},
  url = {http://dx.plos.org/10.1371/journal.pone.0182930},
  doi = {http://doi.org/10.1371/journal.pone.0182930}
}
Rahbar, S., Novin, M.G., Alizadeh, E., Shahnazi, V., Pashaei-Asl, F., AsrBadr, Y.A., Farzadi, L., Ebrahimie, E. and Pashaiasl, M. New insights into the expression profile of MicroRNA-34c and P53 in infertile men spermatozoa and testicular tissue 2017 Cellular and Molecular Biology
Vol. 63(8), pp. 77 
article DOI URL 
Abstract: Spermatogenesis is proliferation and differentiation processes of stem spermatogonia into mature spermatozoa controlled by the genes responsible for transcription and post transcription levels. MicroRNAs (miRNA) are  the key factors during gene expression in RNA silencing and post-transcriptional regulation. They play main roles in regulation of early and late spermatogenesis, and reproduction. In this study, we investigate the role of miRNAs in infertile males. The patients were assigned to five groups based on semen analysis (n=55), including normozoospermic (N), moderate oligoasthenoteratozoospermic (MOAT), severe oligoasthenoteratozoospermic (SOAT), obstructive azoospermia (OA) and non-obstructive azoospermia (NOA). Quantitative RT-PCR was recruited to study the expression of miR-34c and tumor suppressor p53 gene. In addition, malondialdehyde (MDA) and DNA fragmentation was measured. Network analysis was performed using Pathway Studio web tool (Elsevier). Our results revealed statistically significant increased expression of miR-34c in moderate oligoasthenoteratozoospermic, non-obstructive azoospermia and an increased expression of p53 in MOAT, SOAT and NOA males. Also, the percentage of DNA fragmentation and oxidative stress was significantly higher in infertile groups (MOAT and SOAT) than other groups. These findings provide a novel molecular mechanism of gene regulation during cell-cycle and apoptosis in sperm, which gives a new regulatory insight into male infertility in terms of molecular diagnosis.
BibTeX:
@article{Rahbar2017,
  author = {Rahbar, S. and Novin, M. G. and Alizadeh, E. and Shahnazi, V. and Pashaei-Asl, F. and AsrBadr, Y. A. and Farzadi, L. and Ebrahimie, E. and Pashaiasl, M.},
  title = {New insights into the expression profile of MicroRNA-34c and P53 in infertile men spermatozoa and testicular tissue},
  journal = {Cellular and Molecular Biology},
  year = {2017},
  volume = {63},
  number = {8},
  pages = {77},
  url = {https://www.cellmolbiol.org/index.php/CMB/article/view/1348},
  doi = {http://doi.org/10.14715/cmb/2017.63.8.17}
}
Rahman, M.S., Kwon, W.-S. and Pang, M.-G. Prediction of male fertility using capacitation-associated proteins in spermatozoa 2017 Molecular Reproduction and Development  article DOI URL 
BibTeX:
@article{Rahman2017,
  author = {Rahman, Md Saidur and Kwon, Woo-Sung and Pang, Myung-Geol},
  title = {Prediction of male fertility using capacitation-associated proteins in spermatozoa},
  journal = {Molecular Reproduction and Development},
  year = {2017},
  url = {http://doi.wiley.com/10.1002/mrd.22810},
  doi = {http://doi.org/10.1002/mrd.22810}
}
Rahman, N.I.A., Abdul Murad, N.A., Mollah, M.M., Jamal, R. and Harun, R. NFIX as a Master Regulator for Lung Cancer Progression. 2017 Frontiers in pharmacology
Vol. 8, pp. 540 
article DOI URL 
Abstract: About 40% of lung cancer cases globally are diagnosed at the advanced stage. Lung cancer has a high mortality and overall survival in stage I disease is only 70%. This study was aimed at finding a candidate of transcription regulator that initiates the mechanism for metastasis by integrating computational and functional studies. The genes involved in lung cancer were retrieved using in silico software. 10 kb promoter sequences upstream were scanned for the master regulator. Transient transfection of shRNA NFIXs were conducted against A549 and NCI-H1299 cell lines. qRT-PCR and functional assays for cell proliferation, migration and invasion were carried out to validate the involvement of NFIX in metastasis. Genome-wide gene expression microarray using a HumanHT-12v4.0 Expression BeadChip Kit was performed to identify differentially expressed genes and construct a new regulatory network. The in silico analysis identified NFIX as a master regulator and is strongly associated with 17 genes involved in the migration and invasion pathways including IL6ST, TIMP1 and ITGB1. Silencing of NFIX showed reduced expression of IL6ST, TIMP1 and ITGB1 as well as the cellular proliferation, migration and invasion processes. The data was integrated with the in silico analyses to find the differentially expressed genes. Microarray analysis showed that 18 genes were expressed differentially in both cell lines after statistical analyses integration between t-test, LIMMA and ANOVA with Benjamini-Hochberg adjustment at p-value textless 0.05. A transcriptional regulatory network was created using all 18 genes, the existing regulated genes including the new genes PTCH1, NFAT5 and GGCX that were found highly associated with NFIX, the master regulator of metastasis. This study suggests that NFIX is a promising target for therapeutic intervention that is expected to inhibit metastatic recurrence and improve survival rate.
BibTeX:
@article{Rahman2017a,
  author = {Rahman, Nor I A and Abdul Murad, Nor A and Mollah, Mohammad M and Jamal, Rahman and Harun, Roslan},
  title = {NFIX as a Master Regulator for Lung Cancer Progression.},
  journal = {Frontiers in pharmacology},
  publisher = {Frontiers Media SA},
  year = {2017},
  volume = {8},
  pages = {540},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28871224 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5566971},
  doi = {http://doi.org/10.3389/fphar.2017.00540}
}
Rahman, M.S., Kwon, W.-S., Ryu, D.-Y., Khatun, A., Karmakar, P.C., Ryu, B.-Y. and Pang, M.-G. Functional and Proteomic Alterations of F1 Capacitated Spermatozoa of Adult Mice Following Gestational Exposure to Bisphenol A 2017 Journal of Proteome Research, pp. acs.jproteome.7b00668  article DOI URL 
Abstract: Studies regarding bisphenol A (BPA) exposure and male (in)fertility have conventionally focused on modifications in ejaculated spermatozoa function from exposed individuals. However, mammalian spermatozoa are incapable of fertilization prior to achieving capacitation, the penultimate step in maturation. Therefore, it is necessary to investigate BPA-induced changes in capacitated spermatozoa and assess the consequences on subsequent fertilization. Here, we demonstrate the effect of gestational BPA exposure (50 μg, 5 mg, and 50 mg•kg bw-1•day-1) on the functions, biochemical properties, and proteomic profiles of F1 capacitated spermatozoa from adult mice. The data showed that high concentrations of BPA inhibited motility, motion kinematics, and capacitation of spermatozoa, perhaps because of increased lipid peroxidation and protein tyrosine nitration, and decreased intracellular ATP levels and protein kinase-A activity in spermatozoa. We also found that BPA compromised the rates of fertilization and early e...
BibTeX:
@article{Rahman2017b,
  author = {Rahman, Md Saidur and Kwon, Woo-Sung and Ryu, Do-Yeal and Khatun, Amena and Karmakar, Polash Chandra and Ryu, Buom-Yong and Pang, Myung-Geol},
  title = {Functional and Proteomic Alterations of F1 Capacitated Spermatozoa of Adult Mice Following Gestational Exposure to Bisphenol A},
  journal = {Journal of Proteome Research},
  publisher = { American Chemical Society },
  year = {2017},
  pages = {acs.jproteome.7b00668},
  url = {http://pubs.acs.org/doi/abs/10.1021/acs.jproteome.7b00668},
  doi = {http://doi.org/10.1021/acs.jproteome.7b00668}
}
Rastegar-Mojarad, M., Elayavilli, R.K., Wang, Y., Liu, S., Shen, F. and Liu, H. Semantic Information Retrieval : Exploring Dependency and Word Embedding Features in Biomedical Information Retrieval 2017   article URL 
Abstract: We present an information retrieval system developed to retrieve evidence sentences for a given Biological Expression Language (BEL) statement. Previously, as a participant of the BEL challenge in BioCreative V, we proposed and developed a system called BELTracker, which mainly focused on lexical features. In the BEL challenge of BioCreative VI, we explored usage of syntactic and semantic features in identifying and ranking evidence sentences. Similar to BELTracker, the new system has 3 main components: indexing, retrieval, and ranking. In this system, we trained several classifiers for the ranking process. These classifiers have lexical, syntactic, and semantic features such as unigrams, bigrams, word embedding, and dependency-word embedding. Our evaluation showed that the new system obtained higher mean average precision on BioCreative V's test data when compared to BELTracker under full, relaxed, and context criteria. The challenge organizers provided 100 BEL statements as test data and we submitted 2 set of results 1) baseline (using ElasticSearch results), and 2) using the classifiers to re-rank the ElasticSearch results. The baseline system achieved 30.6% and 45.8% precision under full and partial criteria, respectively. Using various classifiers for ranking, the precision of the system increased to 31.6% and 50.2%, respectively, for full and partial criteria Semantic Information Retrieval: Exploring... (PDF Download Available). Available from: https://www.researchgate.net/publication/320335872SemanticInformationRetrievalExploringDependencyandWordEmbeddingFeaturesinBiomedicalInformationRetrieval [accessed Apr 22 2018].
BibTeX:
@article{Rastegar-Mojarad,
  author = {Rastegar-Mojarad, Majid and Elayavilli, Ravikumar Komandur and Wang, Yanshan and Liu, Sijia and Shen, Feichen and Liu, Hongfang},
  title = {Semantic Information Retrieval : Exploring Dependency and Word Embedding Features in Biomedical Information Retrieval},
  year = {2017},
  url = {https://www.researchgate.net/profile/MajidRastegar-Mojarad/publication/320335872SemanticInformationRetrievalExploringDependencyandWordEmbeddingFeaturesinBiomedicalInformationRetrieval/links/59df9adfaca272386b62437a/Semantic-Information-Retri}
}
Reiter, E., Yvinec, R., Crépieux, P. and Poupon, A. Title: " Coupling of recognition and effect in GPCR signaling: computational modelling approaches " 2017   incollection URL 
Abstract: Synopsis (250 words) Understanding how cells process the plethora of signals transduced by G protein-coupled receptors (GPCRs) is of paramount importance, not only to decipher the molecular basis of life, but also to facilitate innovative approaches in drug discovery. Over the last few years, GPCRs structural biology has made huge strides, strengthening the concept that these receptors exist in multiple conformations. Importantly, the nature of the conformers that are stabilized and therefore the effectors they recruit directly depend on the chemical structure of the bound ligand. Selective control of intracellular signaling pathways activated downstream of GPCRs using particular compounds that are referred to as " biased ligands " is becoming a reality, provoking a revision of the classical concept of pharmacological efficacy. Inside the cell, the networks triggered by GPCRs and the way they ultimately generate context-dependent biological responses are extremely intricate; activated GPCRs can couple to multiple transducers; homo-and hetero-receptor dimers can recruit distinct effectors in response to the same ligand; intracellular signaling effectors can be shared by different networks and their local concentrations and trafficking are tightly regulated; cellular outcomes generally require a combination of upstream regulatory events; finally different extracellular signals co-exist, eliciting composite responses. To face this huge complexity, computational modeling has become critical. This chapter reviews the existing modeling strategies and how they can be combined with experimental biology in order to build quantitative and predictive computational models of GPCR-induced transduction mechanisms and intracellular networks.
BibTeX:
@incollection{Reiter,
  author = {Reiter, Eric and Yvinec, Romain and Crépieux, Pascale and Poupon, Anne},
  title = {Title: " Coupling of recognition and effect in GPCR signaling: computational modelling approaches "},
  year = {2017},
  url = {http://prodinra.inra.fr/record/310480}
}
Rengaraj, D., Lee, B.R., Han, J.Y. and Pang, M.-G. Comprehensive analysis on the homology, interaction, and miRNA regulators of human deleted in azoospermia proteins: updated evolutionary relationships with primates 2017 Genes & Genomics, pp. 1-17  article DOI URL 
BibTeX:
@article{Rengaraj2017,
  author = {Rengaraj, Deivendran and Lee, Bo Ram and Han, Jae Yong and Pang, Myung-Geol},
  title = {Comprehensive analysis on the homology, interaction, and miRNA regulators of human deleted in azoospermia proteins: updated evolutionary relationships with primates},
  journal = {Genes & Genomics},
  publisher = {The Genetics Society of Korea},
  year = {2017},
  pages = {1--17},
  url = {http://link.springer.com/10.1007/s13258-017-0598-4},
  doi = {http://doi.org/10.1007/s13258-017-0598-4}
}
Ryu, D.-Y., Rahman, M. and Pang, M.-G. Determination of Highly Sensitive Biological Cell Model Systems to Screen BPA-Related Health Hazards Using Pathway Studio 2017 International Journal of Molecular Sciences
Vol. 18(9), pp. 1909 
article DOI URL 
Abstract: Bisphenol-A (BPA) is a ubiquitous endocrine-disrupting chemical. Recently, many issues have arisen surrounding the disease pathogenesis of BPA. Therefore, several studies have been conducted to investigate the proteomic biomarkers of BPA that are associated with disease processes. However, studies on identifying highly sensitive biological cell model systems in determining BPA health risk are lacking. Here, we determined suitable cell model systems and potential biomarkers for predicting BPA-mediated disease using the bioinformatics tool Pathway Studio. We compiled known BPA-mediated diseases in humans, which were categorized into five major types. Subsequently, we investigated the differentially expressed proteins following BPA exposure in several cell types, and analyzed the efficacy of altered proteins to investigate their associations with BPA-mediated diseases. Our results demonstrated that colon cancer cells (SW480), mammary gland, and Sertoli cells were highly sensitive biological model systems, because of the efficacy of predicting the majority of BPA-mediated diseases. We selected glucose-6-phosphate dehydrogenase (G6PD), cytochrome b-c1 complex subunit 1 (UQCRC1), and voltage-dependent anion-selective channel protein 2 (VDAC2) as highly sensitive biomarkers to predict BPA-mediated diseases. Furthermore, we summarized proteomic studies in spermatozoa following BPA exposure, which have recently been considered as another suitable cell type for predicting BPA-mediated diseases.
BibTeX:
@article{Ryu2017,
  author = {Ryu, Do-Yeal and Rahman, Md and Pang, Myung-Geol},
  title = {Determination of Highly Sensitive Biological Cell Model Systems to Screen BPA-Related Health Hazards Using Pathway Studio},
  journal = {International Journal of Molecular Sciences},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2017},
  volume = {18},
  number = {9},
  pages = {1909},
  url = {http://www.mdpi.com/1422-0067/18/9/1909},
  doi = {http://doi.org/10.3390/ijms18091909}
}
Schlenke, P., Bugert, P., Dreier, J., Frey, B.M., Gassner, C., Humpe, A., Korte, W., Taleghani, B.M., Pruß, A., Sputtek, A., Wagner, F.F., Riestenpatt, S. and Karger Gmbh, S. Transfusion Medicine and Hemotherapy 2017
Vol. 44(5) 
book URL 
BibTeX:
@book{Schlenke2017,
  author = {Schlenke, Peter and Bugert, Peter and Dreier, Jens and Frey, Beat M and Gassner, Christoph and Humpe, Andreas and Korte, Wolfgang and Taleghani, Behrouz Mansouri and Pruß, Axel and Sputtek, Andreas and Wagner, Franz F and Riestenpatt, Sven and Karger Gmbh, S},
  title = {Transfusion Medicine and Hemotherapy},
  year = {2017},
  volume = {44},
  number = {5},
  url = {https://www.karger.com/Article/PDF/481596}
}
Schlenke, P., Bugert, P., Dreier, J., Frey, B.M., Gassner, C., Humpe, A., Korte, W., Taleghani, B.M., Pruß, A., Sputtek, A., Wagner, F.F., Riestenpatt, S. and Karger Gmbh, S. Editor-in-Chief Associate Editors Official Organ of 2017
Vol. 44(4) 
article URL 
BibTeX:
@article{Schlenke2017a,
  author = {Schlenke, Peter and Bugert, Peter and Dreier, Jens and Frey, Beat M and Gassner, Christoph and Humpe, Andreas and Korte, Wolfgang and Taleghani, Behrouz Mansouri and Pruß, Axel and Sputtek, Andreas and Wagner, Franz F and Riestenpatt, Sven and Karger Gmbh, S},
  title = {Editor-in-Chief Associate Editors Official Organ of},
  year = {2017},
  volume = {44},
  number = {4},
  url = {https://www.karger.com/Article/PDF/479670}
}
Schlenke, P., Bugert, P., Dreier, J., Frey, B.M., Gassner, C., Humpe, A., Korte, W., Taleghani, B.M., Pruß, A., Sputtek, A., Wagner, F.F., Riestenpatt, S. and Karger Gmbh, S. Editor-in-Chief Associate Editors Editorial Office O f fi c i a l O r g a n o f 2017
Vol. 44(6) 
article URL 
BibTeX:
@article{Schlenke2017b,
  author = {Schlenke, Peter and Bugert, Peter and Dreier, Jens and Frey, Beat M and Gassner, Christoph and Humpe, Andreas and Korte, Wolfgang and Taleghani, Behrouz Mansouri and Pruß, Axel and Sputtek, Andreas and Wagner, Franz F and Riestenpatt, Sven and Karger Gmbh, S},
  title = {Editor-in-Chief Associate Editors Editorial Office O f fi c i a l O r g a n o f},
  year = {2017},
  volume = {44},
  number = {6},
  url = {https://www.karger.com/Article/PDF/485293}
}
Selva Rupa C. Immanuela, b, c, Avinash D. Ghanateb, c, Dharmeshkumar S. Parmarb, c, Fiona Marriagea, Venkateswarlu Panchagnulab, c, Philip J. Daya, A.R. Integrative analysis of rewired central metabolism in temozolomide resistant cells 2017 Biochemical and Biophysical Research Communications  article URL 
Abstract:
Abstract
An authenticated U87MG clonal glioblastoma cell line was investigated to identify a sub-population of neurospheroidal (NSP) cells within the main epithelial population (U87MG). The NSP cells sorted using Fluorescence Assisted Cell Sorting (FACS) showed varied morphology, 30% lower growth rates, 40% higher IC50 values for temozolomide drug and could differentiate into the glial cell type (NDx). Metabolite profiling using HR-LCMS identified glucose, glutamine and serine in both populations and tryptophan only in U87MG as growth limiting substrates. Glycine, alanine, glutamate and proline were secreted by U87MG, however proline and glycine were re-utilized in NSP. Exo-metabolite profiling and phenotypic microarrays identified differential metabolism of primary carbon sources glucose and derived pyruvate for U87MG; glutamine and derived glutamate metabolism in NSP. Differential mRNA abundance of AKT1, PTEN, PIK3CA controlling metabolism, drug efflux, nutrient transport and epigenetic control MDM2 are potentially critical in shaping DNA methylation effects of temozolomide. Our study provides a new insight into the combined effect of these factors leading to temozolomide resistance in NSP.
BibTeX:
@article{SelvaRupaC.ImmanuelabcAvinashD.GhanatebcDharmeshkumarS.ParmarbcFionaMarriageaVenkateswarluPanchagnulabcPhilipJ.Daya2017,
  author = {Selva Rupa C. Immanuela, b, c, Avinash D. Ghanateb, c, Dharmeshkumar S. Parmarb, c, Fiona Marriagea, Venkateswarlu Panchagnulab, c, Philip J. Daya, Anu Raghunathan},
  title = {Integrative analysis of rewired central metabolism in temozolomide resistant cells},
  journal = {Biochemical and Biophysical Research Communications},
  year = {2017},
  url = {https://www.sciencedirect.com/science/article/pii/S0006291X17324671}
}
Shuptrine, C.W., Ajina, R., Fertig, E.J., Jablonski, S.A., Kim Lyerly, H., Hartman, Z.C. and Weiner, L.M. An unbiased in vivo functional genomics screening approach in mice identifies novel tumor cell-based regulators of immune rejection 2017 Cancer Immunology, Immunotherapy, pp. 1-16  article DOI URL 
BibTeX:
@article{Shuptrine2017,
  author = {Shuptrine, Casey W. and Ajina, Reham and Fertig, Elana J. and Jablonski, Sandra A. and Kim Lyerly, H. and Hartman, Zachary C. and Weiner, Louis M.},
  title = {An unbiased in vivo functional genomics screening approach in mice identifies novel tumor cell-based regulators of immune rejection},
  journal = {Cancer Immunology, Immunotherapy},
  publisher = {Springer Berlin Heidelberg},
  year = {2017},
  pages = {1--16},
  url = {http://link.springer.com/10.1007/s00262-017-2047-2},
  doi = {http://doi.org/10.1007/s00262-017-2047-2}
}
Simon, M., Mesmar, F., Helguero, L. and Williams, C. Genome-wide effects of MELK-inhibitor in triple-negative breast cancer cells indicate context-dependent response with p53 as a key determinant 2017 PLOS ONE
Vol. 12(2), pp. e0172832 
article DOI URL 
BibTeX:
@article{Simon2017,
  author = {Simon, Marisa and Mesmar, Fahmi and Helguero, Luisa and Williams, Cecilia},
  title = {Genome-wide effects of MELK-inhibitor in triple-negative breast cancer cells indicate context-dependent response with p53 as a key determinant},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2017},
  volume = {12},
  number = {2},
  pages = {e0172832},
  url = {http://dx.plos.org/10.1371/journal.pone.0172832},
  doi = {http://doi.org/10.1371/journal.pone.0172832}
}
Slade, G., Fry, B., Maller, J., Daly, M., Shadick, N., Reich, D., Cho, C., Yosefpour, N., Sivaselvachandran, S., Tohyama, S., Cole, T., Khuong, T.M., Mir, E., Gibson, D.G., Wieskopf, J.S., Sotocinal, S.G., Austin, J.S., Meloto, C.B., Gitt, J.H., Gkogkas, C., Sonenberg, N., Greenspan, J.D., Fillingim, R.B., Ohrbach, R., Slade, G.D., Knott, C., Dubner, R., Nackley, A.G., Ribeiro-da-Silva, A., Neely, G.G., Maixner, W., Zaykin, D.V., Mogil, J.S. and Diatchenko, L. Epiregulin and EGFR interactions are involved in pain processing 2017 Pain
Vol. 154(11), pp. 2335-2343 
article DOI URL 
BibTeX:
@article{Slade2017,
  author = {Slade, GD and Fry, B and Maller, J and Daly, MJ and Shadick, NA and Reich, D and Cho, Chulmin and Yosefpour, Noosha and Sivaselvachandran, Sivaani and Tohyama, Sarasa and Cole, Tiffany and Khuong, Thang M. and Mir, Ellen and Gibson, Dustin G. and Wieskopf, Jeffrey S. and Sotocinal, Susana G. and Austin, Jean Sebastien and Meloto, Carolina B. and Gitt, Joseph H. and Gkogkas, Christos and Sonenberg, Nahum and Greenspan, Joel D. and Fillingim, Roger B. and Ohrbach, Richard and Slade, Gary D. and Knott, Charles and Dubner, Ronald and Nackley, Andrea G. and Ribeiro-da-Silva, Alfredo and Neely, G. Gregory and Maixner, William and Zaykin, Dmitri V. and Mogil, Jeffrey S. and Diatchenko, Luda},
  title = {Epiregulin and EGFR interactions are involved in pain processing},
  journal = {Pain},
  publisher = {American Society for Clinical Investigation},
  year = {2017},
  volume = {154},
  number = {11},
  pages = {2335--2343},
  url = {https://www.jci.org/articles/view/87406},
  doi = {http://doi.org/10.1172/JCI87406}
}
Tchio Mantho, C.I., Harbuzariu, A. and Gonzalez-Perez, R.R. Histone deacetylases, microRNA and leptin crosstalk in pancreatic cancer. 2017 World journal of clinical oncology
Vol. 8(3), pp. 178-189 
article DOI URL 
Abstract: Because pancreatic cancer (PC) historically has had poor prognosis and five year survival rates, it has been intensely investigated. Analysis of PC incidence and biology has shown a link between different risk factors such as smoking, alcoholism, and obesity and disease progression. Important factors affecting PC include the epigenomic changes driven by DNA methylation and histone acetylation, and actions of microRNA inducing oncogenic or tumor suppressor effects. Studies have identified markers whose dysregulation seem to play important roles in PC progression. PC markers involve classical histone deacetylases (HDAC), PC stem cell (PCSC), and leptin. In this review, we discuss the role of several PC biomarkers, and the potential crosstalk between HDAC, microRNA, and leptin in PC progression. Dysregulated expression of these molecules can increase proliferation, survival, PCSC, resistance to chemotherapy and tumor angiogenesis. The potential relationships between these molecules are further analyzed using data from The Cancer Genome Atlas and crosstalk pathways generated by the Pathway Studio Platform (Ariadne Genomics, Inc.). Oncogenic miRNA21 and tumor suppressor miRNA200 have been previously linked to leptin signaling. Preliminary analysis of PC biopsies and signaling crosstalk suggests that the main adipokine leptin could affect the expression of microRNA and HDAC in PC. Data analysis suggests that HDAC-microRNA-leptin signaling crosstalk may be a new target for PC therapy.
BibTeX:
@article{TchioMantho2017,
  author = {Tchio Mantho, Cynthia I and Harbuzariu, Adriana and Gonzalez-Perez, Ruben R},
  title = {Histone deacetylases, microRNA and leptin crosstalk in pancreatic cancer.},
  journal = {World journal of clinical oncology},
  publisher = {Baishideng Publishing Group Inc},
  year = {2017},
  volume = {8},
  number = {3},
  pages = {178--189},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28638788 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5465008},
  doi = {http://doi.org/10.5306/wjco.v8.i3.178}
}
Truong, A.D., Rengaraj, D., Hong, Y., Hoang, C.T., Hong, Y.H. and Lillehoj, H.S. Differentially expressed JAK-STAT signaling pathway genes and target microRNAs in the spleen of necrotic enteritis-afflicted chicken lines 2017 Research in Veterinary Science
Vol. 115, pp. 235-243 
article DOI URL 
Abstract: The JAK signal transducer and STAT signaling pathway is an important regulator of cell proliferation, differentiation, survival, motility, apoptosis, immune response, and development. In this study, we used RNA-Sequencing, qRT-PCR, and bioinformatics tools to investigate the differential expression of JAK-STAT pathway genes, their interactions, and regulators in the spleen of two genetically disparate chicken lines (Marek's disease-resistant line 6.3 and MD-susceptible line 7.2) induced necrotic enteritis (NE) disease by co-infection with Eimeria maxima and Clostridium perfringens. Using RNA-Seq analysis, we identified a total of 116 JAK-STAT pathway genes that were differentially expressed in the spleen of these chickens. All of the identified genes were analyzed through clustering, mapping to the KEGG chicken JAK-STAT pathway, and the Pathway Studio program. Of the 116 JAK-STAT pathway genes, 20 were further verified by qRT-PCR. According to the RNA-Seq results, several key genes, including STAT1–6, JAK1–3, TYK2, AKT1, AKT3, SOCS1–5, PIAS1, PIAS2, PIAS4, SHP1, SHP2, and PIK3, showed marked differential expression in the two lines, relative to their respective controls. Moreover, the RNA-Seq results of many key genes were highly correlated with the qRT-PCR results. Finally, we predicted 63 mature miRNAs that variably target JAK-STAT pathway genes and are differentially expressed in the spleen of chickens of both lines. To the best of our knowledge, this study is the first to analyze most of the genes, interactions, and regulators of the JAK-STAT pathway in the innate immune response to NE disease in chickens.
BibTeX:
@article{Truong2017,
  author = {Truong, Anh Duc and Rengaraj, Deivendran and Hong, Yeojin and Hoang, Cong Thanh and Hong, Yeong Ho and Lillehoj, Hyun S.},
  title = {Differentially expressed JAK-STAT signaling pathway genes and target microRNAs in the spleen of necrotic enteritis-afflicted chicken lines},
  journal = {Research in Veterinary Science},
  year = {2017},
  volume = {115},
  pages = {235--243},
  url = {http://www.sciencedirect.com/science/article/pii/S0034528817302370},
  doi = {http://doi.org/10.1016/j.rvsc.2017.05.018}
}
Udvari, E.B., Völgyi, K., Gulyássy, P., Dimén, D., Kis, V., Barna, J., Szabó, É.R., Lubec, G., Juhász, G., Kékesi, K.A. and Dobolyi, Á. Synaptic proteome changes in the hypothalamus of mother rats 2017 Journal of Proteomics  article DOI URL 
BibTeX:
@article{Udvari2017,
  author = {Udvari, Edina Brigitta and Völgyi, Katalin and Gulyássy, Péter and Dimén, Diána and Kis, Viktor and Barna, János and Szabó, Éva Rebeka and Lubec, Gert and Juhász, Gábor and Kékesi, Katalin Adrienna and Dobolyi, Árpád},
  title = {Synaptic proteome changes in the hypothalamus of mother rats},
  journal = {Journal of Proteomics},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S1874391917300908},
  doi = {http://doi.org/10.1016/j.jprot.2017.03.006}
}
V?lgyi, K., Guly?ssy, P., Todorov, M.I., Puska, G., Badics, K., Hlatky, D., K?kesi, K.A., Nyitrai, G., Czurk?, A., Drahos, L. and Dobolyi, A. Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex 2017 Molecular Neurobiology, pp. 1-14  article DOI URL 
Abstract: The bioinformatic pathway analysis to
uncover the linkage between AD and the CCH-induced significantly altered corti- cal synaptic
proteins was performed by Elsevier Pathway Studio Platform.
BibTeX:
@article{V?lgyi2017,
  author = {V?lgyi, Katalin and Guly?ssy, P?ter and Todorov, Mihail Ivilinov and Puska, Gina and Badics, Kata and Hlatky, D?vid and K?kesi, Katalin Adrienna and Nyitrai, Gabriella and Czurk?, Andr?s and Drahos, L?szl? and Dobolyi, Arp?d},
  title = {Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex},
  journal = {Molecular Neurobiology},
  publisher = {Springer US},
  year = {2017},
  pages = {1--14},
  url = {http://link.springer.com/10.1007/s12035-017-0641-0},
  doi = {http://doi.org/10.1007/s12035-017-0641-0}
}
V. Gambardella1,3, J.C., F. Gimeno-Valiente1, N. Tarazona1,4, M.H., D. Roda1, T. Fleitas1, G. Ribas1, S. Rosello1, E. Serna2 and A. Cervantes1 Gene expression changes responsible for lapatinib acquired resistance in HER2 positive gastric cancer cell lines: a microarray analysis 2017 Annals of Oncology  article URL 
Abstract: Background: Despite the identification of several molecular alterations, personalized
medicine for gastric cancer patients still represents a big challenge. HER2, when amplified
or overexpressed, is the only actionable target but Trastuzumab was the only drug
that improves median overall survival. Nevertheless, acquired resistance is a frequent
event.
Methods: In our laboratory, OE 19, HER2 positive gastric cancer cell line, were continuously
treated with increasing doses of lapatinib, a TKi of the HER1-HER2 dimer,
for 6 months to create resistant clones. Viability assays by MTT confirmed resistance.
Genome-wide expression profiles was evaluated by using Clariom S microarray from
Affymetrix. Data were analysed using Partek Genomics Suite v6.6 software and
Pathway Studio v10 (Elsevier).
Results: Lapatinib resistant clones were finally obtained. Resistance was confirmed by
MTT. Data obtained by microarray were analyzed by principal component analysis
(PCA) to determine the significant sources of variability in the data sets. Gene expression
changes are clearly observed between two resistant clones versus parental cell line.
Impressively 132 genes were significant differentially expressed among resistant clones
versus parental line (ANOVA, FDR textless0.05). 76 genes were upregulated and 56 genes
were downregulated in the resistant clones. Unsupervised hierarchical clustering of 132genes revealed a robust classification between three different groups. The most important
biological processes where: metabolic process, oxidation-reduction process and response
to drug. ABCC2 is one of the most upregulated gene that encodes MDR2
(Multidrug Resistance-Associated Proteins).
Conclusions: Lapatinib resistant clones showed a high similar transcriptome compared
with the parental cell line. The microarray analysis allowed us to obtain a list of genes
that could be involved in acquired resistance to anti-Her2 drugs. The most upregulated
gene codes a protein that bellows to Multidrug resistant proteins involved in the transport
of antineoplastic agents.
BibTeX:
@article{V.Gambardella132017,
  author = {V. Gambardella1,3, J. Castillo1 and F. Gimeno-Valiente1 and N. Tarazona1,4, M. Huerta1 and D. Roda1 and T. Fleitas1 and G. Ribas1 and S. Rosello1 and E. Serna2 and A. Cervantes1},
  title = {Gene expression changes responsible for lapatinib acquired resistance in HER2 positive gastric cancer cell lines: a microarray analysis},
  journal = {Annals of Oncology},
  year = {2017},
  url = {https://watermark.silverchair.com/mdx511.007.pdf?token=AQECAHi208BE49Ooan9kkhWErcy7Dm3ZL9Cf3qfKAc485ysgAAAe4wggHqBgkqhkiG9w0BBwagggHbMIIB1wIBADCCAdAGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMPlmGs265VTiNRnbdAgEQgIIBoYf4eRMDpQD-Fb4r2grZhLfzHyi-I0OhqyXW3lmnLgib}
}
Valdivieso, Á.G., Mori, C., Clauzure, M., Massip-Copiz, M. and Santa-Coloma, T.A. CFTR modulates RPS27 gene expression using chloride anion as signaling effector 2017 Archives of Biochemistry and Biophysics  article DOI URL 
Abstract: In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Cl− concentrations ([Cl−]i), we observed several Cl−-dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl− might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl−]i (using the Cl− fluorescent probe SPQ). The [Cl−]i rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl− accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl− behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1β receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1β and JNK signaling downstream of Cl− in RPS27 modulation.
BibTeX:
@article{Valdivieso2017,
  author = {Valdivieso, Ángel G. and Mori, Consuelo and Clauzure, Mariángeles and Massip-Copiz, Macarena and Santa-Coloma, Tomás A.},
  title = {CFTR modulates RPS27 gene expression using chloride anion as signaling effector},
  journal = {Archives of Biochemistry and Biophysics},
  year = {2017},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S0003986117301753},
  doi = {http://doi.org/10.1016/j.abb.2017.09.014}
}
VikasKaushik and BhupenderSinghandJoginderSingh BioinformaticsTechniquesusedinHepatitisCVirusResearch 2017
Vol. 11(2), pp. 921-932 
article DOI URL 
Abstract: See, stats, and : https : / / www . researchgate . net / publication / 318122733 Bioinformatics C Article DOI : 10 . 22207 / JPAM . 11 . 2 . 32 CITATIONS 0 READS 41 3 : Some : Biodegradation Bioinformatics Vikas Lovely 12 SEE Bhupender Lovely 1 SEEJoginderLovely65SEEAll.The.HepatitisCiswidelyspreadandinduceslifethreateningsituations.Researchersfromvariousfieldshavedevelopedvaccine,buttheyarenotthateffectivebecauseofthevariationingenotypeofHepatitisvirusandalsonotmuchaffordable.In-silicoapproachisofgreaterimportanceindesigningandtestingthemodelvaccine.Inthisstudy,investigationhasbeendonefortheavailableBioinformaticstoolsandmethodologiesusedinHCVresearch.Differenttypesoftoolsanddatabasescommonlyusedbyresearcherswerereviewedtogetanoverallpictureofbioinformaticstechniques,computationalbiologytoolsanddatabasesusedinHepatitisCVirusresearch.Exclusivestudyhasalsodonetofigureoutdifferentstatisticalmethodsusedbydifferentresearchgroups.Thispaperwillprovideanup-to-datepictureofcomputationapproachesusedforexploringHepatitisCtreatment.
BibTeX:
@article{VikasKaushik,
  author = {VikasKaushik and BhupenderSinghandJoginderSingh},
  title = {BioinformaticsTechniquesusedinHepatitisCVirusResearch},
  year = {2017},
  volume = {11},
  number = {2},
  pages = {921--932},
  url = {http://dx.doi.org/10.22207/JPAM.11.2.32},
  doi = {http://doi.org/10.22207/JPAM.11.2.32}
}
Villareal, M.O., Kume, S., Neffati, M. and Isoda, H. Upregulation of textlessitextgreaterMitftextless/itextgreater by Phenolic Compounds-Rich textlessitextgreaterCymbopogon schoenanthustextless/itextgreater Treatment Promotes Melanogenesis in B16 Melanoma Cells and Human Epidermal Melanocytes 2017 BioMed Research International
Vol. 2017, pp. 1-11 
article DOI URL 
Abstract: textlessptextgreater Melanin provides inherent protection against skin cancer by absorbing broad-spectrum radiant energy of UV radiation. Cutaneous malignant melanoma incidence has recently been observed to increase and the frequency is closely associated with the skin color, highlighting the importance of skin pigmentation. Here, we showed how melanin biosynthesis is enhanced by treatment with phenolic compounds-rich textlessitalictextgreaterCymbopogon schoenanthustextless/italictextgreater (CYM) in B16 murine melanoma cells and human epidermal melanocytes (HEM). CYM increased the melanin content of the cells by upregulating the expression of tyrosinase (TYR), tyrosinase-related protein 1 (TRP1), and dopachrome tautomerase (DCT) at the protein and mRNA levels, comparable to the effect of textlessitalictextgreaterαtextless/italictextgreater -melanocyte-stimulating hormone (MSH), in both B16 cells and HEM. Moreover, global gene expression analysis showed that at least 44 pigmentation-associated genes were modulated, including the microphthalmia-associated transcription factor textlessitalictextgreater(Mitf)textless/italictextgreater and its transcriptional regulators ( textlessitalictextgreaterSox10textless/italictextgreater , textlessitalictextgreaterPax3textless/italictextgreater , and textlessitalictextgreaterLef1textless/italictextgreater ). Upregulation of copper transport-associated gene textlessitalictextgreaterAtp7btextless/italictextgreater indicates that CYM also promotes tyrosinase activity. CYM upregulated textlessitalictextgreaterMitftextless/italictextgreater and possibly activates tyrosinase enzyme, providing evidence for its possible use to promote melanogenesis and as a therapeutic agent against hypopigmentation disorders. textless/ptextgreater
BibTeX:
@article{Villareal2017,
  author = {Villareal, Myra O. and Kume, Sayuri and Neffati, Mohamed and Isoda, Hiroko},
  title = {Upregulation of textlessitextgreaterMitftextless/itextgreater by Phenolic Compounds-Rich textlessitextgreaterCymbopogon schoenanthustextless/itextgreater Treatment Promotes Melanogenesis in B16 Melanoma Cells and Human Epidermal Melanocytes},
  journal = {BioMed Research International},
  publisher = {Hindawi},
  year = {2017},
  volume = {2017},
  pages = {1--11},
  url = {https://www.hindawi.com/journals/bmri/2017/8303671/},
  doi = {http://doi.org/10.1155/2017/8303671}
}
Wang, K.K.-w., Yang, Z. and Moghieb, A. PROTEIN BIOMARKERS FOR ACUTE, SUBACUTE AND CHRONIC TRAUMATIC INJURIES OF THE CENTRAL NERVOUS SYSTEM 2017   article URL 
BibTeX:
@article{Wang2017,
  author = {Wang, Kevin Ka-wang and Yang, Zhihui and Moghieb, Ahmed},
  title = {PROTEIN BIOMARKERS FOR ACUTE, SUBACUTE AND CHRONIC TRAUMATIC INJURIES OF THE CENTRAL NERVOUS SYSTEM},
  year = {2017},
  url = {http://www.freepatentsonline.com/y2017/0146555.html}
}
Warnke, E., Pietsch, J., Kopp, S., Bauer, J., Sahana, J., Wehland, M., Krüger, M., Hemmersbach, R., Infanger, M., Lützenberg, R. and Grimm, D. Cytokine Release and Focal Adhesion Proteins in Normal Thyroid Cells Cultured on the Random Positioning Machine. 2017 Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Vol. 43(1), pp. 257-270 
article DOI URL 
Abstract: BACKGROUND/AIMS Spaceflight impacts on the function of the thyroid gland in vivo. In vitro normal and malignant thyrocytes assemble in part to multicellular spheroids (MCS) after exposure to the random positioning machine (RPM), while a number of cells remain adherent (AD). We aim to elucidate possible differences between AD and MCS cells compared to 1g-controls of normal human thyroid cells. METHODS Cells of the human follicular epithelial thyroid cell line Nthy-ori 3-1 were incubated for up to 72 h on the RPM. Afterwards, they were investigated by phase-contrast microscopy, quantitative real-time PCR and by determination of cytokines released in their supernatants. RESULTS A significant up-regulation of IL6, IL8 and CCL2 gene expression was found after a 4h RPM-exposure, when the whole population was still growing adherently. MCS and AD cells were detected after 24 h on the RPM. At this time, a significantly reduced gene expression in MCS compared to 1g-controls was visible for IL6, IL8, FN1, ITGB1, LAMA1, CCL2, and TLN1. After a 72 h RPM-exposure, IL-6, IL-8, and TIMP-1 secretion rates were increased significantly. CONCLUSION Normal thyrocytes form MCS within 24 h. Cytokines seem to be involved in the initiation of MCS formation via focal adhesion proteins.
BibTeX:
@article{Warnke2017,
  author = {Warnke, Elisabeth and Pietsch, Jessica and Kopp, Sascha and Bauer, Johann and Sahana, Jayashree and Wehland, Markus and Krüger, Marcus and Hemmersbach, Ruth and Infanger, Manfred and Lützenberg, Ronald and Grimm, Daniela},
  title = {Cytokine Release and Focal Adhesion Proteins in Normal Thyroid Cells Cultured on the Random Positioning Machine.},
  journal = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology},
  publisher = {Karger Publishers},
  year = {2017},
  volume = {43},
  number = {1},
  pages = {257--270},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/28854433},
  doi = {http://doi.org/10.1159/000480368}
}
Xu, F., Gao, Q.Q., Zhu, L.L., Jiang, H.S., Chen, H., Xu, Z.P., Chen, Y. and Dai, Y.T. Impact of varicocelectomy on the proteome profile of testicular tissues of rats with varicocele 2017 Andrologia, pp. e12873  article DOI URL 
BibTeX:
@article{Xu2017,
  author = {Xu, F. and Gao, Q. Q. and Zhu, L. L. and Jiang, H. S. and Chen, H. and Xu, Z. P. and Chen, Y. and Dai, Y. T.},
  title = {Impact of varicocelectomy on the proteome profile of testicular tissues of rats with varicocele},
  journal = {Andrologia},
  year = {2017},
  pages = {e12873},
  url = {http://doi.wiley.com/10.1111/and.12873},
  doi = {http://doi.org/10.1111/and.12873}
}
Yan, Y., Zhang, A., Dong, H., Yan, G., Sun, H., Wu, X., Han, Y. and Wang, X. Toxicity and detoxification effects of herbal Caowu via ultra performance liquid chromatography/mass spectrometry metabolomics analyzed using pattern recognition method 2017 Pharmacognosy Magazine
Vol. 13(52), pp. 683 
article DOI URL 
Abstract: textlessbrtextgreatertextlessbtextgreaterBackground:textless/btextgreater textlessitextgreaterCaowutextless/itextgreater (textlessitextgreaterRadix Aconiti kusnezoffiitextless/itextgreater, CW), the root of textlessitextgreaterAconitum kusnezoffii Reichb.textless/itextgreater, has widely used clinically in rheumatic arthritis, painful joints, and tumors for thousands of years. However, the toxicity of heart and central nervous system induced by CW still limited the application. textlessbtextgreaterMaterials and Methods:textless/btextgreater Metabolomics was performed to identify the sensitive and reliable biomarkers and to characterize the phenotypically biochemical perturbations and potential mechanisms of CW-induced toxicity, and the detoxification by combinatorial intervention of CW with textlessitextgreaterGancaotextless/itextgreater (textlessitextgreaterRadix Glycyrrhizaetextless/itextgreater) (CG), textlessitextgreaterBaishaotextless/itextgreater (textlessitextgreaterRadix Paeoniae Albatextless/itextgreater) (CB), and textlessitextgreaterRenshentextless/itextgreater (textlessitextgreaterRadix Ginsengtextless/itextgreater) (CR) was also analyzed by pattern recognition methods. textlessbtextgreaterResults:textless/btextgreater As a result, the metabolites were characterized and responsible for pentose and glucuronate interconversions, tryptophan metabolism, amino sugar and nucleotide sugar metabolism, taurine and hypotaurine metabolism, fructose and mannose metabolism, and starch and sucrose metabolism, six networks of which were the same to the metabolic pathways of textlessitextgreaterChuanwutextless/itextgreater (textlessitextgreaterRadix Aconititextless/itextgreater, CHW) group. The ascorbate and aldarate metabolism was also characterized by CW group. The urinary metabolomics also revealed CW-induced serious toxicity to heart and liver. Thirteen significant metabolites were identified and had validated as phenotypic toxicity biomarkers of CW, five biomarkers of which were commonly owned in textlessitextgreaterAconitumtextless/itextgreater. The changes of toxicity metabolites obtained from combinatorial intervention of CG, CB, and CR also were analyzed to investigate the regulation degree of toxicity biomarkers adjusted by different combinatorial interventions at 6textlesssuptextgreaterthtextless/suptextgreater month. textlessbtextgreaterConclusion:textless/btextgreater Metabolomics analyses coupled with pattern recognition methods in the evaluation of drug toxicity and finding detoxification methods were highlighted in this work.textlessbrtextgreaterPattern recognition plot reflects the toxicity effects tendency of the urine metabolic fluctuations according to time after treatment of herbal textlessitextgreaterCaowutextless/itextgreater.textlessbrtextgreatertextlessbtextgreaterAbbreviations used:textless/btextgreater CW: Caowu (Radix Aconiti kusnezoffii); CHW: Chuanwu (Radix Aconiti); TCM: Traditional Chinese Medicine; CG: Caowu and Gancao; CB: Caowu and Baishao; CR: Caowu and Renshen; QC: Quality control; UPLC: Ultra performance liquid chromatography; MS: Mass spectrometry; PCA: Principal component analysis; PLS-DA: Partial least squares-discriminant analysis; OPLS: Orthogonal projection to latent structures analysis.textlessbrtextgreater
BibTeX:
@article{Yan2017,
  author = {Yan, Yan and Zhang, Aihua and Dong, Hui and Yan, Guangli and Sun, Hui and Wu, Xiuhong and Han, Ying and Wang, Xijun},
  title = {Toxicity and detoxification effects of herbal Caowu via ultra performance liquid chromatography/mass spectrometry metabolomics analyzed using pattern recognition method},
  journal = {Pharmacognosy Magazine},
  publisher = {Medknow Publications and Media Pvt. Ltd.},
  year = {2017},
  volume = {13},
  number = {52},
  pages = {683},
  url = {http://www.phcog.com/text.asp?2017/13/52/683/218123},
  doi = {http://doi.org/10.4103/pm.pm_475_16}
}
Yang, T., Ahmari, N., Schmidt, J.T., Redler, T., Arocha, R., Pacholec, K., Magee, K.L., Malphurs, W., Owen, J.L., Krane, G.A., Li, E., Wang, G.P., Vickroy, T.W., Raizada, M.K., Martyniuk, C.J. and Zubcevic, J. Shifts in the Gut Microbiota Composition Due to Depleted Bone Marrow Beta Adrenergic Signaling Are Associated with Suppressed Inflammatory Transcriptional Networks in the Mouse Colon 2017 Frontiers in Physiology
Vol. 8, pp. 220 
article DOI URL 
Abstract: The brain-gut axis plays a critical role in the regulation of different diseases, many of which are characterized by sympathetic dysregulation. However, a direct link between sympathetic dysregulation and gut dysbiosis remains to be illustrated. Bone marrow (BM)-derived immune cells continuously interact with the gut microbiota to maintain homeostasis in the host. Their function is largely dependent upon the sympathetic nervous system acting via adrenergic receptors present on the BM immune cells. In this study, we utilized a novel chimera mouse that lacks the expression of BM beta1/2 adrenergic receptors (b1/2-ARs) to investigate the role of the sympathetic drive to the BM in gut and microbiota homeostasis. Fecal analyses demonstrated a shift from a dominance of Firmicutes to Bacteroidetes phylum in the b1/2-ARs KO chimera, resulting in a reduction in Firmicutes/Bacteroidetes ratio. Meanwhile, a significant reduction in Proteobacteria phylum was determined. No changes in the abundance of acetate-, butyrate-, and lactate-producing bacteria, and colon pathology were observed in the b1/2-ARs KO chimera. Transcriptomic profiling in colon identified Killer Cell Lectin-Like Receptor Subfamily D, Member 1 (Klrd1), Membrane-Spanning 4-Domains Subfamily A Member 4A (Ms4a4b), and Casein Kinase 2 Alpha Prime Polypeptide (Csnk2a2) as main transcripts associated with the microbiota shifts in the b1/2-ARs KO chimera. Suppression of leukocyte-related transcriptome networks (i.e. function, differentiation, migration), classical compliment pathway, and networks associated with intestinal function, barrier integrity, and excretion was also observed in the colon of the KO chimera. Moreover, reduced expression of transcriptional networks related to intestinal diseases (i.e. ileitis, enteritis, inflammatory lesions and stress) was noted. The observed suppressed transcriptome networks were associated with a reduction in NK cells, macrophages, and CD4+ T cells in the b1/2-ARs KO chimera colon. Thus, sympathetic regulation of BM-derived immune cells plays a significant role in modifying inflammatory networks in the colon and the gut microbiota composition. To our knowledge, this study is the first to suggest a key role of BM b1/2-ARs signalling in host-microbiota interactions, and reveals specific molecular mechanisms that may lead to generation of novel anti-inflammatory treatments for many immune and autonomic diseases as well as gut dysbiosis across the board.
BibTeX:
@article{Yang2017,
  author = {Yang, Tao and Ahmari, Niousha and Schmidt, Jordan T. and Redler, Ty and Arocha, Rebeca and Pacholec, Kevin and Magee, Kacy L. and Malphurs, Wendi and Owen, Jennifer L. and Krane, Gregory A. and Li, Eric and Wang, Gary P. and Vickroy, Thomas W. and Raizada, Mohan K. and Martyniuk, Christopher J. and Zubcevic, Jasenka},
  title = {Shifts in the Gut Microbiota Composition Due to Depleted Bone Marrow Beta Adrenergic Signaling Are Associated with Suppressed Inflammatory Transcriptional Networks in the Mouse Colon},
  journal = {Frontiers in Physiology},
  publisher = {Frontiers},
  year = {2017},
  volume = {8},
  pages = {220},
  url = {http://journal.frontiersin.org/article/10.3389/fphys.2017.00220/full},
  doi = {http://doi.org/10.3389/fphys.2017.00220}
}
Yu, Q., Chen, C., Du, D., Huang, M., Yao, J., Yu, F., Brlansky, R.H. and Gmitter, F.G. Reprogramming of a defense signaling pathway in rough lemon and sweet orange is a critical element of the early response to 'Candidatus Liberibacter asiaticus' 2017 Horticulture Research
Vol. 463 
article DOI URL 
Abstract: Huanglongbing (HLB) in citrus infected by Candidatus Liberibacter asiaticus (CLas) has caused tremendous losses to the citrus industry. No resistant genotypes have been identified in citrus species or close relatives. Among citrus varieties, rough lemon (Citrus jambhiri) has been considered tolerant due to its ability to produce a healthy flush of new growth after infection. The difference between tolerance and susceptibility is often defined by the speed and intensity of a plant's response to a pathogen, especially early defense responses. RNA-seq data were collected from three biological replicates of CLas-and mock-inoculated rough lemon and sweet orange at week 0 and 7 following infection. Functional analysis of the differentially expressed genes (DEGs) indicated that genes involved in the mitogen activated protein kinase (MAPK) signaling pathway were highly upregulated in rough lemon. MAPK induces the transcription of WRKY and other transcription factors which potentially turn on multiple defense-related genes. A Subnetwork Enrichment Analysis further revealed different patterns of regulation of several functional categories, suggesting DEGs with different functions were subjected to reprogramming. In general, the amplitude of the expression of defense-related genes is much greater in rough lemon than in sweet orange. A quantitative disease resistance response may contribute to the durable tolerance level to HLB observed in rough lemon.
BibTeX:
@article{Yu2017,
  author = {Yu, Qibin and Chen, Chunxian and Du, Dongliang and Huang, Ming and Yao, Jiqiang and Yu, Fahong and Brlansky, Ronald H and Gmitter, Frederick G},
  title = {Reprogramming of a defense signaling pathway in rough lemon and sweet orange is a critical element of the early response to 'Candidatus Liberibacter asiaticus'},
  journal = {Horticulture Research},
  year = {2017},
  volume = {463},
  url = {https://www.nature.com/articles/hortres201763.pdf},
  doi = {http://doi.org/10.1038/hortres.2017.63}
}
Yu Zheng1, Xiaoyang Li1, Qiusheng Chen1, Soyeon Showman2, L.X. A Possible Risk Gene for B-cell Chronic Lymphocytic Leukemia: NRIP1 2017 Med One  article DOI URL 
Abstract: Background: The underlying mechanisms that cause B-cell chronic lymphocytic leukemia (B-CLL), the most common type of leukemia in adults, remain unclear. The aim of this study is to investigate the novel genetic risk of B-CLL through systematic literature review and meta-analysis.
Methods: A comprehensive search of electronic databases was completed using Illumina BioEngine. Twenty one B-CLL case/control bio-sets from four different studies were selected, including 195 B-CLL cases and 31 controls. The selected top B-CLL risk genes were further analyzed by integrating an online open source B-CLL genetic database. Pathway enrichment analysis (PEA) and network connectivity analysis (NCA) were conducted to identify the potential functional association between target genes and B-CLL.
Results: One novel gene (NRIP1) and two known genes (INPP5F and LEF1) were identified through the meta-analysis as top target genes for B-CLL. These genes play important roles within multiple B-CLL genetic pathways and are closely related to known B-CLL target genes. NCA results also revealed strong functional association between these genes and B-CLL.
Conclusion: This study identified known as well as novel B-CLL target genes and their functional pathways that involved in the B-CLL pathogenesis. Our results may provide new insights into the understanding of the genetic mechanisms of B-CLL.
BibTeX:
@article{YuZheng1XiaoyangLi1QiushengChen1SoyeonShowman22017,
  author = {Yu Zheng1, Xiaoyang Li1, Qiusheng Chen1, Soyeon Showman2, Lei Xu2},
  title = {A Possible Risk Gene for B-cell Chronic Lymphocytic Leukemia: NRIP1},
  journal = {Med One},
  year = {2017},
  url = {http://www.qingres.com/htmls/Mo888Detail.html},
  doi = {http://doi.org/10.20900/mo.20170005.}
}
Zeegers, D., Venkatesan, S., Koh, S., Low, G.M., Srivastava, P., Sundaram, N., Sethu, S., Banerjee, B., Jayapal, M., Belyakov, O., Baskar, R., Balajee, A. and Hande, M. Biomarkers of ionizing radiation exposure: A multiparametric approach 2017 Genome Integrity
Vol. 8(1), pp. 6 
article URL 
Abstract: Humans are exposed to ionizing radiation not only through background radiation but also through the ubiquitous presence of devices and sources that generate radiation. With the expanded use of radiation in day.to.day life, the chances of accidents or misuse only increase. Therefore, a thorough understanding of the dynamic effects of radiation exposure on biological entities is necessary. The biological effects of radiation exposure on human cells depend on much variability such as level of exposure, dose rate, and the physiological state of the cells. During potential scenarios of a large.scale radiological event which results in mass casualties, dose estimates are essential to assign medical attention according to individual needs. Many attempts have been made to identify biomarkers which can be used for high throughput biodosimetry screening. In this study, we compare the results of different biodosimetry methods on the same irradiated cells to assess the suitability of current biomarkers and push forward the idea of employing a multiparametric approach to achieve an accurate dose and risk estimation.
BibTeX:
@article{Zeegers2017,
  author = {Zeegers, Dimphy and Venkatesan, Shriram and Koh, ShuWen and Low, GraceKah Mun and Srivastava, Pallavee and Sundaram, Neisha and Sethu, Swaminathan and Banerjee, Birendranath and Jayapal, Manikandan and Belyakov, Oleg and Baskar, Rajamanickam and Balajee, AdayabalamS and Hande, MPrakash},
  title = {Biomarkers of ionizing radiation exposure: A multiparametric approach},
  journal = {Genome Integrity},
  publisher = {Medknow Publications and Media Pvt. Ltd.},
  year = {2017},
  volume = {8},
  number = {1},
  pages = {6},
  url = {http://www.genome-integrity.org/article.asp?issn=2041-9414;year=2017;volume=8;issue=1;spage=6;epage=6;aulast=Zeegers}
}
Zerva, C., Navarro, R.B., Day, P. and Ananiadou, S. Using uncertainty to link and rank evidence from biomedical literature for model curation 2017 Bioinformatics doi
Vol. 10 
article DOI URL 
Abstract: Motivation: In recent years, there has been great progress in the field of automated curation of biomedical networks and models, aided by text mining methods that provide evidence from literature. Such methods must not only extract snippets of text that relate to model interactions, but also be able to contextualise the evidence and provide additional confidence scores for the interaction in question. While various approaches calculating confidence scores have focused primarily on the quality of the extracted information, there has been little work on exploring the textual uncertainty conveyed by the author. Although textual uncertainty is acknowledged in biomedical text mining as an attribute of text mined interactions (events), it is significantly understudied as a means of providing a confidence measure for interactions in pathways or other biomedical models. In this work, we focus on improving identification of textual uncertainty for events and explore how it can be used as an additional measure of confidence for biomedical models. Results: We present a novel method for extracting uncertainty from the literature using a hybrid approach that combines rule induction and machine learning. Variations of this hybrid approach are then discussed, alongside their advantages and disadvantages. We use subjective logic theory to combine multiple uncertainty values extracted from different sources for the same interaction. Our approach achieves an F-scores of 0.76 and 0.88 based on the BioNLP-ST and Genia-MK corpora, respectively, making considerable improvements over previously published work. Moreover, we evaluate our proposed system on pathways related to two different areas, namely leukemia and melanoma cancer research. Availability: The leukemia pathway model used is available in Pathway Studio while the Ras model is available via PathwayCommons. Online demonstration of the uncertainty extraction system is available for research purposes at
BibTeX:
@article{Zerva,
  author = {Zerva, Chrysoula and Navarro, Riza Batista and Day, Philip and Ananiadou, Sophia},
  title = {Using uncertainty to link and rank evidence from biomedical literature for model curation},
  journal = {Bioinformatics doi},
  year = {2017},
  volume = {10},
  url = {https://oup.silverchair-cdn.com/oup/backfile/Contentpublic/Journal/bioinformatics/PAP/10.1093bioinformaticsbtx466/3/btx466.pdf?Expires=1502921160&Signature=TRyzLWgooMNsdevGjK7OwebAEect1MNRHLCLFP9EqfBXCWy HeT0LeeugJMBo YupY1njMmDHrv5Nq9 ZEmcPMKJCuEf5uXP},
  doi = {http://doi.org/10.1093/bioinformatics/xxxxxx}
}
Zheng, Y., Li, X., Manor, L.C., Cao, H. and Chen, Q. An Integrative Computational Approach to Evaluate Genetic Markers for Chronic Lymphocytic Leukemia 2017 Journal of Computational Biology, pp. cmb.2017.0041  article DOI URL 
BibTeX:
@article{Zheng2017,
  author = {Zheng, Yu and Li, Xiaoyang and Manor, Lydia C. and Cao, Hongbao and Chen, Qiusheng},
  title = {An Integrative Computational Approach to Evaluate Genetic Markers for Chronic Lymphocytic Leukemia},
  journal = {Journal of Computational Biology},
  year = {2017},
  pages = {cmb.2017.0041},
  url = {http://online.liebertpub.com/doi/10.1089/cmb.2017.0041},
  doi = {http://doi.org/10.1089/cmb.2017.0041}
}
Comparative Network Analysis of Patients with Non-Small Cell Lung Cancer and Smokers for Representing Potential Therapeutic Targets - ProQuest 2017 Scientific Reports
Vol. 7, pp. 1-15 
article URL 
BibTeX:
@article{,,
  title = {Comparative Network Analysis of Patients with Non-Small Cell Lung Cancer and Smokers for Representing Potential Therapeutic Targets - ProQuest},
  journal = {Scientific Reports},
  year = {2017},
  volume = {7},
  pages = { 1--15},
  url = {https://search.proquest.com/openview/ee3ee568db133a0e3a8d2c82a1a9315d/1?pq-origsite=gscholar&cbl=2041939}
}
Researchers gain greater insights into experimental data by leveraging the growing collections of molecular interactions from published literature - Bio-IT World 2017   techreport URL 
BibTeX:
@techreport{,,
  title = {Researchers gain greater insights into experimental data by leveraging the growing collections of molecular interactions from published literature - Bio-IT World},
  year = {2017},
  url = {http://www.bio-itworld.com/Press-Release/Researchers-gain-greater-insights-into-experimental-data-by-leveraging-the-growing-collections-of-molecular-interactions-from-published-literature/}
}
Abbass, H.A., Bahmad, H., Hassan, H.A.E., Zhu, R., Zhou, S., Dong, X., Hamade, E., Mallah, K., Zebian, A., Ramadan, N., Mondello, S., Fares, J., Comair, Y., Atweh, S., Darwish, H., Zibara, K., Mechref, Y. and Kobeissy, F. Deciphering glycomics and neuroproteomic alterations in experimental TBI: Comparative analysis of aspirin and clopidogrel treatment 2016 ELECTROPHORESIS, pp. n/a-n/a  article URL 
BibTeX:
@article{Abbass2016,
  author = {Abbass, Hussein Abou and Bahmad, Hisham and Hassan, Hadi Abou El and Zhu, Rui and Zhou, Shiyue and Dong, Xue and Hamade, Eva and Mallah, Khalil and Zebian, Abir and Ramadan, Naify and Mondello, Stefania and Fares, Jawad and Comair, Youssef and Atweh, Samir and Darwish, Hala and Zibara, Kazem and Mechref, Yehia and Kobeissy, Firas},
  title = {Deciphering glycomics and neuroproteomic alterations in experimental TBI: Comparative analysis of aspirin and clopidogrel treatment},
  journal = {ELECTROPHORESIS},
  year = {2016},
  pages = {n/a--n/a},
  url = {http://doi.wiley.com/10.1002/elps.201500583}
}
Abdelmoez, A., Coraça-Huber, D.C., Thurner, G.C., Debbage, P., Lukas, P., Skvortsov, S. and Skvortsova, I. Screening and identification of molecular targets for cancer therapy. 2016 Cancer letters  article URL 
Abstract: In recent decades, targeted therapeutics have significantly improved therapy results in patients with malignant tumors of different origins. However, malignant diseases characterized by aggressiveness and increased capacity for metastatic spread still require basic researchers and clinicians to direct enormous efforts towards development of novel therapeutic targets. Potential targets should be selected with the clinical endpoint in view; targeted therapeutics can be developed: for use in combination with currently existing therapeutic approaches in order to improve their efficacy; to overcome the treatment resistance of tumor cells and thus protect the patient from recurrence; to repress molecular mechanisms related to immune escape of cancer cells; to combat the metastatic dissemination of carcinoma cells. Taking into account the specific clinical aim that should be achieved, different strategies and techniques can be proposed to identify the most promising candidate molecules for further development as therapeutic targets. Since cellular membranes contain a large number of druggable molecules, evaluation of the membrane protein profiles of carcinoma cells having different properties can provide a basis for further development of therapeutic targets. This review considers how cellular membranes obtained from different pre-clinical and clinical samples can be used in screening and to identify targets for cancer therapy.
BibTeX:
@article{Abdelmoez2016,
  author = {Abdelmoez, Alshaimaa and Coraça-Huber, Débora C and Thurner, Gudrun C and Debbage, Paul and Lukas, Peter and Skvortsov, Sergej and Skvortsova, Ira},
  title = {Screening and identification of molecular targets for cancer therapy.},
  journal = {Cancer letters},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S0304383516301380}
}
Ahmari, N., Schmidt, J.T., Krane, G.A., Malphurs, W., Cunningham, B.E., Owen, J.L., Martyniuk, C.J. and Zubcevic, J. Loss of bone marrow adrenergic beta 1 and 2 receptors modifies transcriptional networks, reduces circulating inflammatory factors, and regulates blood pressure. 2016 Physiological genomics
Vol. 48(7), pp. 526-36 
article URL 
Abstract: Hypertension (HTN) is a prevalent condition with complex etiology and pathophysiology. Evidence exists of significant communication between the nervous system and the immune system (IS), and there appears to be a direct role for inflammatory bone marrow (BM) cells in the pathophysiology of hypertension. However, the molecular and neural mechanisms underlying this interaction have not been characterized. Here, we transplanted whole BM cells from the beta 1 and 2 adrenergic receptor (AdrB1(tm1Bkk)AdrB2(tm1Bkk)/J) knockout (KO) mice into near lethally irradiated C57BL/6J mice to generate a BM AdrB1.B2 KO chimera. This allowed us to evaluate the role of the BM beta 1 and beta 2 adrenergic receptors in mediating BM IS homeostasis and regulating blood pressure (BP) in an otherwise intact physiological setting. Fluorescence-activated cell sorting demonstrated that a decrease in systolic and mean BP in the AdrB1.B2 KO chimera is associated with a decrease in circulating inflammatory T cells, macrophage/monocytes, and neutrophils. Transcriptomics in the BM identified 7,419 differentially expressed transcripts between the C57 and AdrB1.B2 KO chimera. Pathway analysis revealed differentially expressed transcripts related to several cell processes in the BM of C57 compared with AdrB1.B2 KO chimera, including processes related to immunity (e.g., T-cell activation, T-cell recruitment, cytokine production, leukocyte migration and function), the cardiovascular system (e.g., blood vessel development, peripheral nerve blood flow), and the brain (e.g., central nervous system development, neurite development) among others. This study generates new insight into the molecular events that underlie the interaction between the sympathetic drive and IS in modulation of BP.
BibTeX:
@article{Ahmari2016,
  author = {Ahmari, Niousha and Schmidt, Jordan T and Krane, Gregory A and Malphurs, Wendi and Cunningham, Bruce E and Owen, Jennifer L and Martyniuk, Christopher J and Zubcevic, Jasenka},
  title = {Loss of bone marrow adrenergic beta 1 and 2 receptors modifies transcriptional networks, reduces circulating inflammatory factors, and regulates blood pressure.},
  journal = {Physiological genomics},
  year = {2016},
  volume = {48},
  number = {7},
  pages = {526--36},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/27235450}
}
Alam, M. Nucleotide Sequence Encoding Wuschel-Related Homeobox4 (WOX4) Protein From Corchorus Olitorius and Corchorus Capsularis and Methods of Use For Same 2016   article  
BibTeX:
@article{Alam2016,
  author = {Alam, Maqsudul},
  title = {Nucleotide Sequence Encoding Wuschel-Related Homeobox4 (WOX4) Protein From Corchorus Olitorius and Corchorus Capsularis and Methods of Use For Same},
  year = {2016}
}
Alamri, A.M., Liu, X., Wang, W., Zhong, X., Kallakury, B., Davidson, B. and Furth, P.A. Abstract 4280: Paralleled workflow for expansion of limited patient material using CRC for textlessitextgreaterin vitrotextless/itextgreater /PDX/biological/genetic studies of a low-grade mucoepidermoid carcinoma 2016 Cancer Research
Vol. 76(14 Supplement), pp. 4280-4280 
article DOI URL 
Abstract: Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA

Acquiring live cancer cells preserving original characteristics is a critical step for precision medicine. Here we illustrate a paralleled workflow using a low-grade sublingual salivary mucoepidermoid carcinoma (MEC) as an example. Methods: Working under IRB approval, tissue from two distinct regions of a MEC were obtained and primary epithelial cell cultures established using CRC (F medium with Rho Kinase (ROCK) inhibitor Y-27632 with irradiated Swiss 3T3-J2 mouse fibroblast feeder cells). Epithelial cells were separated from feeders to test under non-CRC conditions including 2D (MammoCult™), colony formation in Matrigel (F medium, Y-27632), patient derived xenograft (PDX) formation (10*6 cells/50:50 matrigel/PBS/mammary fatpad), and RNA and DNA extracted for RNAseq, exome sequencing and PCR/RT-PCR for a CRTC1-MAML2 fusion gene (reported in MEC). Sequences were analyzed for relative transcript abundance, differentially expressed genes (DEGs), and single nucleotide polymorphisms (SNPs) (TopHat/CuffLinks, SAMTOOLS, variant database: dbSNP & 1000G, UCSC hg19) between the two MEC regions and fusion genes (FusionCatcher). Potentially pathophysiological SNPs were identified (OMIM and SNPedia). Gene ontology was performed on transcriptome data (PARTEK Genomic Suite, Pathway Studio). Immunohistochemistry (IHC) was used to compare protein expression of selected DEG and downstream effectors in original cancer and surrounding normal tissue, cell pellets, Matrigel colonies and PDX (confirmed as human using MAB1273). Results: CRC cultures established from both sites grew similarly under all in vitro and in vivo conditions. PDX showed well-differentiated histology comparable to original cancer. One of the 11 DEG was amphiregulin but protein expression was equivalent in the two cell cultures. Amphiregulin, EGFR, p-EGFR, p-AKT, and mTOR were expressed in vitro (CRC and non-CRC), in vivo (PDX) and in original cancer, where they were up-regulated as compared to surrounding normal tissue. Five potentially pathophysiologically significant SNPs were detected (BRCA2 (rs144848), TP53 (rs1042522), AURKA (rs2273535), DBYD (rs1801265), and (SOD2 rs4880)) but no CRCTC1-MAML2 fusion gene. FusionCatcher detected a possible novel fusion product currently under investigation. Conclusion: The paralleled approach provided sufficient material to identify amphiregulin as an upregulated growth factor pathway in a CRTC1-MAML2 fusion gene negative MEC. Previously, amphiregulin upregulation was pathophysiologically linked to the CRTC1-MAML2 fusion gene. Results from the two MEC sites were biologically concordant and genetically similar. In summary, CRC can be used to expand limited patient derived material for more extensive studies under non-CRC conditions. Support: R56DE023259 (PAF)

Citation Format: Ahmad M. Alamri, Xuefeng Liu, Weisheng Wang, Xiaogang Zhong, Bhaskar Kallakury, Bruce Davidson, Priscilla A. Furth. Paralleled workflow for expansion of limited patient material using CRC for in vitro /PDX/biological/genetic studies of a low-grade mucoepidermoid carcinoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4280.
BibTeX:
@article{Alamri2016,
  author = {Alamri, Ahmad M. and Liu, Xuefeng and Wang, Weisheng and Zhong, Xiaogang and Kallakury, Bhaskar and Davidson, Bruce and Furth, Priscilla A.},
  title = {Abstract 4280: Paralleled workflow for expansion of limited patient material using CRC for textlessitextgreaterin vitrotextless/itextgreater /PDX/biological/genetic studies of a low-grade mucoepidermoid carcinoma},
  journal = {Cancer Research},
  publisher = {American Association for Cancer Research},
  year = {2016},
  volume = {76},
  number = {14 Supplement},
  pages = {4280--4280},
  url = {http://cancerres.aacrjournals.org/lookup/doi/10.1158/1538-7445.AM2016-4280},
  doi = {http://doi.org/10.1158/1538-7445.AM2016-4280}
}
Alanazi, I.O. and Ebrahimie, E. Computational Systems Biology Approach Predicts Regulators and Targets of microRNAs and Their Genomic Hotspots in Apoptosis Process. 2016 Molecular biotechnology  article URL 
Abstract: Novel computational systems biology tools such as common targets analysis, common regulators analysis, pathway discovery, and transcriptomic-based hotspot discovery provide new opportunities in understanding of apoptosis molecular mechanisms. In this study, after measuring the global contribution of microRNAs in the course of apoptosis by Affymetrix platform, systems biology tools were utilized to obtain a comprehensive view on the role of microRNAs in apoptosis process. Network analysis and pathway discovery highlighted the crosstalk between transcription factors and microRNAs in apoptosis. Within the transcription factors, PRDM1 showed the highest upregulation during the course of apoptosis, with more than 9-fold expression increase compared to non-apoptotic condition. Within the microRNAs, MIR1208 showed the highest expression in non-apoptotic condition and downregulated by more than 6 fold during apoptosis. Common regulators algorithm showed that TNF receptor is the key upstream regulator with a high number of regulatory interactions with the differentially expressed microRNAs. BCL2 and AKT1 were the key downstream targets of differentially expressed microRNAs. Enrichment analysis of the genomic locations of differentially expressed microRNAs led us to the discovery of chromosome bands which were highly enriched (p textless 0.01) with the apoptosis-related microRNAs, such as 13q31.3, 19p13.13, and Xq27.3 This study opens a new avenue in understanding regulatory mechanisms and downstream functions in the course of apoptosis as well as distinguishing genomic-enriched hotspots for apoptosis process.
BibTeX:
@article{Alanazi2016,
  author = {Alanazi, Ibrahim O and Ebrahimie, Esmaeil},
  title = {Computational Systems Biology Approach Predicts Regulators and Targets of microRNAs and Their Genomic Hotspots in Apoptosis Process.},
  journal = {Molecular biotechnology},
  year = {2016},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/27178576}
}
An, F., Chen, T., Stéphanie, D.M.A., Li, K., Li, Q.X., Carvalho, L.J.C.B., Tomlins, K., Li, J., Gu, B. and Chen, S. Domestication Syndrome Is Investigated by Proteomic Analysis between Cultivated Cassava (Manihot esculenta Crantz) and Its Wild Relatives. 2016
Vol. 11(3)PloS one, pp. e0152154 
misc URL 
Abstract: Cassava (Manihot esculenta Crantz) wild relatives remain a largely untapped potential for genetic improvement. However, the domestication syndrome phenomena from wild species to cultivated cassava remain poorly understood. The analysis of leaf anatomy and photosynthetic activity showed significantly different between cassava cultivars SC205, SC8 and wild relative M. esculenta ssp. Flabellifolia (W14). The dry matter, starch and amylose contents in the storage roots of cassava cultivars were significantly more than that in wild species. In order to further reveal the differences in photosynthesis and starch accumulation of cultivars and wild species, the globally differential proteins between cassava SC205, SC8 and W14 were analyzed using 2-DE in combination with MALDI-TOF tandem mass spectrometry. A total of 175 and 304 proteins in leaves and storage roots were identified, respectively. Of these, 122 and 127 common proteins in leaves and storage roots were detected in SC205, SC8 and W14, respectively. There were 11, 2 and 2 unique proteins in leaves, as well as 58, 9 and 12 unique proteins in storage roots for W14, SC205 and SC8, respectively, indicating proteomic changes in leaves and storage roots between cultivated cassava and its wild relatives. These proteins and their differential regulation across plants of contrasting leaf morphology, leaf anatomy pattern and photosynthetic related parameters and starch content could contribute to the footprinting of cassava domestication syndrome. We conclude that these global protein data would be of great value to detect the key gene groups related to cassava selection in the domestication syndrome phenomena.
BibTeX:
@misc{An2016,
  author = {An, Feifei and Chen, Ting and Stéphanie, Djabou Mouafi Astride and Li, Kaimian and Li, Qing X and Carvalho, Luiz J C B and Tomlins, Keith and Li, Jun and Gu, Bi and Chen, Songbi},
  title = {Domestication Syndrome Is Investigated by Proteomic Analysis between Cultivated Cassava (Manihot esculenta Crantz) and Its Wild Relatives.},
  booktitle = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {3},
  pages = {e0152154},
  url = {https://demo.elseviertextmining.com/demo/search?query=pathway+studio&s=d&t=LHi4PF5&category=r&view=d&start=3 http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0152154}
}
An, F., Li, G., Li, Q.X., Li, K., Carvalho, L.J.C.B., Ou, W. and Chen, S. The Comparatively Proteomic Analysis in Response to Cold Stress in Cassava Plantlets. 2016 Plant Molecular Biology Reporter
Vol. 34(6), pp. 1095-1110 
article URL 
Abstract: Cassava (Manihot esculenta Crantz) is a tropical root crop and sensitive to low temperature. However, it is poorly to know how cassava can modify its metabolism and growth to adapt to cold stress. An investigation aimed at a better understanding of cold-tolerant mechanism of cassava plantlets was carried out with the approaches of physiology and proteomics in the present study. The principal component analysis of seven physiological characteristics showed that electrolyte leakage (EL), chlorophyll content, and malondialdehyde (MDA) may be the most important physiological indexes for determining cold-resistant abilities of cassava. The genome-wide proteomic analysis showed that 20 differential proteins had the same patterns in the apical expanded leaves of cassava SC8 and Col1046. They were mainly related to photosynthesis, carbon metabolism and energy metabolism, defense, protein synthesis, amino acid metabolism, signal transduction, structure, detoxifying and antioxidant, chaperones, and DNA-binding proteins, in which 40 % were related with photosynthesis. The remarkable variation in photosynthetic activity and expression level of peroxiredoxin is closely linked with expression levels of proteomic profiles. Moreover, analysis of differentially expressed proteins under cold stress is an important step toward further elucidation of mechanisms of cold stress resistance.
BibTeX:
@article{An2016a,
  author = {An, Feifei and Li, Genghu and Li, Qing X. and Li, Kaimian and Carvalho, Luiz J. C. B. and Ou, Wenjun and Chen, Songbi},
  title = {The Comparatively Proteomic Analysis in Response to Cold Stress in Cassava Plantlets.},
  journal = {Plant Molecular Biology Reporter},
  publisher = {Springer US},
  year = {2016},
  volume = {34},
  number = {6},
  pages = {1095--1110},
  url = {http://link.springer.com/article/10.1007/s11105-016-0987-x http://link.springer.com/10.1007/s11105-016-0987-x}
}
An, R. and Grewal, P.S. Comparative Analysis of Xenorhabdus koppenhoeferi Gene Expression during Symbiotic Persistence in the Host Nematode. 2016 PloS one
Vol. 11(1), pp. e0145739 
article URL 
Abstract: Species of Xenorhabdus and Photorhabdus bacteria form mutualistic associations with Steinernema and Heterorhabditis nematodes, respectively and serve as model systems for studying microbe-animal symbioses. Here, we profiled gene expression of Xenorhabdus koppenhoeferi during their symbiotic persistence in the newly formed infective juveniles of the host nematode Steinernema scarabaei through the selective capture of transcribed sequences (SCOTS). The obtained gene expression profile was then compared with other nematode-bacteria partnerships represented by Steinernema carpocapsae-Xenorhabdus nematophila and Heterorhabditis bacteriophora-Photorhabdus temperata. A total of 29 distinct genes were identified to be up-regulated and 53 were down-regulated in X. koppenhoeferi while in S. scarabaei infective juveniles. Of the identified genes, 8 of the up-regulated and 14 of the down-regulated genes were similarly expressed in X. nematophila during persistence in its host nematode S. carpocapsae. However, only one from each of these up- and down-regulated genes was common to the mutualistic partnership between the bacterium P. temperata and the nematode H. bacteriophora. Interactive network analysis of the shared genes between X. koppenhoeferi and X. nematophila demonstrated that the up-regulated genes were mainly involved in bacterial survival and the down-regulated genes were more related to bacterial virulence and active growth. Disruption of two selected genes pta (coding phosphotransacetylase) and acnB (coding aconitate hydratase) in X. nematophila with shared expression signature with X. koppenhoeferi confirmed that these genes are important for bacterial persistence in the nematode host. The results of our comparative analyses show that the two Xenorhabdus species share a little more than a quarter of the transcriptional mechanisms during persistence in their nematode hosts but these features are quite different from those used by P. temperata bacteria in their nematode host H. bacteriophora.
BibTeX:
@article{An2016b,
  author = {An, Ruisheng and Grewal, Parwinder S},
  title = {Comparative Analysis of Xenorhabdus koppenhoeferi Gene Expression during Symbiotic Persistence in the Host Nematode.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {1},
  pages = {e0145739},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145739 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4706420&tool=pmcentrez&rendertype=abstract}
}
Azimova, J., Kondratieva, N., Sergeev, A., Skorobogatykh, K. and Kokaeva, Z. The Role of BDNF Gene Polymorphism in Formation of Clinical Characteristics of Migraine 2/7 2016 J Neurol Stroke
Vol. 4(2) 
article DOI  
BibTeX:
@article{Azimova2016,
  author = {Azimova, J and Kondratieva, N and Sergeev, A and Skorobogatykh, K and Kokaeva, Z},
  title = {The Role of BDNF Gene Polymorphism in Formation of Clinical Characteristics of Migraine 2/7},
  journal = {J Neurol Stroke},
  year = {2016},
  volume = {4},
  number = {2},
  doi = {http://doi.org/10.15406/jnsk.2016.04.00123}
}
Bahamonde, P.A., McMaster, M.E., Servos, M.R., Martyniuk, C.J. and Munkittrick, K.R. Characterizing Transcriptional Networks in Male Rainbow Darter (Etheostoma caeruleum) that Regulate Testis Development over a Complete Reproductive Cycle. 2016 PloS one
Vol. 11(11), pp. e0164722 
article URL 
Abstract: Intersex is a condition that has been associated with exposure to sewage effluents in male rainbow darter (Etheostoma caeruleum). To better understand changes in the transcriptome that are associated with intersex, we characterized annual changes in the testis transcriptome in wild, unexposed fish. Rainbow darter males were collected from the Grand River (Ontario, Canada) in May (spawning), August (post-spawning), October (recrudescence), January (developing) and March (pre-spawning). Histology was used to determine the proportion of spermatogenic cell types that were present during each period of testicular maturation. Regression analysis determined that the proportion of spermatozoa versus spermatocytes in all stages of development (R2 ≥ 0.58) were inversely related; however this was not the case when males were in the post-spawning period. Gene networks that were specific to the transition from developing to pre-spawning stages included nitric oxide biosynthesis, response to wounding, sperm cell function, and stem cell maintenance. The pre-spawning to spawning transition included gene networks related to amino acid import, glycogenesis, Sertoli cell proliferation, sperm capacitation, and sperm motility. The spawning to post-spawning transition included unique gene networks associated with chromosome condensation, ribosome biogenesis and assembly, and mitotic spindle assembly. Lastly, the transition from post-spawning to recrudescence included gene networks associated with egg activation, epithelial to mesenchymal transition, membrane fluidity, and sperm cell adhesion. Noteworthy was that there were a significant number of gene networks related to immune system function that were differentially expressed throughout reproduction, suggesting that immune network signalling has a prominent role in the male testis. Transcripts in the testis of post-spawning individuals showed patterns of expression that were most different for the majority of transcripts investigated when compared to the other stages. Interestingly, many transcripts associated with female sex differentiation (i.e. esr1, sox9, cdca8 and survivin) were significantly higher in the testis during the post-spawning season compared to other testis stages. At post-spawning, there were higher levels of estrogen and androgen receptors (esr1, esr2, ar) in the testis, while there was a decrease in the levels of sperm associated antigen 1 (spag1) and spermatogenesis associated 4 (spata4) mRNA. Cyp17a was more abundant in the testis of fish in the pre-spawning, spawning, and post-spawning seasons compared to those individuals that were recrudescent while aromatase (cyp19a) did not vary in expression over the year. This study identifies cell process related to testis development in a seasonally spawning species and improves our understanding regarding the molecular signaling events that underlie testicular growth. This is significant because, while there are a number of studies characterizing molecular pathways in the ovary, there are comparatively less describing transcriptomic patterns in the testis in wild fish.
BibTeX:
@article{Bahamonde2016,
  author = {Bahamonde, Paulina A and McMaster, Mark E and Servos, Mark R and Martyniuk, Christopher J and Munkittrick, Kelly R},
  title = {Characterizing Transcriptional Networks in Male Rainbow Darter (Etheostoma caeruleum) that Regulate Testis Development over a Complete Reproductive Cycle.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {11},
  pages = {e0164722},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0164722}
}
Bauer, J., Bussen, M., Wise, P., Wehland, M., Schneider, S. and Grimm, D. Searching the literature for proteins facilitates the identification of biological processes, if advanced methods of analysis are linked: A case study on microgravity-caused changes in cells 2016 Expert Review of Proteomics, pp. 14789450.2016.1197775  article DOI URL 
BibTeX:
@article{Bauer2016,
  author = {Bauer, Johann and Bussen, Markus and Wise, Petra and Wehland, Markus and Schneider, Sabine and Grimm, Daniela},
  title = {Searching the literature for proteins facilitates the identification of biological processes, if advanced methods of analysis are linked: A case study on microgravity-caused changes in cells},
  journal = {Expert Review of Proteomics},
  year = {2016},
  pages = {14789450.2016.1197775},
  url = {http://www.tandfonline.com/doi/full/10.1080/14789450.2016.1197775},
  doi = {http://doi.org/10.1080/14789450.2016.1197775}
}
Bhardwaj,  A. A Bioinformatics Approach to construct Regulatory Networks using Microarray Data 2016 INROADS- An International Journal of Jaipur National University
Vol. 5(1), pp. 18-20 
article URL 
Abstract: In a given cell, multiple genes coordinate to ensure the process of life. A disease is rarely a consequence of an abnormality in a single gene but reflects perturbations of the complex intracellular network (Barabási et al., 2010). Recent advancements in technology have led to the ability to measure the vast catalogues of expression of thousands of genes and transcription factors, simultaneously. The discovery of microarray technique was a major milestone which has revolutionised current research and diagnostics. It has generated a large amount of freely available information, opening the door to a postgenome era. Microarray rapidly uncovers the broad patterns of genetic activity and shows insight into gene function, processes and pathways which allow Insilco research and further mining of available data. The emerging tools of network offer a platform to explore systematically not only the molecular complexity of a particular disease, leading to the identification of disease modules and pathways, but also molecular relationships between apparently distinct phenotypes (Barabási et al., 2010). In this paper, we propose a pipeline to assess the possibility of identifying diseasemarker genes and potent drug targets.
BibTeX:
@article{Bhardwaj2016,
  author = {Bhardwaj,  Anuradha},
  title = {A Bioinformatics Approach to construct Regulatory Networks using Microarray Data},
  journal = {INROADS- An International Journal of Jaipur National University},
  publisher = {Jaipur National University},
  year = {2016},
  volume = {5},
  number = {1},
  pages = {18--20},
  url = {http://www.indianjournals.com/ijor.aspx?target=ijor:inroads&volume=5&issue=1&article=004}
}
Brauze, D., Zawierucha, P., Kiwerska, K., Bednarek, K., Oleszak, M., Rydzanicz, M. and Jarmuz-Szymczak, M. Induction of expression of aryl hydrocarbon receptor-dependent genes in human HepaRG cell line modified by shRNA and treated with β-naphthoflavone 2016 Molecular and Cellular Biochemistry, pp. 1-17  article DOI URL 
BibTeX:
@article{Brauze2016,
  author = {Brauze, Damian and Zawierucha, Piotr and Kiwerska, Katarzyna and Bednarek, Kinga and Oleszak, Martyna and Rydzanicz, Malgorzata and Jarmuz-Szymczak, Malgorzata},
  title = {Induction of expression of aryl hydrocarbon receptor-dependent genes in human HepaRG cell line modified by shRNA and treated with β-naphthoflavone},
  journal = {Molecular and Cellular Biochemistry},
  publisher = {Springer US},
  year = {2016},
  pages = {1--17},
  url = {http://link.springer.com/10.1007/s11010-016-2862-3},
  doi = {http://doi.org/10.1007/s11010-016-2862-3}
}
Brym, P., Bojarojć-Nosowicz, B., Oleʼnski, K., Hering, D., Ruść, A., Kaczmarczyk, E. and Kamiʼnski, S. Genome-wide association study for host response to bovine leukemia virus in Holstein cows 2016 Veterinary Immunology and Immunopathology  article URL 
Abstract: The mechanisms of leukemogenesis induced by bovine leukemia virus (BLV) and the processes underlying the phenomenon of differential host response to BLV infection still remain poorly understood. The aim of the study was to screen the entire cattle genome to identify markers and candidate genes that might be involved in host response to bovine leukemia virus infection. A genome-wide association study was performed using Holstein cows naturally infected by BLV. A data set included 43 cows (BLV positive) and 30 cows (BLV negative) genotyped for 54 609 SNP markers (Illumina Bovine SNP50 BeadChip). The BLV status of cows was determined by serum ELISA, nested-PCR and hematological counts. Linear Regression Analysis with a False Discovery Rate and kinship matrix (computed on the autosomal SNPs) was calculated to find out which SNP markers significantly differentiate BLV-positive and BLV-negative cows. Nine markers reached genome-wide significance. The most significant SNPs were located on chromosomes 23 (rs41583098), 3 (rs109405425, rs110785500) and 8 (rs43564499) in close vicinity of a patatin-like phospholipase domain containing 1 (PNPLA1); adaptor-related protein complex 4, beta 1 subunit (AP4B1); tripartite motif-containing 45 (TRIM45) and cell division cycle associated 2 (CDCA2) genes, respectively. Furthermore, a list of 41 candidate genes was composed based on their proximity to significant markers (within a distance of ca. 1 Mb) and functional involvement in processes potentially underlying BLV-induced pathogenesis. In conclusion, it was demonstrated that host response to BLV infection involves nine sub-regions of the cattle genome (represented by 9 SNP markers), containing many genes which, based on the literature, could be involved to enzootic bovine leukemia progression. New group of promising candidate genes associated with the host response to BLV infection were identified and could therefore be a target for future studies. The functions of candidate genes surrounding significant SNP markers imply that there is no single regulatory process that is solely targeted by BLV infection, but rather the network of interrelated pathways is deregulated, leading to the disruption of the control of B-cell proliferation and programmed cell death.
BibTeX:
@article{Brym2016,
  author = {Brym, P. and Bojarojć-Nosowicz, B. and Oleʼnski, K. and Hering, D.M. and Ruść, A. and Kaczmarczyk, E. and Kamiʼnski, S.},
  title = {Genome-wide association study for host response to bovine leukemia virus in Holstein cows},
  journal = {Veterinary Immunology and Immunopathology},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S0165242716300691}
}
Castillos, L. and Yuryev, A. Cancer and Clinical Research Developing Pathway Collection for Personalized Anti-cancer Therapy 2016 International Library Citation: Castillos L Int J Cancer Clin Res Int J Cancer Clin Res
Vol. 3(3) 
article  
Abstract: " Curse of dimensionality " is the contradiction between mathematical requirement for optimal gene signatures to contain no more than 20-30 genes [5] and biological reality observing10-100 times more differentially expressed genes in cancer tumors. Such short optimal signature are the consequence of the small number of patient samples available in a training set for signature calculation compared to the number of correlated DE genes [6,7]. The shortage of cancer samples for large signature calculation is so significant that even 10-fold increase in the number of available samples will not yield substantial improvement in predictability of transcriptional signatures. Biological considerations can provide solution to the " curse of dimensionality " of microarray data. Indeed, observed transcriptional profile in a patient is due to the activity of transcription factors and micro RNAs. The number of these direct transcriptional regulators is much smaller than the number of genes on the microarray and in human genome. Thus, the transformation of transcriptional profile into activity of few upstream expression regulators should provide significant reduction in the data space dimensionality which in turn should help calculating more powerful signatures [8]. Two similar algorithms were developed to calculate the activity of upstream expression regulators from microarray data using prior knowledge about expression regulatory events reported in the literature: sub-network enrichment analysis (SNEA) [9] and reverse causal reasoning (RCR) [10]. We used SNEA algorithm implemented in Pathway Studio software from Elsevier. It relies on the knowledge base of expression regulation events automatically extracted from biomedical research literature by natural processing technology. Pathway Studio knowledge base has the biggest number of regulatory events and therefore provides the most comprehensive and up-to-date snapshot of transcriptional activity in cancer samples. SNEA uses non-parametric Mann-Whitney enrichment test to evaluate transcriptional activity of upstream regulators which was shown to provide superior results for microarray data analysis over overlap hyper geometric test implemented in RCR [11,12]. The activity of upstream expression regulators in turn depends on activity of pathways altered in the tumor. Therefore projecting the activity of upstream expression regulators identified by SNEA onto collection of relatively small number of biological pathways relevant for cancer progression should allow us to identify cancer mechanism in an individual patient reducing the complexity in interpretation of large number of differentially expressed genes in Abstract We describe methodology for developing personalized anti-cancer drug therapy using pathway analysis. We successfully applied this methodology to treat several cancer patients that were terminally diagnosed by standard of care criteria at the hospital. Our approach consists of profiling patient tumor using gene expression microarray and calculating pathways responsible for the differential expression between tumor and normal control tissue. Pathways are selected for treatment targeting based on their enrichment with major expression regulators identified by sub-network enrichment analysis (SNEA) in Pathway Studio. We then select FDA approved drugs inhibiting activated pathways and prescribe them to the patient. To facilitate interpretation of patient data we built collection of cancer pathways based on ten cancer hallmarks described in the literature. This collection explains function of more than half of expression regulators identified in patient's tumors by SNEA. This paper focuses on description of pathways built for interpretation of expression profiles of cancer patients.
BibTeX:
@article{Castillos2016,
  author = {Castillos, Luminita and Yuryev, Anton},
  title = {Cancer and Clinical Research Developing Pathway Collection for Personalized Anti-cancer Therapy},
  journal = {International Library Citation: Castillos L Int J Cancer Clin Res Int J Cancer Clin Res},
  year = {2016},
  volume = {3},
  number = {3}
}
Cha, H.J., Choi, M.-J., Ahn, J.-I., Jeon, S.-H., Kang, H., Kim, E.J., Seong, W.-K., Kim, H.S. and Jeong, H.-S. Comparison of gene expression profiles in drug-withdrawn rats 2016 Molecular & Cellular Toxicology
Vol. 12(2), pp. 197-207 
article DOI URL 
BibTeX:
@article{Cha2016,
  author = {Cha, Hye Jin and Choi, Mun-Ji and Ahn, Joon-Ik and Jeon, Seol-Hee and Kang, Hoil and Kim, Eun Jung and Seong, Won-Keun and Kim, Hyung Soo and Jeong, Ho-Sang},
  title = {Comparison of gene expression profiles in drug-withdrawn rats},
  journal = {Molecular & Cellular Toxicology},
  publisher = {The Korean Society of Toxicogenomics and Toxicoproteomics},
  year = {2016},
  volume = {12},
  number = {2},
  pages = {197--207},
  url = {http://link.springer.com/10.1007/s13273-016-0024-z},
  doi = {http://doi.org/10.1007/s13273-016-0024-z}
}
Chandrasekaran, S. and Bonchev, D. Network analysis of Human Post-mortem microarrays reveals novel genes, MicroRNAs, and mechanistic scenarios of potential importance in fighting Huntington's disease 2016 Computational and Structural Biotechnology Journal  article URL 
Abstract: Huntington's disease is a progressive neurodegenerative disorder characterized by motor disturbances, cognitive decline, and neuropsychiatric symptoms. In this study, we utilized network-based analysis in an attempt to explore and understand the underlying molecular mechanism and to identify critical molecular players of this disease condition. Using human post-mortem microarrays from three brain regions (cerebellum, frontal cortex and caudate nucleus) we selected in a four-step procedure a seed set of highly modulated genes. Several protein–protein interaction networks, as well as microRNA–mRNA networks were constructed for these gene sets with the Elsevier Pathway Studio software and its associated ResNet database. We applied a gene prioritizing procedure based on vital network topological measures, such as high node connectivity and centrality. Adding to these criteria the guilt-by-association rule and exploring their innate biomolecular functions, we propose 19 novel genes from the analyzed microarrays, from which CEBPA, CDK1, CX3CL1, EGR1, E2F1, ERBB2, LRP1, HSP90AA1 and ZNF148 might be of particular interest for experimental validation. A possibility is discussed for dual-level gene regulation by both transcription factors and microRNAs in Huntington's disease mechanism. We propose several possible scenarios for experimental studies initiated via the extra-cellular ligands TGFB1, FGF2 and TNF aiming at restoring the cellular homeostasis in Huntington's disease.
BibTeX:
@article{Chandrasekaran2016,
  author = {Chandrasekaran, Sreedevi and Bonchev, Danail},
  title = {Network analysis of Human Post-mortem microarrays reveals novel genes, MicroRNAs, and mechanistic scenarios of potential importance in fighting Huntington's disease},
  journal = {Computational and Structural Biotechnology Journal},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S2001037016000027}
}
Chandrasekaran, S. and Bonchev, D. Network Topology Analysis of Post-Mortem Brain Microarrays Identifies More Alzheimer's Related Genes and MicroRNAs and Points to Novel Routes for Fighting with the Disease. 2016 PloS one
Vol. 11(1), pp. e0144052 
article URL 
Abstract: Network-based approaches are powerful and beneficial tools to study complex systems in their entirety, elucidating the essential factors that turn the multitude of individual elements into a functional system. In this study we used critical network topology descriptors and guilt-by-association rule to explore and understand the significant molecular players, drug targets and underlying biological mechanisms of Alzheimer's disease. Analyzing two post-mortem brain gene microarrays (GSE4757 and GSE28146) with Pathway Studio software package we constructed and analyzed a set of protein-protein interaction, as well as miRNA-target networks. In a 4-step procedure the expression datasets were normalized using Robust Multi-array Average approach, while the modulation of gene expression by the disease was statistically evaluated by the empirical Bayes method from the limma Bioconductor package. Representative set of 214 seed-genes (ptextless0.01) common for the three brain sections of the two microarrays was thus created. The Pathway Studio analysis of the networks built identified 15 new potential AD-related genes and 17 novel AD-involved microRNAs. Using KEGG pathways relevant in Alzheimer's disease we built an integrated mechanistic network from the interactions between the overlapping genes in these pathways. Routes of possible disease initiation process were thus revealed through the CD4, DCN, and IL8 extracellular ligands. DAVID and IPA enrichment analysis uncovered a number of deregulated biological processes and pathways including neuron projection/differentiation, aging, oxidative stress, chemokine/ neurotrophin signaling, long-term potentiation and others. The findings in this study offer information of interest for subsequent experimental studies.
BibTeX:
@article{Chandrasekaran2016a,
  author = {Chandrasekaran, Sreedevi and Bonchev, Danail},
  title = {Network Topology Analysis of Post-Mortem Brain Microarrays Identifies More Alzheimer's Related Genes and MicroRNAs and Points to Novel Routes for Fighting with the Disease.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {1},
  pages = {e0144052},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0144052}
}
Chao, W.S., Doğramaci, M., Horvath, D.P., Anderson, J.V. and Foley, M.E. Phytohormone balance and stress-related cellular responses are involved in the transition from bud to shoot growth in leafy spurge. 2016 BMC plant biology
Vol. 16(1), pp. 47 
article URL 
Abstract: BACKGROUND: Leafy spurge (Euphorbia esula L.) is an herbaceous weed that maintains a perennial growth pattern through seasonal production of abundant underground adventitious buds (UABs) on the crown and lateral roots. During the normal growing season, differentiation of bud to shoot growth is inhibited by physiological factors external to the affected structure; a phenomenon referred to as paradormancy. Initiation of shoot growth from paradormant UABs can be accomplished through removal of the aerial shoots (hereafter referred to as paradormancy release).

RESULTS: In this study, phytohormone abundance and the transcriptomes of paradormant UABs vs. shoot-induced growth at 6, 24, and 72 h after paradormancy release were compared based on hormone profiling and RNA-seq analyses. Results indicated that auxin, abscisic acid (ABA), and flavonoid signaling were involved in maintaining paradormancy in UABs of leafy spurge. However, auxin, ABA, and flavonoid levels/signals decreased by 6 h after paradormancy release, in conjunction with increase in gibberellic acid (GA), cytokinin, jasmonic acid (JA), ethylene, and brassinosteroid (BR) levels/signals. Twenty four h after paradormancy release, auxin and ABA levels/signals increased, in conjunction with increase in GA levels/signals. Major cellular changes were also identified in UABs at 24 h, since both principal component and Venn diagram analysis of transcriptomes clearly set the 24 h shoot-induced growth apart from other time groups. In addition, increase in auxin and ABA levels/signals and the down-regulation of 40 over-represented AraCyc pathways indicated that stress-derived cellular responses may be involved in the activation of stress-induced re-orientation required for initiation of shoot growth. Seventy two h after paradormancy release, auxin, cytokinin, and GA levels/signals were increased, whereas ABA, JA, and ethylene levels/signals were decreased.

CONCLUSION: Combined results were consistent with different phytohormone signals acting in concert to direct cellular changes involved in bud differentiation and shoot growth. In addition, shifts in balance of these phytohormones at different time points and stress-related cellular responses after paradormancy release appear to be critical factors driving transition of bud to shoot growth.
BibTeX:
@article{Chao2016,
  author = {Chao, Wun S and Doğramaci, Münevver and Horvath, David P and Anderson, James V and Foley, Michael E},
  title = {Phytohormone balance and stress-related cellular responses are involved in the transition from bud to shoot growth in leafy spurge.},
  journal = {BMC plant biology},
  year = {2016},
  volume = {16},
  number = {1},
  pages = {47},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4761131&tool=pmcentrez&rendertype=abstract}
}
Chatterjee, N., Yang, J., Atluri, R., Lee, W., Hong, J. and Choi, J. Amorphous silica nanoparticle induced perturbation of cholesterol homeostasis as a function of surface area highlight safe-by-design implementation: an integrated Multi-OMICS analysis 2016 RSC Adv.  article DOI URL 
Abstract: To fulfill the knowledge gap between wide application of amorphous silica nanoparticles (aSiNPs) and its health impacts, the present study endeavored to investigate the molecular mechanisms involved in aSiNPs' mediated hepatotoxicity with systems toxicology approach and how it is related to the physico-chemical properties of aSiNPs. To this end we used four types of aSiNPs which differ in their surface area - aSiNP-116 (surface area: 116 m2/g), aSiNP-189 (surface area: 189 m2/g), aSiNP-26 (surface area: 26 m2/g) and aSiNP-8 (surface area: 8.3 m2/g) and human hepatoma (HepG2) cell line as model system. We applied multi-OMICS (DNA microarray based transcriptomics and GC-MS based lipidomics) followed by bioinformatics analysis in aSiNP-116 treated HepG2 cells. The perturbations of steroid-cholesterol biosynthesis was revealed from KEGG (with significantly altered genes) and IMPaLA (with integrated significantly altered genes and metabolites) pathway analysis. Furthermore, in corroboration with in silico analysis, the biochemical tests exhibited concentration dependent increase in total cholesterol level due to aSiNP-116 treatment. In subsequent step, the hypothesis derived in aSiNP-116 was further tested in other aSiNPs (aSiNP-189, aSiNP-26 and aSiNP-8) exposed cells with GC-MS based lipidomics as well as biochemical tests. The alterations of cholesterol biosynthesis were found as directly proportional with the surface area of aSiNPs, i.e., the larger the surface area the higher the cholesterol level. Taken together, perturbation of cholesterol biosynthesis as a function of surface area was found as principal mode-of-action of aSiNPs' exposure which necessitates the safe-by-design approach for its biological applications.
BibTeX:
@article{Chatterjee2016,
  author = {Chatterjee, Nivedita and Yang, Jisu and Atluri, Rambabu and Lee, Wonwoong and Hong, Jongki and Choi, Jinhee},
  title = {Amorphous silica nanoparticle induced perturbation of cholesterol homeostasis as a function of surface area highlight safe-by-design implementation: an integrated Multi-OMICS analysis},
  journal = {RSC Adv.},
  publisher = {The Royal Society of Chemistry},
  year = {2016},
  url = {http://pubs.rsc.org/en/Content/ArticleLanding/2016/RA/C6RA06006D},
  doi = {http://doi.org/10.1039/C6RA06006D}
}
Chavan, R., Feillet, C., Costa, S.S.F., Delorme, J.E., Okabe, T., Ripperger, J.A. and Albrecht, U. Liver-derived ketone bodies are necessary for food anticipation. 2016 Nature communications
Vol. 7, pp. 10580 
article URL 
Abstract: The circadian system has endowed animals with the ability to anticipate recurring food availability at particular times of day. As daily food anticipation (FA) is independent of the suprachiasmatic nuclei, the central pacemaker of the circadian system, questions arise of where FA signals originate and what role components of the circadian clock might play. Here we show that liver-specific deletion of Per2 in mice abolishes FA, an effect that is rescued by viral overexpression of Per2 in the liver. RNA sequencing indicates that Per2 regulates β-hydroxybutyrate (βOHB) production to induce FA leading to the conclusion that liver Per2 is important for this process. Unexpectedly, we show that FA originates in the liver and not in the brain. However, manifestation of FA involves processing of the liver-derived βOHB signal in the brain, indicating that the food-entrainable oscillator is not located in a single tissue but is of systemic nature.
BibTeX:
@article{Chavan2016,
  author = {Chavan, Rohit and Feillet, Céline and Costa, Sara S Fonseca and Delorme, James E and Okabe, Takashi and Ripperger, Jürgen A and Albrecht, Urs},
  title = {Liver-derived ketone bodies are necessary for food anticipation.},
  journal = {Nature communications},
  year = {2016},
  volume = {7},
  pages = {10580},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4742855&tool=pmcentrez&rendertype=abstract}
}
Cheadle, C., Cao, H., Kalinin, A. and Hodgkinson, J. Advanced literature analysis in a Big Data world 2016 Annals of the New York Academy of Sciences  article DOI  
BibTeX:
@article{Cheadle2016,
  author = {Cheadle, Chris and Cao, Hongbao and Kalinin, Andrey and Hodgkinson, Jaqui},
  title = {Advanced literature analysis in a Big Data world},
  journal = {Annals of the New York Academy of Sciences},
  year = {2016},
  doi = {http://doi.org/10.1111/NYAS.13270}
}
Chen, C.-X., Mao, Y.-S., Foster, P., Zhu, Z.-W., Du, J. and Guo, C.-Y. Possible association between helicobacter pylori infection and non-alcoholic fatty liver disease 2016 Applied Physiology, Nutrition, and Metabolism, pp. apnm-2016-0499  article URL 
Abstract: Possible association between Helicobacter pylori infection (HPI) and nonalcoholic fatty liver disease (NAFLD) has been proposed by several studies with inconsistent conclusions. Here, we studied the association between HPI and NAFLD at three levels: 1.) Genetic level; 2.) Small molecular level; and 3.) Clinical level. Relation data between diseases, genes, and small molecules were acquired from Pathway Studio ResNet Mammalian database. Clinical data were acquired from 2,263 elderly South Chinese subjects, including 603 NAFLD patients and 1660 non-NAFLD subjects. Results showed that HPI and NAFLD present significantly shared genetic bases (95 genes, p-value=2.5E-72), demonstrating multiple common genetic pathways (enrichment p-value 4.38E-20 for the top 10 pathways). Genetic network analysis suggested that mutual regulation may exist between HPI and NAFLD through 21 out of 95 genes. Furthermore, 85 out of the 95 genes manifested strong interaction with 12 small molecules/drugs that demonstrate effectivenes...
BibTeX:
@article{Chen2016,
  author = {Chen, Chang-Xi and Mao, Yu-Shan and Foster, Parker and Zhu, Zhong-Wei and Du, Juan and Guo, Chuan-Yong},
  title = {Possible association between helicobacter pylori infection and non-alcoholic fatty liver disease},
  journal = {Applied Physiology, Nutrition, and Metabolism},
  year = {2016},
  pages = {apnm--2016--0499},
  url = {http://www.nrcresearchpress.com/doi/abs/10.1139/apnm-2016-0499.WDRbA7IrJrR}
}
Collí-Dulá, R.C., Martyniuk, C.J., Streets, S., Denslow, N.D. and Lehr, R. Molecular impacts of perfluorinated chemicals (PFASs) in the liver and testis of male largemouth bass (Micropterus salmoides) in Minnesota Lakes 2016 Comparative Biochemistry and Physiology Part D: Genomics and Proteomics  article URL 
Abstract: Perfluorinated chemicals (PFASs) stem from a wide range of sources and have been detected in aquatic ecosystems worldwide, including the upper Midwest and the state of Minnesota in the USA. This study investigated whether fish with high body burden levels of PFASs in the Twin Cities Metro Areas showed any evidence of adverse effects at the level of the transcriptome. We hypothesized that fish with higher body burden levels of PFASs would exhibit molecular responses in the liver and testis that were suggestive of oxidative and general stress, as well as impaired reproduction. Concentrations of PFASs in largemouth bass varied significantly across the sampled lakes, with the lowest concentrations of PFASs found in fish from Steiger and Upper Prior Lakes and the highest concentrations found in fish from Calhoun and Twin Lakes. Largemouth bass with high PFAS concentrations exhibited changes in the expression of genes related to lipid metabolism, energy production, RNA processing, protein production/degradation and contaminant detoxification, all of which are consistent with biomarker responses observed in other studies with PFASs. However, given the wide range of genes that were differentially expressed across the lakes and the variability observed in the mechanisms through which biological processes were affected, it is unlikely that PFASs are the only stressors affecting largemouth bass in the Twin Cities Metro Areas lakes. Indeed, Twin Lake is affected by the Joslyn superfund site which contains polycyclic aromatic hydrocarbons, pentachlorophenol, polychlorinated biphenyls, and dioxins. These compounds are also expected to drive the transcriptomics responses observed, but to what degree is difficult to ascertain at this time.
BibTeX:
@article{Colli-Dula2016,
  author = {Collí-Dulá, Reyna Cristina and Martyniuk, Christopher J. and Streets, Summer and Denslow, Nancy D. and Lehr, Randy},
  title = {Molecular impacts of perfluorinated chemicals (PFASs) in the liver and testis of male largemouth bass (Micropterus salmoides) in Minnesota Lakes},
  journal = {Comparative Biochemistry and Physiology Part D: Genomics and Proteomics},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S1744117X16300168}
}
Corydon, T.J., Mann, V., Slumstrup, L., Kopp, S., Sahana, J., Askou, A.L., Magnusson, N.E., Echegoyen, D., Bek, T., Sundaresan, A., Riwaldt, S., Bauer, J., Infanger, M. and Grimm, D. Reduced Expression of Cytoskeletal and Extracellular Matrix Genes in Human Adult Retinal Pigment Epithelium Cells Exposed to Simulated Microgravity. 2016 Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Vol. 40(1-2), pp. 1-17 
article DOI URL 
Abstract: BACKGROUND/AIMS Microgravity (µg) has adverse effects on the eye of humans in space. The risk of visual impairment is therefore one of the leading health concerns for NASA. The impact of µg on human adult retinal epithelium (ARPE-19) cells is unknown. METHODS In this study we investigated the influence of simulated µg (s-µg; 5 and 10 days (d)), using a Random Positioning Machine (RPM), on ARPE-19 cells. We performed phase-contrast/fluorescent microscopy, qRT-PCR, Western blotting and pathway analysis. RESULTS Following RPM-exposure a subset of ARPE-19 cells formed multicellular spheroids (MCS), whereas the majority of the cells remained adherent (AD). After 5d, alterations of F-actin and fibronectin were observed which reverted after 10d-exposure, suggesting a time-dependent adaptation to s-µg. Gene expression analysis of 12 genes involved in cell structure, shape, adhesion, migration, and angiogenesis suggested significant changes after a 10d-RPM-exposure. 11 genes were down-regulated in AD and MCS 10d-RPM-samples compared to 1g, whereas FLK1 was up-regulated in 5d- and 10d-RPM-MCS-samples. Similarly, TIMP1 was up-regulated in 5d-RPM-samples, whereas the remaining genes were down-regulated in 5d-RPM-samples. Western blotting revealed similar changes in VEGF, β-actin, laminin and fibronectin of 5d-RPM-samples compared to 10d, whereas different alterations of β-tubulin and vimentin were observed. The pathway analysis showed complementing effects of VEGF and integrin β-1. CONCLUSIONS These findings clearly show that s-µg induces significant alterations in the F-actin-cytoskeleton and cytoskeleton-related proteins of ARPE-19, in addition to changes in cell growth behavior and gene expression patterns involved in cell structure, growth, shape, migration, adhesion and angiogenesis.
BibTeX:
@article{Corydon2016,
  author = {Corydon, Thomas J and Mann, Vivek and Slumstrup, Lasse and Kopp, Sascha and Sahana, Jayashree and Askou, Anne Louise and Magnusson, Nils E and Echegoyen, David and Bek, Toke and Sundaresan, Alamelu and Riwaldt, Stefan and Bauer, Johann and Infanger, Manfred and Grimm, Daniela},
  title = {Reduced Expression of Cytoskeletal and Extracellular Matrix Genes in Human Adult Retinal Pigment Epithelium Cells Exposed to Simulated Microgravity.},
  journal = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology},
  publisher = {Karger Publishers},
  year = {2016},
  volume = {40},
  number = {1-2},
  pages = {1--17},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/27842307},
  doi = {http://doi.org/10.1159/000452520}
}
Devaux, S., Cizkova, D., Quanico, J., Franck, J., Nataf, S., Pays, L., Hauberg-Lotte, L., Maass, P., Kobarg, J.H., Kobeissy, F., Meriaux, C., Wisztorski, M., Slovinska, L., Blasko, J., Cigankova, V., Fournier, I. and Salzet, M. Proteomic analysis of the spatio-temporal based molecular kinetics of acute spinal cord injury identifies a time- and segment-specific window for effective tissue repair 2016 Molecular & Cellular Proteomics, pp. mcp.M115.057794  article DOI URL 
Abstract: Subnetwork enrichment pathway analyses and statistical testing The Elsevier's Pathway Studio
version 9.0 (Ariadne Genomics/Elsevier) was used to deduce relationships among differentially
expressed proteomics protein candidates using the Ariadne ResNetdatabase
BibTeX:
@article{Devaux2016,
  author = {Devaux, Stephanie and Cizkova, Dasa and Quanico, Jusal and Franck, Julien and Nataf, Serge and Pays, Laurent and Hauberg-Lotte, Lena and Maass, Peter and Kobarg, Jan H. and Kobeissy, Firas and Meriaux, Celine and Wisztorski, Maxence and Slovinska, Lucia and Blasko, Juraj and Cigankova, Viera and Fournier, Isabelle and Salzet, Michel},
  title = {Proteomic analysis of the spatio-temporal based molecular kinetics of acute spinal cord injury identifies a time- and segment-specific window for effective tissue repair},
  journal = {Molecular & Cellular Proteomics},
  year = {2016},
  pages = {mcp.M115.057794},
  url = {http://www.mcponline.org/lookup/doi/10.1074/mcp.M115.057794},
  doi = {http://doi.org/10.1074/mcp.M115.057794}
}
Dong, X., Ritter, M., Cao, H. and Yang, D. Literature Data Mining Based Enrichment Analysis Med One Literature Data Mining Based Enrichment Analysis on 1,925 for Lung Cancer 2016
Vol. 11(2) 
article DOI  
Abstract: Background: Approximately 8% of lung cancer is due to inherited factors, and the risk is more than doubled in those with relatives who have lung cancer. To date, numerous genetic studies reported a large group of genes that are related to lung cancer. However, a majority of the studies are focused on separate activities of genes that influence the development of the disease. Method: We conducted a literature data mining (LDM) of over 17,884 articles covering publications from 1978 to Feb. 2016. These articles reported multiple types of marker-disease associations between 1,925 genes and lung cancer. Then we conducted a gene set enrichment analysis (GSEA) and a sub-network enrichment analysis (SNEA) to study the functional profile and validate the pathogenic significance of these genes to lung cancer. Last, we performed a network connectivity analysis (NCA) to study the associations between the reported genes. Results: The reported genes demonstrate multiple types of association with lung cancer. Results from the enrichment analysis confirm the reports and suggest that these genes play significant roles in the pathogenesis of lung cancer, as well as in the pathogenesis of other lung cancer related disorders. Moreover, NCA results demonstrate that these genes, especially the ones with high RScores, present strong functional associations with each other. Conclusion: Our results suggest that the genetic causes of lung cancer are linked to a network composed of a large group of genes. LDM together with enrichment and network analysis could serve as an effective approach in finding these potential target genes.
BibTeX:
@article{Dong2016,
  author = {Dong, Xinming and Ritter, McKenzie and Cao, Hongbao and Yang, DeXiang},
  title = {Literature Data Mining Based Enrichment Analysis Med One Literature Data Mining Based Enrichment Analysis on 1,925 for Lung Cancer},
  year = {2016},
  volume = {11},
  number = {2},
  doi = {http://doi.org/10.20900/mo.20160006}
}
Ebrahimie, E., Moussavi-Nik, S.H., Newman, M., Van Der Hoek, M. and Lardelli, M. The Zebrafish Equivalent of Alzheimer's Disease-Associated PRESENILIN Isoform PS2V Regulates Inflammatory and Other Responses to Hypoxic Stress. 2016 Journal of Alzheimer's disease : JAD
Vol. Preprint(Preprint), pp. 1-28 
article DOI URL 
Abstract: Dominant mutations in the PRESENILIN genes PSEN1 and PSEN2 cause familial Alzheimer's disease (fAD) that usually shows onset before 65 years of age. In contrast, genetic variation at the PSEN1 and PSEN2 loci does not appear to contribute to risk for the sporadic, late onset form of the disease (sAD), leading to doubts that these genes play a role in the majority of AD cases. However, a truncated isoform of PSEN2, PS2V, is upregulated in sAD brains and is induced by hypoxia and high cholesterol intake. PS2V can increase γ-secretase activity and suppress the unfolded protein response (UPR), but detailed analysis of its function has been hindered by lack of a suitable, genetically manipulable animal model since mice and rats lack this PRESENILIN isoform. We recently showed that zebrafish possess an isoform, PS1IV, that is cognate to human PS2V. Using an antisense morpholino oligonucleotide, we can block specifically the induction of PS1IV that normally occurs under hypoxia. Here, we exploit this ability to identify gene regulatory networks that are modulated by PS1IV. When PS1IV is absent under hypoxia-like conditions, we observe changes in expression of genes controlling inflammation (particularly sAD-associated IL1B and CCR5), vascular development, the UPR, protein synthesis, calcium homeostasis, catecholamine biosynthesis, TOR signaling, and cell proliferation. Our results imply an important role for PS2V in sAD as a component of a pathological mechanism that includes hypoxia/oxidative stress and support investigation of the role of PS2V in other diseases, including schizophrenia, when these are implicated in the pathology.
BibTeX:
@article{Ebrahimie2016,
  author = {Ebrahimie, Esmaeil and Moussavi-Nik, Seyyed Hani and Newman, Morgan and Van Der Hoek, Mark and Lardelli, Michael},
  title = {The Zebrafish Equivalent of Alzheimer's Disease-Associated PRESENILIN Isoform PS2V Regulates Inflammatory and Other Responses to Hypoxic Stress.},
  journal = {Journal of Alzheimer's disease : JAD},
  publisher = {IOS Press},
  year = {2016},
  volume = {Preprint},
  number = {Preprint},
  pages = {1--28},
  url = {http://content.iospress.com/articles/journal-of-alzheimers-disease/jad150678},
  doi = {http://doi.org/10.3233/JAD-150678}
}
El Husseini, N., Schlisser, A.E. and Hales, B.F. Hydroxyurea Exposure Activates the P53 Signaling Pathway in Murine Organogenesis-Stage Embryos 2016 Toxicological Sciences, pp. kfw089  article URL 
Abstract: Hydroxyurea, an anticancer agent and potent teratogen, induces oxidative stress and activates a DNA damage response pathway in the gestation day (GD) 9 mouse embryo. To delineate the stress response pathways activated by this drug, we investigated the effect of hydroxyurea exposure on the transcriptome of GD 9 embryos. Timed pregnant CD-1 mice were treated with saline or hydroxyurea (400 mg/kg or 600 mg/kg) on GD 9; embryonic gene and protein expression were examined 3 h later. Microarray analysis revealed that the expression of 1346 probe sets changed significantly in embryos exposed to hydroxyurea compared to controls; the P53 signaling pathway was highly affected. In addition, P53 related family members, P63 and P73, were predicted to be activated and had common and unique downstream targets. Western blot analysis revealed that active phospho-P53 was significantly increased in drug-exposed embryos; confocal microscopy showed that the translocation of phospho-P53 to the nucleus was widespread in the embryo. Furthermore, qRT-PCR showed that the expression of P53-regulated genes (Cdkn1A, Fas, Trp53inp1) was significantly upregulated in hydroxyurea-exposed embryos; the concentration of the redox sensitive P53INP1 protein was also increased in a hydroxyurea dose-dependent fashion. Thus, hydroxyurea elicits a significant effect on the transcriptome of the organogenesis stage murine embryo, activating several key developmental signaling pathways related to DNA damage and oxidative stress. We propose that the P53 pathway plays a central role in the embryonic stress response and the developmental outcome after teratogen exposure.
BibTeX:
@article{ElHusseini2016,
  author = {El Husseini, Nazem and Schlisser, Ava E. and Hales, Barbara F.},
  title = {Hydroxyurea Exposure Activates the P53 Signaling Pathway in Murine Organogenesis-Stage Embryos},
  journal = {Toxicological Sciences},
  year = {2016},
  pages = {kfw089},
  url = {http://toxsci.oxfordjournals.org/content/early/2016/05/12/toxsci.kfw089.abstract}
}
Eric Leclerca, Keiichi Kimurab, Marie Shinoharab, Mathieu Danoya, c, Morgane Le Galld, Taketomo Kidoe, Atsushi Miyajimae, Teruo Fujiib, a, Yasuyuki Sakaib, a. Comparison of the transcriptomic profile of hepatic human induced pluripotent stem like cells cultured in plates and in a 3D microscale dynamic environment 2016   misc URL 
Abstract: We have compared the transcriptomic profiles of human induced pluripotent stem cells after their differentiation in hepatocytes like cells in plates and microfluidic biochips. The biochips provided a 3D and dynamic support during the cell differentiation when compared to the 2D static cultures in plates. The microarray have demonstrated the up regulation of important pathway related to liver development and maturation during the culture in biochips. Furthermore, the results of the transcriptomic profile, coupled with immunostaining, and RTqPCR analysis have shown typical biomarkers illustrating the presence of responders of biliary like cells, hepatocytes like cells, and endothelial like cells. However, the overall tissue still presented characteristic of immature and foetal patterns. Nevertheless, the biochip culture provided a specific micro-environment in which a complex multicellular differentiation toward liver could be oriented.
BibTeX:
@misc{EricLeclercaKeiichiKimurabMarieShinoharabMathieuDanoyacMorganeLeGalldTaketomoKidoeAtsushiMiyajimaeTeruoFujiibaYasuyukiSakaib2016,
  author = {Eric Leclerca, Keiichi Kimurab, Marie Shinoharab, Mathieu Danoya, c, Morgane Le Galld, Taketomo Kidoe, Atsushi Miyajimae, Teruo Fujiib, a, Yasuyuki Sakaib, a},
  title = {Comparison of the transcriptomic profile of hepatic human induced pluripotent stem like cells cultured in plates and in a 3D microscale dynamic environment},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S0888754316301288}
}
Esmaeili, F., Shiran, B., Fallahi, H., Mirakhorli, N., Budak, H. and Martínez-Gómez, P. In silico search and biological validation of microRNAs related to drought response in peach and almond. 2016 Functional & integrative genomics  article URL 
Abstract: Plant responses to drought stress are regulated at the transcriptional and post-transcriptional levels through noncoding endogenous microRNAs. These microRNAs play key roles in gene expression, mainly by down-regulating target mRNAs. In this work, an in silico search and validation for microRNAs related to drought response in peach ('G.H. Hill'), almond ('Sefied') and an interspecific peach-almond hybrid ('GN 15') has been performed. We used qPCR to analyse the gene expression of several miRNAs described as being related to drought response in peach, including miR156, miR159, miR160, miR167, miR171, miR172, miR398, miR403, miR408, miR842 and miR2275 under mild and severe water deficit. These miRNAs were in silico selected on the basis of previous works, their conservation in plants and their drought response. qPCR analysis confirmed the implication of these miRNAs in the dehydration stress response in the three assayed genotypes. Comparison of miRNA expression patterns in the three evaluated genotypes indicated that the hybrid GN 15 showed higher expression levels of specific miRNAs which should be related to the observed drought tolerance. mRNA target transcripts of the miRNAs studied were predicted using the Rose database, which includes transcription factors that regulate plant growth and development. In addition, results showed that the promoter region contains responsive elements to hormone-mediated regulatory elements. Network analysis not only unravelled the interaction between miRNAs and their predicted gene targets but also highlighted the roles of miRNAs in response to drought stress.
BibTeX:
@article{Esmaeili2016,
  author = {Esmaeili, Fazileh and Shiran, Behrouz and Fallahi, Hossein and Mirakhorli, Neda and Budak, Hikmet and Martínez-Gómez, Pedro},
  title = {In silico search and biological validation of microRNAs related to drought response in peach and almond.},
  journal = {Functional & integrative genomics},
  year = {2016},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/27068847}
}
Fan, F. and Manor, L.C. Genetic Network underlying Eating Disorder The Genetic Network underlying Eating Disorder and its Small Molecular Level Supports 2016 JPBS 2016
Vol. 12(4) 
article DOI  
Abstract: Background: It is believed that the genetic cause of complex diseases, such as Eating Disorder (ED), is linked to a large genetic network. In recent years, there has been an increased number of studies reporting dozens of genes associated with ED, posing an increased need of a systematically evaluation of the genetic markers underlying the disease. Methods: ED-Gene relation data were extracted from the ResNet Mammalian database, containing 69 ED candidate genes. Pathway Enrichment Analysis, Sub-Network Enrichment Analysis, Network Connectivity Analysis and Network Metrics Analysis were conducted to study network attributes and select the top genes for ED. Additionally, ED-Drug and Drug-Gene relation data were employed to study the ED-Gene relation at the small molecule level. Results: 66 out of 69 genes enriched 104 ED candidate pathways (p-values textless 1e-5), demonstrating strong gene-gene interactions. Metrics analysis suggest 6 genes worthy of further study for ED, including CHR, DRD2, AVP, OPRM1, IL6, and ESR2. Additionally, the majority of the ED candidate genes (64/69) demonstrated strong interaction with 46/55 ED effective drugs, providing support for the ED-gene relationships identified. Conclusion: Our results suggested that the genetic causes of ED were linked to a genetic network composed of a large group of genes. The gene network, together with the literature and enrichment metrics provided in this study, laid the groundwork for further biological/genetic studies in the field.
BibTeX:
@article{Fan2016,
  author = {Fan, Fengmei and Manor, Lydia C},
  title = {Genetic Network underlying Eating Disorder The Genetic Network underlying Eating Disorder and its Small Molecular Level Supports},
  journal = {JPBS 2016},
  year = {2016},
  volume = {12},
  number = {4},
  doi = {http://doi.org/10.20900/jpbs.20160016}
}
Feswick, A., Loughery, J.R., Isaacs, M.A., Munkittrick, K.R. and Martyniuk, C.J. Low-dose exposure to 17alpha-ethinylestradiol rapidly regulates molecular networks associated with gonad differentiation in the adult fathead minnow testes 2016 Aquatic Toxicology  article DOI  
Abstract: Intersex, or the presence of oocytes in the testes, has been documented in fish following exposure to wastewater effluent and estrogenic compounds. However, the molecular networks leading to the intersex condition are not completely characterized. To address this, we exposed male fathead minnows to a low, environmentally-relevant concentration of 17alpha-ethinylestradiol (EE2) (15ng/μl) and measured the transcriptome response in the testis after 96h to identify early molecular initiating events that may proceed the intersex condition. The short-term exposure to EE2 did not affect gonadosomatic index and proportion of gametes within the testes. However, the production of 11-ketotestosterone and testosterone from the testis in vitro was decreased relative to controls. Expression profiling using a 8×60K fathead minnow microarray identified 10 transcripts that were differentially expressed in the testes, the most dramatic change being that of coagulation factor XIII A chain (20-fold increase). Transcripts that included guanine nucleotide binding protein (Beta Polypeptide 2), peroxisome proliferator-activated receptor delta, and WNK lysine deficient protein kinase 1a, were down-regulated by EE2. Subnetwork enrichment analysis revealed that EE2 suppressed transcriptional networks associated with steroid metabolism, hormone biosynthesis, and sperm mobility. Most interesting was that gene networks associated with doublesex and mab-3 related transcription factor 1 (dmrt1) were suppressed in the adult testis, despite the fact that dmrt1 itself was not different in expression from control males. Cell processes involving forkhead box L2 (foxl2) (transcript involved in ovarian follicle development) were increased in expression in the testis. Noteworthy was that a gene network associated to granulosa cell development was increased over 100%, suggesting that this transcriptome network may be important for monitoring early estrogenic exposures. Other cell processes rapidly downregulated by EE2 at the transcript level included glucose homeostasis, response to heavy metal, amino acid catabolism, and the cyclooxygenase pathway. Conversely, lymphocyte chemotaxis, intermediate filament polymerization, glucocorticoid metabolism, carbohydrate utilization, and anterior/posterior axis specification were increased. These data provide new insight into the transcriptional responses that are perturbed prior to gonadal remodeling and intersex following exposure to estrogens. These data demonstrate that low concentrations of EE2 (1) rapidly suppresses male hormone production, (2) down-regulate molecular networks related to male sex differentiation, and (3) induce transcriptional networks related to granulosa cell development in the adult testis. These responses are hypothesized to be key molecular initiating events that occur prior to the development of the intersex phenotype following estrogenic exposures.
BibTeX:
@article{Feswick2016,
  author = {Feswick, April and Loughery, Jennifer R. and Isaacs, Meghan A. and Munkittrick, Kelly R. and Martyniuk, Christopher J.},
  title = {Low-dose exposure to 17alpha-ethinylestradiol rapidly regulates molecular networks associated with gonad differentiation in the adult fathead minnow testes},
  journal = {Aquatic Toxicology},
  year = {2016},
  doi = {http://doi.org/10.1016/j.aquatox.2016.10.021}
}
Gao, J.-R., Qin, X.-J., Jiang, H., Wang, T., Song, J.-M. and Xu, S.-Z. The effects of Qi Teng Xiao Zhuo granules, traditional Chinese medicine, on the expression of genes in chronic glomerulonephritis rats 2016 Journal of Ethnopharmacology  article DOI  
Abstract: Background and Aim: Chronic glomerulonephritis (CGN) is a primary glomerular disease that is related to immune-mediated inflammatory diseases. Qi Teng Xiao Zhuo granules have been proposed as a prescription of traditional Chinese medicine for treatment of CGN, but the comprehensive molecular mechanism underlying this therapeutic effect is not clear to date. The aim of this study was to evaluate and analyze the possible roles and molecular mechanisms of Qi Teng Xiao Zhuo granule-mediated treatment of CGN induced by adriamycin in rats. Methods: For gene expression analysis, four samples of glomerular tissue from rats in the Qi Teng Xiao Zhuo granule group and four samples each from the adriamycin treated and control groups were hybridized with Agilent Rat 4 × 44K whole genome microarrays. KEGG and Gene Ontology (GO) analyses and LIMMA, String and Cytoscape software were used to analyze the functional microarray data and screen differentially expressed genes. Hub genes were identified using Pathway Studio software. Real-time PCR was performed to verify the selected genes. Results: Microarray gene expression analysis showed that Pnoc, Cacfd1, Fos, Igll1, Lcn2, and Syk were among the most downregulated genes in the Qi Teng Xiao Zhuo granule group compared with the adriamycin treated group, whereas Cyp2c7, Hsd3b6, Acsm5, and Ugt2b15 were significantly upregulated. Functional analysis demonstrated that metabolism of xenobiotics by cytochrome P450, the B cell receptor signaling pathway, and cytokine-cytokine receptor interaction pathways were significantly downregulated in the Qi Teng Xiao Zhuo granule group and that GO terms related to positive regulation of immune response, immune response-activating signal transduction, cell differentiation, cell cycle, proliferation, and adhesion were significantly affected. Fos and Syk were considered to be potential hub genes. Conclusions: In the adriamycin-induced CGN rat model, comprehensive molecular mechanisms were involved with complex gene expression alterations containing many altered pathways and GO terms. However, how Qi Teng Xiao Zhuo granules regulate these events warrants further investigation.
BibTeX:
@article{Gao2016,
  author = {Gao, Jia-Rong and Qin, Xiu-Juan and Jiang, Hui and Wang, Ting and Song, Jun-Mei and Xu, Shuang-Zhi},
  title = {The effects of Qi Teng Xiao Zhuo granules, traditional Chinese medicine, on the expression of genes in chronic glomerulonephritis rats},
  journal = {Journal of Ethnopharmacology},
  year = {2016},
  doi = {http://doi.org/10.1016/j.jep.2016.08.011}
}
Gellén, B., Völgyi, K., Györffy, B.A., Balogh, B., Darula, Z., Éva, H.-G., Baracskay, P., Czurkó, A., Hernádi, I., Juhász, G., Dobolyi, Á. and Kékesi, K.A. Proteomic investigation of the prefrontal cortex in the rat clomipramine model of depression 2016 Journal of Proteomics  article DOI  
Abstract: Neonatal rodents chronically treated with the tricyclic antidepressant clomipramine show depression-like behavior, which persists throughout adulthood. Therefore, this animal model is suitable to investigate the pathomechanism of depression, which is still largely unknown at the molecular level beyond monoaminergic dysfunctions. Here, we describe protein level changes in the prefrontal cortex of neonatally clomipramine-treated adult rats correlating with behavioral abnormalities. Clomipramine was administered to rat pups twice daily between postnatal days 8–21, while controls received saline injections. Behavioral tests were performed on 3months old rats. The proteomic study was conducted using two-dimensional differential gel electrophoresis. We have identified 32 proteins by mass spectrometry analysis of the significantly altered protein spots. The changed proteins are related to several biological functions, such as inflammation, transcription, cell metabolism and cytoskeleton organization. Among the altered proteins, the level of macrophage migration inhibitory factor showed the largest alteration, which was confirmed with Western blot. Macrophage migration inhibitory factor showed widespread distribution and was predominantly expressed in astrocytes in the forebrain of rats which were described using immunohistochemistry. We conclude that neonatal clomipramine exposure induces sustained modification in the proteome, which may form the molecular basis of the observed depression-like behavior in adult rats.

BIOLOGICAL SIGNIFICANCE
It is known that some of the psychiatric disorders, such as autism, depression or schizophrenia may be at least in part, developmental disorders. We hypothesized that clomipramine treatment in early stage of brain development, which is known to induce depression-like behavior in adult rats, results in pathological distortion in neuronal and glial network development, which can be reflected by the cellular proteome in adulthood. Thus, we performed an unbiased proteomics experiment in adult rats, which were neonatally administered with clomipramine to reveal protein level changes three months after treatment. Many of the identified changed proteins are previously associated with depressive symptoms, e.g., the macrophage migration inhibitory factor (MIF), the level of which showed the largest alteration among the identified proteins. Based on our data, we suggest that neonatal clomipramine treatment is a reliable model to study the developmental effect of psychoactive drugs applied in the sensitive early phase of brain development. Furthermore, our findings support the idea that the alteration of early development of the brain induced by antidepressant treatment could result in sustained pathological changes in the cellular phenotype in the prefrontal cortex leading to depression-like behavioral symptoms.
BibTeX:
@article{Gellen2016,
  author = {Gellén, Barbara and Völgyi, Katalin and Györffy, Balázs András and Balogh, Boróka and Darula, Zsuzsa and Éva, Hunyadi-Gulyás and Baracskay, Péter and Czurkó, András and Hernádi, István and Juhász, Gábor and Dobolyi, Árpád and Kékesi, Katalin Adrienna},
  title = {Proteomic investigation of the prefrontal cortex in the rat clomipramine model of depression},
  journal = {Journal of Proteomics},
  year = {2016},
  doi = {http://doi.org/10.1016/j.jprot.2016.06.027}
}
Gholizadeh-Ghaleh Aziz, S., Pashaei-Asl, F., Fardyazar, Z., Pashaiasl, M., Csermely, P., Hódsági, J., Korcsmáros, T., Módos, D., Perez-Lopez, Á., Szalay, K., Ludlow, J., Buehrer, B., Stocum, D., Rossant, J., Thomson, J., Itskovitz-Eldor, J., Shapiro, S., Waknitz, M., Swiergiel, J., Marshall, V., Menasché, P., Vanneaux, V., Hagège, A., Bel, A., Cholley, B., Cacciapuoti, I., Wichterle, H., Jessell, T., Peljto, M., Reubinoff, B., Pera, M., Fong, C.-Y., Trounson, A., Bongso, A., Huskey, N., Guo, T., Evason, K., Momcilovic, O., Pardo, D., Creasman, K., Takahashi, K., Ichisaka, T., Yamanaka, S., Gritti, A., Bonfanti, L., Doetsch, F., Caille, I., Alvarez-Buylla, A., Lim, D., Gargett, C., Schwab, K., Zillwood, R., Nguyen, H., Wu, D., Beltrami, A., Barlucchi, L., Torella, D., Baker, M., Limana, F., Chimenti, S., Murrell, W., Féron, F., Wetzig, A., Cameron, N., Splatt, K., Bellette, B., Asahara, T., Murohara, T., Sullivan, A., Silver, M., van der Zee, R., Li, T., Almond, S., Lindley, R., Kenny, S., Connell, M., Edgar, D., Suetsugu, A., Nagaki, M., Aoki, H., Motohashi, T., Kunisada, T., Moriwaki, H., Polgar, K., Adany, R., Abel, G., Kappelmayer, J., Muszbek, L., Papp, Z., Priest, R., Marimuthu, K., Priest, J., Coppi, P.D., Bartsch, G., Siddiqui, M., Xu, T., Santos, C., Perin, L., Scherjon, S., der Keur, C.K.-v., Noort, W., Claas, F., Willemze, R., Fibbe, W., Tsai, M., Lee, J., Chang, Y., Hwang, S., R Prusa, A, Marton, E., Rosner, M., Bettelheim, D., Lubec, G., Pollack, A., Perin, L., Sedrakyan, S., Sacco, S.D., Filippo, R.D., Gosden, C., Hoehn, H., Salk, D., Li, C., Zhou, J., Shi, G., Ma, Y., Yang, Y., Gu, J., Bossolasco, P., Montemurro, T., Cova, L., Zangrossi, S., Calzarossa, C., Buiatiotis, S., Yuan, J., Reed, A., Chen, F., Jr, C.S., Phermthai, T., Odglun, Y., Julavijitphong, S., Titapant, V., Chuenwattana, P., Vantanasiri, C., Diecke, S., Lu, J., Lee, J., Termglinchan, V., Kooreman, N., Burridge, P., Pashaiasl, M., Khodadadi, K., Richings, N., Holland, M., Verma, P., Nikitin, A., Egorov, S., Daraselia, N., Mazo, I., Novichkova, S., Egorov, S., Daraselia, N., Subramanian, A., Tamayo, P., Mootha, V., Mukherjee, S., Ebert, B., Gillette, M., Ebrahimie, E., Moussavi-Nik, S., Newman, M., Hoek, M.V.D., Lardelli, M., Pashaiasl, M., Khodadadi, K., Kayvanjoo, A., Pashaei-asl, R., Ebrahimie, E., Ebrahimi, M., Alanazi, I., Ebrahimie, E., Alanazi, I., Ebrahimie, E., Hoffmann, P., Adelson, D., Ebrahimie, M., Esmaeili, F., Cheraghi, S., Houshmand, F., Shabani, L., Ebrahimie, E., Alisoltani, A., Fallahi, H., Ebrahimi, M., Ebrahimi, M., Ebrahimie, E., Hosseinpour, B., HajiHoseini, V., Kashfi, R., Ebrahimie, E., Hemmatzadeh, F., Ebrahimie, E., Nurollah, Z., Ebrahimi, M., Hemmatzadeh, F., Ignjatovic, J., Fruzangohar, M., Ebrahimie, E., Adelson, D., Fruzangohar, M., Ebrahimie, E., Ogunniyi, A., Mahdi, L., Paton, J., Adelson, D., Diarra, D., Stolina, M., Polzer, K., Zwerina, J., Ominsky, M., Dwyer, D., Wang, B.-E., Wang, X.-D., Ernst, J., Polakis, P., Gao, W.-Q., Hendy, G., D'Souza-Li, L., Yang, B., Canaff, L., Cole, D., Ruat, M., Molliver, M., Snowman, A., Snyder, S., Swiatek, P., Lindsell, C., Amo, F.D., Weinmaster, G., Gridley, T., Maki, R., Nicolaides, K., Brizot, M., Patel, F., Snijders, R., Underwood, M., Gilbert, W., Sherman, M., Loh, Y.-H., Wu, Q., Chew, J.-L., Vega, V., Zhang, W., Chen, X., Gholizadeh-Ghalehaziz, S., Farahzadi, R., Fathi, E., Pashaiasl, M., Klemmt, P., Vafaizadeh, V., Groner, B., Prusa, A., Marton, E., Rosner, M., Bernaschek, G., Hengstschläger, M., Fauza, D., Kaviani, A., Perry, T., Dzakovic, A., Jennings, R., Ziegler, M., Fauza, D., Pozzobon, M., Piccoli, M., Coppi, P.D., Roubelakis, M., Bitsika, V., Zagoura, D., Trohatou, O., Pappa, K., Makridakis, M., Sartore, S., Lenzi, M., Angelini, A., Chiavegato, A., Gasparotto, L., Coppi, P.D., Rossi, B., Merlo, B., Colleoni, S., Iacono, E., Tazzari, P., Ricci, F., You, Q., Cai, L., Zheng, J., Tong, X., Zhang, D., Zhang, Y., Hauser, P., Fazio, R.D., Bruno, S., Sdei, S., Grange, C., Bussolati, B., Martin, G., Perin, L., Sedrakyan, S., Sacco, S.D., Filippo, R.D., Evans, M., Kaufman, M., Ilancheran, S., Michalska, A., Peh, G., Wallace, E., Pera, M., Manuelpillai, U., Card, D.G., Hebbar, P., Li, L., Trotter, K., Komatsu, Y., Mishina, Y., Lee, Y., Ramakrishna, S., Chauhan, H., Park, W., Hong, S., Kim, K., Rosa, A., Brivanlou, A., Lin, S.-L., Chang, D., Lin, C.-H., Ying, S.-Y., Leu, D., Wu, D., Lin, S.-L., Chang, D., Chang-Lin, S., Lin, C.-H., Wu, D., Chen, D., Subramanyam, D., Lamouille, S., Judson, R., Liu, J., Bucay, N., Derynck, R., Turner, J., Williamson, R., Almefty, K., Nakaji, P., Porter, R., Tse, V., Bhatti, I., Lee, A., Lund, J., Larvin, M., Vidal, D., Marques, M., Lopes, L. and Reis, R. Isolation, Characterization, Cryopreservation of Human Amniotic Stem Cells and Differentiation to Osteogenic and Adipogenic Cells 2016 PLOS ONE
Vol. 11(7), pp. e0158281 
article DOI URL 
BibTeX:
@article{Gholizadeh-GhalehAziz2016,
  author = {Gholizadeh-Ghaleh Aziz, Shiva and Pashaei-Asl, Fatima and Fardyazar, Zahra and Pashaiasl, Maryam and Csermely, P and Hódsági, J and Korcsmáros, T and Módos, D and Perez-Lopez, ÁR and Szalay, K and Ludlow, J and Buehrer, B and Stocum, DL and Rossant, J and Thomson, JA and Itskovitz-Eldor, J and Shapiro, SS and Waknitz, MA and Swiergiel, JJ and Marshall, VS and Menasché, P and Vanneaux, V and Hagège, A and Bel, A and Cholley, B and Cacciapuoti, I and Wichterle, H and Jessell, TM and Peljto, M and Reubinoff, BE and Pera, MF and Fong, C-Y and Trounson, A and Bongso, A and Huskey, NE and Guo, T and Evason, KJ and Momcilovic, O and Pardo, D and Creasman, KJ and Takahashi, K and Ichisaka, T and Yamanaka, S and Gritti, A and Bonfanti, L and Doetsch, F and Caille, I and Alvarez-Buylla, A and Lim, DA and Gargett, CE and Schwab, KE and Zillwood, RM and Nguyen, HP and Wu, D and Beltrami, AP and Barlucchi, L and Torella, D and Baker, M and Limana, F and Chimenti, S and Murrell, W and Féron, F and Wetzig, A and Cameron, N and Splatt, K and Bellette, B and Asahara, T and Murohara, T and Sullivan, A and Silver, M and van der Zee, R and Li, T and Almond, S and Lindley, RM and Kenny, SE and Connell, MG and Edgar, DH and Suetsugu, A and Nagaki, M and Aoki, H and Motohashi, T and Kunisada, T and Moriwaki, H and Polgar, K and Adany, R and Abel, G and Kappelmayer, J and Muszbek, L and Papp, Z and Priest, R and Marimuthu, K and Priest, J and Coppi, P De and Bartsch, G and Siddiqui, MM and Xu, T and Santos, CC and Perin, L and Scherjon, SA and der Keur, C Kleijburg-van and Noort, WA and Claas, FH and Willemze, R and Fibbe, WE and Tsai, MS and Lee, JL and Chang, YJ and Hwang, SM and A-, R Prusa and Marton, E and Rosner, M and Bettelheim, D and Lubec, G and Pollack, A and Perin, L and Sedrakyan, S and Sacco, S Da and Filippo, R De and Gosden, CM and Hoehn, H and Salk, D and Li, C and Zhou, J and Shi, G and Ma, Y and Yang, Y and Gu, J and Bossolasco, P and Montemurro, T and Cova, L and Zangrossi, S and Calzarossa, C and Buiatiotis, S and Yuan, JS and Reed, A and Chen, F and Jr, CN Stewart and Phermthai, T and Odglun, Y and Julavijitphong, S and Titapant, V and Chuenwattana, P and Vantanasiri, C and Diecke, S and Lu, J and Lee, J and Termglinchan, V and Kooreman, NG and Burridge, PW and Pashaiasl, M and Khodadadi, K and Richings, NM and Holland, MK and Verma, PJ and Nikitin, A and Egorov, S and Daraselia, N and Mazo, I and Novichkova, S and Egorov, S and Daraselia, N and Subramanian, A and Tamayo, P and Mootha, VK and Mukherjee, S and Ebert, BL and Gillette, MA and Ebrahimie, E and Moussavi-Nik, SH and Newman, M and Hoek, M Van Der and Lardelli, M and Pashaiasl, M and Khodadadi, K and Kayvanjoo, AH and Pashaei-asl, R and Ebrahimie, E and Ebrahimi, M and Alanazi, IO and Ebrahimie, E and Alanazi, I and Ebrahimie, E and Hoffmann, P and Adelson, DL and Ebrahimie, M and Esmaeili, F and Cheraghi, S and Houshmand, F and Shabani, L and Ebrahimie, E and Alisoltani, A and Fallahi, H and Ebrahimi, M and Ebrahimi, M and Ebrahimie, E and Hosseinpour, B and HajiHoseini, V and Kashfi, R and Ebrahimie, E and Hemmatzadeh, F and Ebrahimie, E and Nurollah, Z and Ebrahimi, M and Hemmatzadeh, F and Ignjatovic, J and Fruzangohar, M and Ebrahimie, E and Adelson, DL and Fruzangohar, M and Ebrahimie, E and Ogunniyi, AD and Mahdi, LK and Paton, JC and Adelson, DL and Diarra, D and Stolina, M and Polzer, K and Zwerina, J and Ominsky, MS and Dwyer, D and Wang, B-E and Wang, X-D and Ernst, JA and Polakis, P and Gao, W-Q and Hendy, GN and D'Souza-Li, L and Yang, B and Canaff, L and Cole, DE and Ruat, M and Molliver, ME and Snowman, AM and Snyder, SH and Swiatek, PJ and Lindsell, CE and Amo, FF Del and Weinmaster, G and Gridley, T and Maki, RG and Nicolaides, K and Brizot, M and Patel, F and Snijders, R and Underwood, MA and Gilbert, WM and Sherman, MP and Loh, Y-H and Wu, Q and Chew, J-L and Vega, VB and Zhang, W and Chen, X and Gholizadeh-Ghalehaziz, S and Farahzadi, R and Fathi, E and Pashaiasl, M and Klemmt, PA and Vafaizadeh, V and Groner, B and Prusa, AR and Marton, E and Rosner, M and Bernaschek, G and Hengstschläger, M and Fauza, D and Kaviani, A and Perry, TE and Dzakovic, A and Jennings, RW and Ziegler, MM and Fauza, DO and Pozzobon, M and Piccoli, M and Coppi, P De and Roubelakis, MG and Bitsika, V and Zagoura, D and Trohatou, O and Pappa, KI and Makridakis, M and Sartore, S and Lenzi, M and Angelini, A and Chiavegato, A and Gasparotto, L and Coppi, P De and Rossi, B and Merlo, B and Colleoni, S and Iacono, E and Tazzari, P and Ricci, F and You, Q and Cai, L and Zheng, J and Tong, X and Zhang, D and Zhang, Y and Hauser, PV and Fazio, R De and Bruno, S and Sdei, S and Grange, C and Bussolati, B and Martin, GR and Perin, L and Sedrakyan, S and Sacco, S Da and Filippo, R De and Evans, MJ and Kaufman, MH and Ilancheran, S and Michalska, A and Peh, G and Wallace, EM and Pera, M and Manuelpillai, U and Card, DA Greer and Hebbar, PB and Li, L and Trotter, KW and Komatsu, Y and Mishina, Y and Lee, YJ and Ramakrishna, S and Chauhan, H and Park, WS and Hong, SH and Kim, KS and Rosa, A and Brivanlou, AH and Lin, S-L and Chang, DC and Lin, C-H and Ying, S-Y and Leu, D and Wu, DT and Lin, S-L and Chang, DC and Chang-Lin, S and Lin, C-H and Wu, DT and Chen, DT and Subramanyam, D and Lamouille, S and Judson, RL and Liu, JY and Bucay, N and Derynck, R and Turner, JD and Williamson, R and Almefty, KK and Nakaji, P and Porter, R and Tse, V and Bhatti, I and Lee, A and Lund, J and Larvin, M and Vidal, DO and Marques, MMC and Lopes, LF and Reis, RM},
  title = {Isolation, Characterization, Cryopreservation of Human Amniotic Stem Cells and Differentiation to Osteogenic and Adipogenic Cells},
  journal = {PLOS ONE},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {7},
  pages = {e0158281},
  url = {http://dx.plos.org/10.1371/journal.pone.0158281},
  doi = {http://doi.org/10.1371/journal.pone.0158281}
}
Grabiec, K., Majewska, A., Wicik, Z., Milewska, M., Błaszczyk, M. and Grzelkowska-Kowalczyk, K. The effect of palmitate supplementation on gene expression profile in proliferating myoblasts. 2016 Cell biology and toxicology  article URL 
Abstract: High-fat diet, exposure to saturated fatty acids, or the presence of adipocytes in myoblast microenvironment affects skeletal muscle growth and function. The aim of the present study was to investigate the effect of palmitate supplementation on transcriptomic profile of mouse C2C12 myoblasts. Global gene expression was evaluated using whole mouse genome oligonucleotide microarrays, and the results were validated through qPCR. A total of 4047 genes were identified as differentially expressed, including 3492 downregulated and 555 upregulated genes, during a 48-h exposure to palmitate (0.1 mmol/l). Functional classification showed the involvement of these genes in several processes which regulate cell growth. In conclusion, the addition of palmitate modifies the expression of genes associated with (1) myoblast responsiveness to hormones and growth factors, (2) cytokine and growth factor expression, and (3) regulation of cell-cell and cell-matrix communication. Such alterations can affect myoblast growth and differentiation; however, further studies in this field are required.
BibTeX:
@article{Grabiec2016,
  author = {Grabiec, K and Majewska, A and Wicik, Z and Milewska, M and Błaszczyk, M and Grzelkowska-Kowalczyk, K},
  title = {The effect of palmitate supplementation on gene expression profile in proliferating myoblasts.},
  journal = {Cell biology and toxicology},
  year = {2016},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/27114085}
}
Haustead, D.J., Stevenson, A., Saxena, V., Marriage, F., Firth, M., Silla, R., Martin, L., Adcroft, K.F., Rea, S., Day, P.J., Melton, P., Wood, F.M. and Fear, M.W. Transcriptome analysis of human ageing in male skin shows mid-life period of variability and central role of NF-κB. 2016 Scientific reports
Vol. 6, pp. 26846 
article URL 
Abstract: Age is well-known to be a significant factor in both disease pathology and response to treatment, yet the molecular changes that occur with age in humans remain ill-defined. Here, using transcriptome profiling of healthy human male skin, we demonstrate that there is a period of significantly elevated, transcriptome-wide expression changes occurring predominantly in middle age. Both pre and post this period, the transcriptome appears to undergo much smaller, linear changes with increasing age. Functional analysis of the transient changes in middle age suggest a period of heightened metabolic activity and cellular damage associated with NF-kappa-B and TNF signaling pathways. Through meta-analysis we also show the presence of global, tissue independent linear transcriptome changes with age which appear to be regulated by NF-kappa-B. These results suggest that aging in human skin is associated with a critical mid-life period with widespread transcriptome changes, both preceded and proceeded by a relatively steady rate of linear change in the transcriptome. The data provides insight into molecular changes associated with normal aging and will help to better understand the increasingly important pathological changes associated with aging.
BibTeX:
@article{Haustead2016,
  author = {Haustead, Daniel J and Stevenson, Andrew and Saxena, Vishal and Marriage, Fiona and Firth, Martin and Silla, Robyn and Martin, Lisa and Adcroft, Katharine F and Rea, Suzanne and Day, Philip J and Melton, Phillip and Wood, Fiona M and Fear, Mark W},
  title = {Transcriptome analysis of human ageing in male skin shows mid-life period of variability and central role of NF-κB.},
  journal = {Scientific reports},
  publisher = {Nature Publishing Group},
  year = {2016},
  volume = {6},
  pages = {26846},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4882522&tool=pmcentrez&rendertype=abstract http://www.nature.com/srep/2016/160527/srep26846/full/srep26846.html}
}
Ishido, M., Suzuki, J. and Masuo, Y. Neonatal rotenone lesions cause onset of hyperactivity during juvenile and adulthood in the rat. 2016 Toxicology Letters  article DOI  
Abstract: Attention deficit hyperactivity disorder (ADHD) is characterized by behavioral and cognitive symptoms. Longitudinal studies demonstrated that the symptoms remains clinically significant for the majority of ADHD children into adulthood. Furthermore, a population-based birth cohort provided the initial evidence of adult ADHD that lacks a history of childhood ADHD. We previously demonstrated that neonatal exposure to bisphenol A, an environmental chemical caused hyperactivity in the juvenile. Here, we extend to examine other chemical such as rotenone, a dopaminergic toxins. Oral administration of rotenone (3mg/kg) into 5-day-old male Wistar rats significantly caused hyperactivity at adulthood (8∼11 weeks old; ptextless0.05). It was about 1.3∼1.4-fold more active in the nocturnal phase after administration of rotenone than control rats. Higher dose (16mg/kg) or repeated lower dose of rotenone (1mg/kg/day for 4 days) caused hyperactivity in the juvenile. Furthermore, DNA array analyses showed that neonatal exposure to rotenone altered the levels of gene expression of several molecules related to apoptosis/cell cycle, ATPase, skeletal molecule, and glioma. Bivariate normal distribution analysis indicates no correlation in gene expression between a hyperactivity disorder model and a Parkinson's disease model by rotenone. Thus, we demonstrate a rotenone models of ADHD whose onset varies during juvenile and adulthood.
BibTeX:
@article{Ishido2016,
  author = {Ishido, Masami and Suzuki, Junko and Masuo, Yoshinori},
  title = {Neonatal rotenone lesions cause onset of hyperactivity during juvenile and adulthood in the rat.},
  journal = {Toxicology Letters},
  year = {2016},
  doi = {http://doi.org/10.1016/j.toxlet.2016.12.008}
}
Jaber, Z., Aouad, P., Al Medawar, M., Bahmad, H., Abou-Abbass, H., Ghandour, H., Mondello, S. and Kobeissy, F. Role of Systems Biology in Brain Injury Biomarker Discovery: Neuroproteomics Application 2016 , pp. 157-174  incollection DOI URL 
Abstract: tudies conducted by Kobeissy et al. used Pathway Studio to construct a functional
interaction map linking 59 proteins significantly increased or decreased post-TBI
[4, 34].
BibTeX:
@incollection{Jaber2016,
  author = {Jaber, Zaynab and Aouad, Patrick and Al Medawar, Mohamad and Bahmad, Hisham and Abou-Abbass, Hussein and Ghandour, Hiba and Mondello, Stefania and Kobeissy, Firas},
  title = {Role of Systems Biology in Brain Injury Biomarker Discovery: Neuroproteomics Application},
  year = {2016},
  pages = {157--174},
  url = {http://link.springer.com/10.1007/978-1-4939-3816-210},
  doi = {http://doi.org/10.1007/978-1-4939-3816-2_10}
}
Jaber, Z., Aouad, P., Al Medawar, M., Bahmad, H., Abou-Abbass, H. and Kobeissy, F. Application of Systems Biology to Neuroproteomics: The Path to Enhanced Theranostics in Traumatic Brain Injury 2016 , pp. 139-155  incollection DOI URL 
Abstract: It is now possible to generate visual presentations of network models by incorporating genome,
proteome, and metabolome data through such bioinformatics software as Pathway Studio (Ariadne,
Rockville, MD)
BibTeX:
@incollection{Jaber2016a,
  author = {Jaber, Zaynab and Aouad, Patrick and Al Medawar, Mohamad and Bahmad, Hisham and Abou-Abbass, Hussein and Kobeissy, Firas},
  title = {Application of Systems Biology to Neuroproteomics: The Path to Enhanced Theranostics in Traumatic Brain Injury},
  year = {2016},
  pages = {139--155},
  url = {http://link.springer.com/10.1007/978-1-4939-3816-29},
  doi = {http://doi.org/10.1007/978-1-4939-3816-2_9}
}
Januchowski, R., Wojtowicz, K., Sterzyʼnska, K., Sosiʼnska, P., Andrzejewska, M., Zawierucha, P., Nowicki, M. and Zabel, M. Inhibition of ALDH1A1 activity decreases expression of drug transporters and reduces chemotherapy resistance in ovarian cancer cell lines. 2016 The International Journal of Biochemistry & Cell Biology  article DOI  
Abstract: The high mortality of ovarian cancer patients results from the failure of treatment caused by the inherent or acquired chemotherapy drug resistance. It was reported that overexpression of aldehyde dehydrogenase A1 (ALDH1A1) in cancer cells can be responsible for the development of drug resistance. To add the high expression of the drug transporter proteins the ALDHA1 is considered as a molecular target in cancer therapy. Therefore, we analysed drug-resistant ovarian cancer cell lines according to ALDHA1 expression and the association with drug resistance. The expression of ALDH1A1, P-glycoprotein (P-gp) or breast cancer resistance protein (BCRP) was determined using a microarray and confirmed by Q-PCR, western blot and fluorescence analysis. ALDH1A1 activity was determined using an Aldefluor assay. The impact of all-trans retinoic acid (ATRA) and diethylaminobenzaldehyde (DEAB) on chemotherapy resistance was assessed by the MTT chemosensitivity assay. The most abundant expression of ALDH1A1 was noted in paclitaxel- and topotecan-resistant cell lines where two populations of ALDH-positive and ALDH-negative cells could be observed. Those cell lines also revealed the overexpression of P-gp and BCRP respectively, and were able to form spheres in non-adherent conditions. Pre-treatment with ATRA and DEAB reduced chemotherapy resistance in both cell lines. ATRA treatment led to downregulation of the ALDH1A1, P-gp and BCRP proteins. DEAB treatment led to downregulation of the P-gp protein and BCRP transcript and protein. Our results indicate that ALDH1A1-positive cancer cells can be responsible for drug resistance development in ovarian cancer. Developing more specific ALDH1A1 inhibitors can increase chemotherapy effectiveness in ovarian cancer.
BibTeX:
@article{Januchowski2016,
  author = {Januchowski, Radosław and Wojtowicz, Karolina and Sterzyʼnska, Karolina and Sosiʼnska, Patrycja and Andrzejewska, Małgorzata and Zawierucha, Piotr and Nowicki, Michał and Zabel, Maciej},
  title = {Inhibition of ALDH1A1 activity decreases expression of drug transporters and reduces chemotherapy resistance in ovarian cancer cell lines.},
  journal = {The International Journal of Biochemistry & Cell Biology},
  year = {2016},
  doi = {http://doi.org/10.1016/j.biocel.2016.07.017}
}
Jeong, Y.-D., Cho, E.S., Woo, J.-S. and Sa, S.J. Low birth weight can be influencing reproductive functions in piglets 2016 , pp. 54-54  misc  
Abstract: Swine industry has been focusing selection of excellent breeding pigs for post decades. This result is created to superior breeding sows with larger litter size, which are leads to low birth weight piglets (LBW) because of intrauterine growth retardation. The LBW on development of pigs have well known to postpone growth performance and to disrupt body metabolisms than normal birth weight piglets (NBW). However, effect of LBW on reproductive functions is very not documented. Therefore, this study was conducted to identify effect of birth weight on reproductive function in the LBW compared with normal birth weight piglets (NBW) by RNA sequencing and pathway studio. The experimental animals utilized 3d old LBW (0.96±95.07 kg, n=4) and NBW (1.69±83.39 kg, n=4). The differentially expressed genes were approximately 800 genes above 2 fold. The genes were related to steroid hormone synthesis, estrogen receptors signaling and growth and proliferation of cells. These results may be suggested to affect development of reproductive organ. However, our data are restricted using young experimental animals.
BibTeX:
@misc{Jeong2016,
  author = {Jeong, Yong-Dae and Cho, Eun Seok and Woo, Jae-Seok and Sa, Soo Jin},
  title = {Low birth weight can be influencing reproductive functions in piglets},
  year = {2016},
  pages = {54--54}
}
Jiefeng Liao, Chris Cheadle, Hongbao Cao, V.R. Qingres-An academic Publisher 2016 Journal of Psychiatry and Brain Science
Vol. 1(3) 
article DOI URL 
Abstract: Background:It is believed that the genetic cause of complex diseases, such as anxiety, is linked to a large genetic network. In recent years, there has been an increased number of studies reporting hundreds of genes associated with anxiety, posing the necessity of systematically study of the genetic network underlying the disease.
Methods:Anxiety-Gene relation data were extracted from the ResNet 11 Mammalian database, containing 592 anxiety candidate genes (nodes). Pathway enrichment analysis, Sub-Network Enrichment Analysis, Network Connectivity Analysis and Network Metrics Analysis were conducted to study network attributes and select the top nodes (genes). Additionally, Anxiety-Drug and Drug-Gene relation data were employed to study the Anxiety-Gene relation at the small molecule level.
Results:526 out of 592 genes enriched 100 anxiety candidate pathways (ptextless 1e-15), demonstrating strong gene-gene interactions. Metrics analysis revealed 6 genes, DRD2, ADORA2A, IL1B, CRH, AVP, CRHR1, as top candidates for anxiety, in terms of replication frequency, network centrality and functional diversity. Additionally, the majority of the anxiety candidate genes (538/592) demonstrated strong interaction with 548/618 anxiety effective drugs, supporting the identified anxiety-gene relationship.
Conclusion:Our results suggested that the genetic causes of anxiety were linked to a genetic network composed of a large group of genes. The gene network, together with the literature and enrichment metrics provided in this study, laid the groundwork for further biological/genetic studies in the field.
BibTeX:
@article{JiefengLiaoChrisCheadleHongbaoCao2016,
  author = {Jiefeng Liao, Chris Cheadle, Hongbao Cao, Vindhya Rao},
  title = {Qingres-An academic Publisher},
  journal = {Journal of Psychiatry and Brain Science},
  year = {2016},
  volume = {1},
  number = {3},
  url = {http://jpbs.qingres.com/htmls/JPBS849Detail.html},
  doi = {http://doi.org/10.20900/jpbs.20160013}
}
Jufvas, Å., Rajan, M.R., Jönsson, C., Strålfors, P. and Turkina, M. Scaffolding Protein IQGAP1 - an Insulin-dependent Link between Caveolae and the Cytoskeleton in Primary Human Adipocytes? 2016 The Biochemical journal, pp. BCJ20160581  article DOI URL 
Abstract: The ubiquitously expressed IQ motif-containing GTPase activating protein-1 (IQGAP1) is a scaffolding protein implicated in an array of cellular functions, in particular by binding to cytoskeletal elements and signaling proteins. A role for IQGAP1 in adipocytes has not been reported. We therefore investigated the cellular IQGAP1 interactome in primary human adipocytes. Immunoprecipitation and quantitative mass spectrometry identified caveolae and caveolae-associated proteins as the major IQGAP1 interactors alongside cytoskeletal proteins. We confirmed colocalization of IQGAP1 with the defining caveolar marker protein caveolin-1 by confocal microscopy and proximity ligation assay. Most interestingly, insulin enhanced the number of IQGAP1 interactions with caveolin-1 by 5-fold. Moreover, we found significantly reduced abundance of IQGAP1 in adipocytes from patients with type 2 diabetes compared with cells from non-diabetic control subjects. Both the abundance of IQGAP1 protein and mRNA were reduced, indicating a transcriptional defect in diabetes. Our findings suggest a novel role for IQGAP1 in insulin-regulated interaction between caveolae and cytoskeletal elements of the adipocyte, and that this is quelled in the diabetic state.
BibTeX:
@article{Jufvas2016,
  author = {Jufvas, Åsa and Rajan, Meenu Rohini and Jönsson, Cecilia and Strålfors, Peter and Turkina, Maria},
  title = {Scaffolding Protein IQGAP1 - an Insulin-dependent Link between Caveolae and the Cytoskeleton in Primary Human Adipocytes?},
  journal = {The Biochemical journal},
  publisher = {Portland Press Limited},
  year = {2016},
  pages = {BCJ20160581},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/27458251},
  doi = {http://doi.org/10.1042/BCJ20160581}
}
Kim, I., Lee, S.H., Jeong, J., Park, J.H., Yoo, M.A. and Kim, C.M. Functional Profiling of Human MeCP2 by Automated Data Comparison Analysis and Computerized Expression Pathway Modeling. 2016 Healthcare informatics research
Vol. 22(2), pp. 120-8 
article URL 
Abstract: OBJECTIVES: Methyl-CpG binding protein 2 (MeCP2) is a ubiquitous epigenetic factor that represses gene expression by modifying chromatin. Mutations in the MeCP2 gene cause Rett syndrome, a progressive neurodevelopmental disorder. Recent studies also have shown that MeCP2 plays a role in carcinogenesis. Specifically, functional ablation of MeCP2 suppresses cell growth and leads to the proliferation of cancer cells. However, MeCP2's function in adult tissues remains poorly understood. We utilized a weight matrix-based comparison software to identify transcription factor binding site (TFBS) of MeCP2-regulated genes, which were recognized by cDNA microarray analysis. METHODS: MeCP2 expression was silenced using annealed siRNA in HEK293 cells, and then a cDNA microarray analysis was performed. Functional analysis was carried out, and transcriptional levels in target genes regulated by MeCP2 were investigated. TFBS analysis was done within genes selected by the cDNA microarray analysis, using a weight matrix-based program and the TRANSFAC 6.0 database. RESULTS: Among the differentially expressed genes with a change in expression greater than two-fold, 189 genes were up-regulated and 91 genes were down-regulated. Genes related to apoptosis and cell proliferation (JUN, FOSL2, CYR61, SKIL, ATF3, BMABI, BMPR2, RERE, and FALZ) were highly up-regulated. Genes with anti-apoptotic and anti-proliferative functions (HNRPA0, HIS1, and FOXC1) were down-regulated. Using TFBS analysis within putative promoters of novel candidate target genes of MeCP2, disease-related transcription factors were identified. CONCLUSIONS: The present results provide insights into the new target genes regulated by MeCP2 under epigenetic control. This information will be valuable for further studies aimed at clarifying the pathogenesis of Rett syndrome and neoplastic diseases.
BibTeX:
@article{Kim2016,
  author = {Kim, Injoo and Lee, Shin Hae and Jeong, Jinwoo and Park, Jun Hyung and Yoo, Mi Ae and Kim, Cheol Min},
  title = {Functional Profiling of Human MeCP2 by Automated Data Comparison Analysis and Computerized Expression Pathway Modeling.},
  journal = {Healthcare informatics research},
  year = {2016},
  volume = {22},
  number = {2},
  pages = {120--8},
  url = {http://synapse.koreamed.org/search.php?where=aview&id=10.4258/hir.2016.22.2.120&code=1088HIR&vmode=FULL}
}
Kim, H.J., Kim, S.Y., Kwon, J.Y., Kim, Y.J., Hun Kang, S., Jang, W.-H., Lee, J.H., Seo, M.-W., Song, J.-J., Seo, Y.R. and Park, M.K. Identification of Potential Novel Biomarkers and Signaling Pathways Related to Otitis Media Induced by Diesel Exhaust Particles Using Transcriptomic Analysis in an In Vivo System 2016 PLOS ONE
Vol. 11(11), pp. e0166044 
article DOI URL 
BibTeX:
@article{Kim2016a,
  author = {Kim, Hyo Jeong and Kim, So Young and Kwon, Jee Young and Kim, Yeo Jin and Hun Kang, Seung and Jang, Won-Hee and Lee, Jun Ho and Seo, Myung-Whan and Song, Jae-Jun and Seo, Young Rok and Park, Moo Kyun},
  title = {Identification of Potential Novel Biomarkers and Signaling Pathways Related to Otitis Media Induced by Diesel Exhaust Particles Using Transcriptomic Analysis in an In Vivo System},
  journal = {PLOS ONE},
  year = {2016},
  volume = {11},
  number = {11},
  pages = {e0166044},
  url = {http://dx.plos.org/10.1371/journal.pone.0166044},
  doi = {http://doi.org/10.1371/journal.pone.0166044}
}
Kim, J.-h., Kwon, D.-n., Lee, K. and Prather, R.S. INTERLEUKIN 2 RECEPTOR GAMMA GENE TARGETING VECTOR, PRODUCTION OF IMMUNE CELL-DEFICIENT TRANSGENIC CLONED MINI PIG HAVING VECTOR INTRODUCED THEREIN, PREPARATION METHOD THEREFOR AND USE THEREOF 2016   article  
BibTeX:
@article{Kim2016b,
  author = {Kim, Jin-hoi and Kwon, Deug-nam and Lee, Kiho and Prather, Randall S.},
  title = {INTERLEUKIN 2 RECEPTOR GAMMA GENE TARGETING VECTOR, PRODUCTION OF IMMUNE CELL-DEFICIENT TRANSGENIC CLONED MINI PIG HAVING VECTOR INTRODUCED THEREIN, PREPARATION METHOD THEREFOR AND USE THEREOF},
  year = {2016}
}
Kim, N., Jeong, Y.-M., Jeong, S., Kim, G.-B., Baek, S., Kwon, Y.-E., Cho, A., Choi, S.-B., Kim, J., Lim, W.-J., Kim, K.H., Park, W., Kim, J.-Y., Kim, J.-H., Yim, B., Lee, Y.J., Chun, B.-M., Lee, Y.-P., Park, B.-S., Yu, H.-J. and Mun, J.-H. Identification of candidate domestication regions in the radish genome based on high-depth resequencing analysis of 17 genotypes 2016 Theoretical and Applied Genetics, pp. 1-18  article DOI URL 
BibTeX:
@article{Kim2016c,
  author = {Kim, Namshin and Jeong, Young-Min and Jeong, Seongmun and Kim, Goon-Bo and Baek, Seunghoon and Kwon, Young-Eun and Cho, Ara and Choi, Sang-Bong and Kim, Jiwoong and Lim, Won-Jun and Kim, Kyoung Hyoun and Park, Won and Kim, Jae-Yoon and Kim, Jin-Hyun and Yim, Bomi and Lee, Young Joon and Chun, Byung-Moon and Lee, Young-Pyo and Park, Beom-Seok and Yu, Hee-Ju and Mun, Jeong-Hwan},
  title = {Identification of candidate domestication regions in the radish genome based on high-depth resequencing analysis of 17 genotypes},
  journal = {Theoretical and Applied Genetics},
  publisher = {Springer Berlin Heidelberg},
  year = {2016},
  pages = {1--18},
  url = {http://link.springer.com/10.1007/s00122-016-2741-z},
  doi = {http://doi.org/10.1007/s00122-016-2741-z}
}
Klimov, E., Kondratieva, N., Skorobogatykh, K., Azimova, J., Sergeev, A., Kokaeva, Z., Naumova, E., Rachin, A., Tabeeva, G. and Nathaniel, T.I. The Polymorphism of Regulatory Region of NOS3 Gene (rs2070744, Genotype CC) Protect Patients from Chronic Migraine 2016 British Journal of Medicine & Medical Research Texas Institute of Rehabilitation Research India. Original Research Article Klimov et al
Vol. 16(1610), pp. 1-7 
article DOI URL 
Abstract: Aims: There is evidence that endothelial nitric oxide synthase has a role in migraine pathophysiology. In our research, the role of SNP rs2070744 (c.-813CtextgreaterT) in promoter region of NOS3 gene in the episodic and chronic forms of migraine is considered. Methodology: The study included 138 patients with migraine (44 with chronic and 96 with episodic migraine). The control group included 348 unexamined subjects. Genotypes were determined using real-time PCR with allelic discrimination test. Statistical processing was performed using Fisher test and Pearson's chi-squared test. Results: Our study evaluated the link of CC genotype of rs2070744 with migraine (Fisher's p=0.026) and episodic migraine (Fisher's p=0.022). Conclusion: Genotype CC of SNP rs2070744 in the regulatory region of NOS3 gene is more specific for episodic migraine and may prevents the chronification of migraine.
BibTeX:
@article{Klimov2016,
  author = {Klimov, Eugene and Kondratieva, Natalia and Skorobogatykh, Kirill and Azimova, Julia and Sergeev, Alexey and Kokaeva, Zarema and Naumova, Elena and Rachin, Andrey and Tabeeva, Gyuzyal and Nathaniel, Thomas I},
  title = {The Polymorphism of Regulatory Region of NOS3 Gene (rs2070744, Genotype CC) Protect Patients from Chronic Migraine},
  journal = {British Journal of Medicine & Medical Research Texas Institute of Rehabilitation Research India. Original Research Article Klimov et al},
  publisher = {Robert Perna},
  year = {2016},
  volume = {16},
  number = {1610},
  pages = {1--7},
  url = {www.sciencedomain.org http://sciencedomain.org/review-history/15326},
  doi = {http://doi.org/10.9734/BJMMR/2016/26738}
}
Kondratieva, N., Azimova, J., Skorobogatykh, K., Sergeev, A., Naumova, E., Kokaeva, Z., Anuchina, A., Rudko, O., Tabeeva, G. and Klimov, E. Biomarkers of migraine: Part 1 – Genetic markers 2016   article DOI  
Abstract: a b s t r a c t Background: Migraine is a multifactorial socially significant disease affecting the peripheral and central nervous system. The diagnosis of " migraine " is still the only clinical, and additional methods of inspection are only re-quired to avoid secondary headaches if certain " signs of danger " . Accordingly, the search for biomarkers of mi-graine, confirming the diagnosis, rather than refuting others, is the leading vector in this scientific field. Aim: In this paper we have analyzed the literature data on the genetic markers associated with migraine. Methods: List of genes was compiled using Pathway Studio 10® software and abstract database ResNet12 ® made by Elsevier. Addition search (last time on 15 March 2016) was performed by using PubMed or TargetInsights. In-formation about 185 polymorphic loci in 98 genes associated with migraine was extracted and described. Results: The genes associated with migraine could be classified into 8 major groups: homeostasis of blood vessels -26.5%, metabolism of neurotransmitters -11.2%, transport and reception of neurotransmitters -24.5%, neurogenesis -5.1%, inflammation -8.2%, sex hormones -5.1%, ion channels and membrane potential -11.2%, other -8.2%. Conclusion: These findings parallel the range of mechanisms implicated in migraine pathogenesis.
BibTeX:
@article{Kondratieva2016,
  author = {Kondratieva, Natalia and Azimova, Julia and Skorobogatykh, Kirill and Sergeev, Alexey and Naumova, Elena and Kokaeva, Zarema and Anuchina, Arina and Rudko, Olga and Tabeeva, Gyuzyal and Klimov, Eugene},
  title = {Biomarkers of migraine: Part 1 – Genetic markers},
  year = {2016},
  doi = {http://doi.org/10.1016/j.jns.2016.08.008}
}
Kopp, S., Slumstrup, L., Corydon, T.J., Sahana, J., Aleshcheva, G., Islam, T., Magnusson, N.E., Wehland, M., Bauer, J., Infanger, M. and Grimm, D. Identifications of novel mechanisms in breast cancer cells involving duct-like multicellular spheroid formation after exposure to the Random Positioning Machine. 2016 Scientific reports
Vol. 6, pp. 26887 
article URL 
Abstract: Many cell types form three-dimensional aggregates (MCS; multicellular spheroids), when they are cultured under microgravity. MCS often resemble the organ, from which the cells have been derived. In this study we investigated human MCF-7 breast cancer cells after a 2 h-, 4 h-, 16 h-, 24 h- and 5d-exposure to a Random Positioning Machine (RPM) simulating microgravity. At 24 h few small compact MCS were detectable, whereas after 5d many MCS were floating in the supernatant above the cells, remaining adherently (AD). The MCS resembled the ducts formed in vivo by human epithelial breast cells. In order to clarify the underlying mechanisms, we harvested MCS and AD cells separately from each RPM-culture and measured the expression of 29 selected genes with a known involvement in MCS formation. qPCR analyses indicated that cytoskeletal genes were unaltered in short-term samples. IL8, VEGFA, and FLT1 were upregulated in 2 h/4 h AD-cultures. The ACTB, TUBB, EZR, RDX, FN1, VEGFA, FLK1 Casp9, Casp3, PRKCA mRNAs were downregulated in 5d-MCS-samples. ESR1 was upregulated in AD, and PGR1 in both phenotypes after 5d. A pathway analysis revealed that the corresponding gene products are involved in organization and regulation of the cell shape, in cell tip formation and membrane to membrane docking.
BibTeX:
@article{Kopp2016,
  author = {Kopp, Sascha and Slumstrup, Lasse and Corydon, Thomas J and Sahana, Jayashree and Aleshcheva, Ganna and Islam, Tawhidul and Magnusson, Nils E and Wehland, Markus and Bauer, Johann and Infanger, Manfred and Grimm, Daniela},
  title = {Identifications of novel mechanisms in breast cancer cells involving duct-like multicellular spheroid formation after exposure to the Random Positioning Machine.},
  journal = {Scientific reports},
  publisher = {Nature Publishing Group},
  year = {2016},
  volume = {6},
  pages = {26887},
  url = {http://www.nature.com/srep/2016/160527/srep26887/full/srep26887.html}
}
Krzystyniak, J., Ceppi, L., Dizon, D.S. and Birrer, M.J. Epithelial ovarian cancer: the molecular genetics of epithelial ovarian cancer. 2016 Annals of oncology : official journal of the European Society for Medical Oncology / ESMO
Vol. 27(suppl 1), pp. i4-i10 
article URL 
Abstract: BACKGROUND: Epithelial ovarian cancer (EOC) remains one of the leading causes of cancer-related deaths among women worldwide, despite gains in diagnostics and treatments made over the last three decades. Existing markers of ovarian cancer possess very limited clinical relevance highlighting the emerging need for identification of novel prognostic biomarkers as well as better predictive factors that might allow the stratification of patients who could benefit from a more targeted approach.

PATIENTS AND METHODS: A summary of molecular genetics of EOC.

RESULTS: Large-scale high-throughput genomic technologies appear to be powerful tools for investigations into the genetic abnormalities in ovarian tumors, including studies on dysregulated genes and aberrantly activated signaling pathways. Such technologies can complement well-established clinical histopathology analysis and tumor grading and will hope to result in better, more tailored treatments in the future. Genomic signatures obtained by gene expression profiling of EOC may be able to predict survival outcomes and other important clinical outcomes, such as the success of surgical treatment. Finally, genomic analyses may allow for the identification of novel predictive biomarkers for purposes of treatment planning. These data combined suggest a pathway to progress in the treatment of advanced ovarian cancer and the promise of fulfilling the objective of providing personalized medicine to women with ovarian cancer.

CONCLUSIONS: The understanding of basic molecular events in the tumorigenesis and chemoresistance of EOC together with discovery of potential biomarkers may be greatly enhanced through large-scale genomic studies. In order to maximize the impact of these technologies, however, extensive validation studies are required.
BibTeX:
@article{Krzystyniak2016,
  author = {Krzystyniak, J and Ceppi, L and Dizon, D S and Birrer, M J},
  title = {Epithelial ovarian cancer: the molecular genetics of epithelial ovarian cancer.},
  journal = {Annals of oncology : official journal of the European Society for Medical Oncology / ESMO},
  year = {2016},
  volume = {27},
  number = {suppl 1},
  pages = {i4--i10},
  url = {http://annonc.oxfordjournals.org/content/27/suppl1/i4.full}
}
Lefevre, P.L.C., Wade, M., Goodyer, C., Hales, B.F. and Robaire, B. A Mixture Reflecting Polybrominated Diphenyl Ether (PBDE) Profiles Detected in Human Follicular Fluid Significantly Affects Steroidogenesis and Induces Oxidative Stress in a Female Human Granulosa Cell Line 2016 Endocrinology
Vol. 157(7), pp. 2698-2711 
article DOI URL 
BibTeX:
@article{Lefevre2016,
  author = {Lefevre, Pavine L. C. and Wade, Mike and Goodyer, Cindy and Hales, Barbara F. and Robaire, Bernard},
  title = {A Mixture Reflecting Polybrominated Diphenyl Ether (PBDE) Profiles Detected in Human Follicular Fluid Significantly Affects Steroidogenesis and Induces Oxidative Stress in a Female Human Granulosa Cell Line},
  journal = {Endocrinology},
  publisher = {Oxford University Press},
  year = {2016},
  volume = {157},
  number = {7},
  pages = {2698--2711},
  url = {https://academic.oup.com/endo/article-lookup/doi/10.1210/en.2016-1106},
  doi = {http://doi.org/10.1210/en.2016-1106}
}
Le Provost, G., Lesur, I., Lalanne, C., Da Silva, C., Labadie, K., Aury, J.M., Leple, J.C. and Plomion, C. Implication of the suberin pathway in adaptation to waterlogging and hypertrophied lenticels formation in pedunculate oak ( textlessitextgreaterQuercus roburtextless/itextgreater L.) 2016 Tree Physiology, pp. tpw056  article DOI URL 
BibTeX:
@article{LeProvost2016,
  author = {Le Provost, Gregoire and Lesur, Isabelle and Lalanne, Celine and Da Silva, Corinne and Labadie, Karine and Aury, Jean Marc and Leple, Jean Charles and Plomion, Christophe},
  title = {Implication of the suberin pathway in adaptation to waterlogging and hypertrophied lenticels formation in pedunculate oak ( textlessitextgreaterQuercus roburtextless/itextgreater L.)},
  journal = {Tree Physiology},
  publisher = {Oxford University Press},
  year = {2016},
  pages = {tpw056},
  url = {http://treephys.oxfordjournals.org/lookup/doi/10.1093/treephys/tpw056},
  doi = {http://doi.org/10.1093/treephys/tpw056}
}
Leung, A.W.Y., Hung, S.S., Backstrom, I., Ricaurte, D., Kwok, B., Poon, S., McKinney, S., Segovia, R., Rawji, J., Qadir, M.A., Aparicio, S., Stirling, P.C., Steidl, C., Bally, M.B. and Leung AW, Hung SS, Backstrom I, Ricaurte D, Kwok B, Poon S, McKinney S, Segovia R, Rawji J, Qadir MA, Aparicio S, Stirling PC, Steidl C, B.M. Combined Use of Gene Expression Modeling and siRNA Screening Identifies Genes and Pathways Which Enhance the Activity of Cisplatin When Added at No Effect Levels to Non-Small Cell Lung Cancer Cells In Vitro 2016
Vol. 11(3)PloS one, pp. e0150675 
misc URL 
Abstract: Platinum-based combination chemotherapy is the standard treatment for advanced non-small cell lung cancer (NSCLC). While cisplatin is effective, its use is not curative and resistance often emerges. As a consequence of microenvironmental heterogeneity, many tumour cells are exposed to sub-lethal doses of cisplatin. Further, genomic heterogeneity and unique tumor cell sub-populations with reduced sensitivities to cisplatin play a role in its effectiveness within a site of tumor growth. Being exposed to sub-lethal doses will induce changes in gene expression that contribute to the tumour cell's ability to survive and eventually contribute to the selective pressures leading to cisplatin resistance. Such changes in gene expression, therefore, may contribute to cytoprotective mechanisms. Here, we report on studies designed to uncover how tumour cells respond to sub-lethal doses of cisplatin. A microarray study revealed changes in gene expressions that occurred when A549 cells were exposed to a no-observed-effect level (NOEL) of cisplatin (e.g. the IC10). These data were integrated with results from a genome-wide siRNA screen looking for novel therapeutic targets that when inhibited transformed a NOEL of cisplatin into one that induced significant increases in lethality. Pathway analyses were performed to identify pathways that could be targeted to enhance cisplatin activity. We found that over 100 genes were differentially expressed when A549 cells were exposed to a NOEL of cisplatin. Pathways associated with apoptosis and DNA repair were activated. The siRNA screen revealed the importance of the hedgehog, cell cycle regulation, and insulin action pathways in A549 cell survival and response to cisplatin treatment. Results from both datasets suggest that RRM2B, CABYR, ALDH3A1, and FHL2 could be further explored as cisplatin-enhancing gene targets. Finally, pathways involved in repairing double-strand DNA breaks and INO80 chromatin remodeling were enriched in both datasets, warranting further research into combinations of cisplatin and therapeutics targeting these pathways.
BibTeX:
@misc{Leung2016,
  author = {Leung, Ada W Y and Hung, Stacy S and Backstrom, Ian and Ricaurte, Daniel and Kwok, Brian and Poon, Steven and McKinney, Steven and Segovia, Romulo and Rawji, Jenna and Qadir, Mohammed A and Aparicio, Samuel and Stirling, Peter C and Steidl, Christian and Bally, Marcel B and Leung AW, Hung SS, Backstrom I, Ricaurte D, Kwok B, Poon S, McKinney S, Segovia R, Rawji J, Qadir MA, Aparicio S, Stirling PC, Steidl C, Bally MB},
  title = {Combined Use of Gene Expression Modeling and siRNA Screening Identifies Genes and Pathways Which Enhance the Activity of Cisplatin When Added at No Effect Levels to Non-Small Cell Lung Cancer Cells In Vitro},
  booktitle = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {3},
  pages = {e0150675},
  url = {https://demo.elseviertextmining.com/demo/search?query=pathway+studio&s=d&t=LHi4PF5&category=r&view=d&start=1 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0150675}
}
Li, J., Sheng, N., Cui, R., Feng, Y., Shao, B., Guo, X., Zhang, H. and Dai, J. Gestational and lactational exposure to bisphenol AF in maternal rats increases testosterone levels in 23-day-old male offspring 2016 Chemosphere
Vol. 163, pp. 552-561 
article DOI  
Abstract: During prenatal and postnatal development, exposure to environmental chemicals with estrogenic activity, such as bisphenol AF (BPAF), may result in reproductive disorders. Currently, the mechanisms behind such disorders in male offspring induced by gestational and lactational exposure to BPAF remain poorly understood. Here, female rats from gestational day (GD) 3–19 were exposed to 100 mg BPAF/kg/day by oral gavage. On the day of birth (postnatal day (PD) 0), cross-fostering took place between treated and control litters, and cross-fostered mother rats were given BPAF 100 mg/kg/day during the postnatal period (PD 3 to PD 19). HPLC-MS/MS analysis showed that BPAF was transferred via cord blood and lactation, finally bio-accumulating in the offspring testes. Pups exposed to BPAF both prenatally and postnatally showed a significant increase in testis testosterone levels compared with that of the control, while all pups exposed to BPAF showed a significant decrease in testis inhibin B (INHB) levels. Compared with the control, RNA-seq revealed that 279 genes were significantly differentially expressed in the testes of pups exposed to BPAF both prenatally and postnatally, including genes involved in cell differentiation and meiosis. These results indicate that gestational and lactational exposure to BPAF in the mother can impair reproductive function in male offspring.
BibTeX:
@article{Li2016,
  author = {Li, Jing and Sheng, Nan and Cui, Ruina and Feng, Yixing and Shao, Bing and Guo, Xuejiang and Zhang, Hongxia and Dai, Jiayin},
  title = {Gestational and lactational exposure to bisphenol AF in maternal rats increases testosterone levels in 23-day-old male offspring},
  journal = {Chemosphere},
  year = {2016},
  volume = {163},
  pages = {552--561},
  doi = {http://doi.org/10.1016/j.chemosphere.2016.08.059}
}
Li, S., Kapoor, K. and Manor, L.C. Literature Data Mining and Enrichment Analysis on Top 235 Genes for Attention Deficit Hyperactivity Disorder 2016 Journal of Psychiatry and Brain Science
Vol. 1313(2210) 
article DOI  
Abstract: Background: Attention deficit hyperactivity disorder (ADHD) is a psychiatric disorder of the neuro-developmental type, marked by an ongoing pattern of inattention or hyperactivity/impulsivity, which interferes with functioning or development. The disorder affects approximately 5-7 % children and 2-5 % of adults worldwide. Numerous studies have indicated that genetic factors predominate the causes for ADHD. Nevertheless, no systematic study has summarized these findings and provided an objective and complete list of genes with a reported association to ADHD. Methods: Literature and enrichment metrics analyses were used to discover genes of specific significance associated with ADHD. We conducted a literature data mining (LDM) of over 2,410 articles covering publications from Jan. 1988 to Apr. 2016, where 235 genes were reported to be associated with the disease. Then we performed a gene set enrichment analysis (GSEA) and a sub-network enrichment analysis (SNEA) to study the functional profile and pathogenic significance of these genes associated with ADHD. Lastly, we performed a network connectivity analysis (NCA) to study the associations between the reported genes. Results: 181/235 genes enriched 100 pathways (ptextless1.1e-007), demonstrating multiple associations with ADHD. Twelve genes were discovered to be associated with ADHD, in terms of both functional diversity and replication frequency, including SLC6A3, DRD4, BDNF, DRD2, HTR2A, DBH, HTR1B, DRD5, GRM7, DRD3, TH and GRIN2A. In addition, one novel gene, SHANK2, was suggested worthy of further study. Moreover, SNEA and NCA results indicated that many of these genes form a functional network, playing roles in the pathogenesis of other ADHD related disorders. Conclusion: Our results suggest that the genetic causes of ADHD are linked to a genetic and functional network composed of a large group of genes. The gene lists, together with the literature and enrichment metrics provided in this study, could serve as groundwork for further biological/genetic studies in the field.
BibTeX:
@article{Li2016a,
  author = {Li, Shunan and Kapoor, Karan and Manor, Lydia C},
  title = {Literature Data Mining and Enrichment Analysis on Top 235 Genes for Attention Deficit Hyperactivity Disorder},
  journal = {Journal of Psychiatry and Brain Science},
  year = {2016},
  volume = {1313},
  number = {2210},
  doi = {http://doi.org/10.20900/jpbs.20160008}
}
Lian, X., Yang, D. and Cao, S. Genetic marker for lewis lung cancer Network based genetic marker evaluation for Lewis lung carcinoma 2016   article DOI  
Abstract: Background: Lung cancer is the most common cancer among males and females. During past years, many studies has been performed seeking genetic impact factors associated with lung cancer, posing the necessity of systematically study of the genetic network underlying Lewis lung carcinoma (LLC) model.
BibTeX:
@article{Lian2016,
  author = {Lian, Xiangyao and Yang, Dexiang and Cao, Shaolong},
  title = {Genetic marker for lewis lung cancer Network based genetic marker evaluation for Lewis lung carcinoma},
  year = {2016},
  doi = {http://doi.org/10.20900/mo.20160024}
}
Liang, X., Martyniuk, C.J., Zha, J. and Wang, Z. Brain quantitative proteomic responses reveal new insight of benzotriazole neurotoxicity in female Chinese rare minnow (Gobiocypris rarus) 2016 Aquatic Toxicology
Vol. 181, pp. 67-75 
article DOI  
Abstract: Benzotriazole (BT) is a high-production volume chemical which has been ubiquitously detected in aquatic environments. Although adverse effects from acute and chronic exposure to BT have been reported, the neurotoxic effect of BT and the mechanisms of toxicity are not well documented. In this study, adult female Chinese rare minnow (Gobiocypris rarus) were exposed to 0.05, 0.5, and 5mg/L BT for 28days. The brain proteome showed that BT exposure mainly involved in metabolic process, signal transduction, stress response, cytoskeleton, and transport. Pathway analysis revealed that cellular processes affected by BT included cellular respiration, G-protein signal cascades, Ca2+-dependent signaling, cell cycle and apoptosis. Moreover, data on relative mRNA levels demonstrated that genes related to these toxic pathways were also significantly affected by BT. Furthermore, proteins affected by BT such as CKBB, GS, HPCA, VDAC1, and FLOT1A are associated with neurological disorders. Therefore, our finding suggested that BT induced molecular responses in the brain and could provide new insight into BT neurotoxicity in Chinese rare minnow.
BibTeX:
@article{Liang2016,
  author = {Liang, Xuefang and Martyniuk, Christopher J. and Zha, Jinmiao and Wang, Zijian},
  title = {Brain quantitative proteomic responses reveal new insight of benzotriazole neurotoxicity in female Chinese rare minnow (Gobiocypris rarus)},
  journal = {Aquatic Toxicology},
  year = {2016},
  volume = {181},
  pages = {67--75},
  doi = {http://doi.org/10.1016/j.aquatox.2016.10.030}
}
Lim, K.S., Lee, K.T., Park, J.E., Chung, W.H., Jang, G.W., Choi, B.H., Hong, K.C. and Kim, T.H. Identification of differentially expressed genes in longissimus muscle of pigs with high and low intramuscular fat content using RNA sequencing 2016 Animal Genetics  article DOI URL 
BibTeX:
@article{Lim2016,
  author = {Lim, K. S. and Lee, K. T. and Park, J. E. and Chung, W. H. and Jang, G. W. and Choi, B. H. and Hong, K. C. and Kim, T. H.},
  title = {Identification of differentially expressed genes in longissimus muscle of pigs with high and low intramuscular fat content using RNA sequencing},
  journal = {Animal Genetics},
  year = {2016},
  url = {http://doi.wiley.com/10.1111/age.12518},
  doi = {http://doi.org/10.1111/age.12518}
}
Liu, F., Chen, J., Jagannatha, A. and Yu, H. Learning for Biomedical Information Extraction: Methodological Review of Recent Advances 2016   article URL 
Abstract: Biomedical information extraction (BioIE) is important to many applications, including clinical decision support, integrative biology, and pharmacovigilance, and therefore it has been an active research. Unlike existing reviews covering a holistic view on BioIE, this review focuses on mainly recent advances in learning based approaches, by systematically summarizing them into different aspects of methodological development. In addition, we dive into open information extraction and deep learning, two emerging and influential techniques and envision next generation of BioIE.
BibTeX:
@article{Liu2016,
  author = {Liu, Feifan and Chen, Jinying and Jagannatha, Abhyuday and Yu, Hong},
  title = {Learning for Biomedical Information Extraction: Methodological Review of Recent Advances},
  year = {2016},
  url = {http://arxiv.org/abs/1606.07993}
}
Ljunggren, A.S., Iggland, M., Rönn, M., Lind, L., Lind, P.M. and Karlsson, H. Altered heart proteome in fructose-fed Fisher 344 rats exposed to bisphenol A. 2016 Toxicology  article URL 
Abstract: Bisphenol A (BPA), is an artificial estrogen initially produced for medical purposes but is today widely used in polycarbonate plastics and epoxy resins. Exposure-related reproductive disorders have been found, but recently it has also been suggested that BPA may be involved in obesity, diabetes, myocardial hypertrophy and myocardial infarction in humans. To mimic a modern lifestyle, female rats were fed with fructose or fructose plus BPA (0.25mg/L drinking water). The myocardial left ventricle proteome of water controls, fructose-fed and fructose-fed plus BPA supplemented rats was explored. The proteome was investigated using nano-liquid chromatography tandem mass spectrometry and two-dimensional gel electrophoresis followed by matrix assisted laser desorption/ionization mass spectrometry identification. In total, 41 proteins were significantly altered by BPA exposure compared to water or fructose controls. Principal component analysis and cellular process enrichment analysis of altered proteins suggested increased fatty acid transport and oxidation, increased ROS generation and altered structural integrity of the myocardial left ventricle in the fructose-fed BPA-exposed rats, indicating unfavorable effects on the myocardium. In conclusion, BPA exposure in the rats induces major alterations in the myocardial proteome.
BibTeX:
@article{Ljunggren2016,
  author = {Ljunggren, A S and Iggland, M and Rönn, M and Lind, L and Lind, P M and Karlsson, H},
  title = {Altered heart proteome in fructose-fed Fisher 344 rats exposed to bisphenol A.},
  journal = {Toxicology},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S0300483X1630018X}
}
Mahmoud, A.M., Aboul-Soud, M.A.M., Han, J., Al-Sheikh, Y.A., Al-Abd, A.M. and El-Shemy, H.A. Transcriptional profiling of breast cancer cells in response to mevinolin: Evidence of cell cycle arrest, DNA degradation and apoptosis. 2016 International journal of oncology
Vol. 48(5), pp. 1886-94 
article DOI URL 
Abstract: The merging of high-throughput gene expression techniques, such as microarray, in the screening of natural products as anticancer agents, is considered the optimal solution for gaining a better understanding of the intervention mechanism. Red yeast rice (RYR), a Chinese dietary product, contains a mixture of hypocholesterolemia agents such as statins. Typically, statins have this effect via the inhibition of HMG‑CoA reductase, the key enzyme in the biosynthesis of cholesterol. Recently, statins have been shown to exhibit various beneficial antineoplastic properties through the disruption of tumor angiogenesis and metastatic processes. Mevinolin (MVN) is a member of statins and is abundantly present in RYR. Early experimental trials suggested that the mixed apoptotic/necrotic cell death pathway is activated in response to MVN exposure. In the current study, the cytotoxic profile of MVN was evaluated against MCF‑7, a breast cancer‑derived cell line. The obtained results indicated that MVN‑induced cytotoxicity is multi‑factorial involving several regulatory pathways in the cytotoxic effects of MVN on breast cancer cell lines. In addition, MVN‑induced transcript abundance profiles inferred from microarrays showed significant changes in some key cell processes. The changes were predicted to induce cell cycle arrest and reactive oxygen species generation but inhibit DNA repair and cell proliferation. This MVN‑mediated multi‑factorial stress triggered specific programmed cell death (apoptosis) and DNA degradation responses in breast cancer cells. Taken together, the observed MVN‑induced effects underscore the potential of this ubiquitous natural compound as a selective anticancer activity, with broad safety margins and low cost compared to benchmarked traditional synthetic chemotherapeutic agents. Additionally, the data support further pre‑clinical and clinical evaluations of MVN as a novel strategy to combat breast cancer and overcome drug resistance.
BibTeX:
@article{Mahmoud2016,
  author = {Mahmoud, Ali M and Aboul-Soud, Mourad A M and Han, Junkyu and Al-Sheikh, Yazeed A and Al-Abd, Ahmed M and El-Shemy, Hany A},
  title = {Transcriptional profiling of breast cancer cells in response to mevinolin: Evidence of cell cycle arrest, DNA degradation and apoptosis.},
  journal = {International journal of oncology},
  publisher = {Spandidos Publications},
  year = {2016},
  volume = {48},
  number = {5},
  pages = {1886--94},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/26983896 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4809649},
  doi = {http://doi.org/10.3892/ijo.2016.3418}
}
Majewska, A., Gajewska, M., Dembele, K., Maciejewski, H., Prostek, A., Jank, M., Olivry, T., DeBoer, D., Griffin, C., Halliwell, R., Hill, P., Hillier, A., Marsella, R., Olivry, T., Carlotti, D., Bieber, T., Nuttall, T., Knight, P., McAleese, S., Lamb, J., Hill, P., Schlotter, Y., Rutten, V., Riemers, F., Knol, E., Willemse, T., Martinez, G., Nurieva, R., Yang, X., Dong, C., Jutel, M., Akdis, C., Hennino, A., Jean-Decoster, C., Giordano-Labadie, F., Debeer, S., Vanbervliet, B., Rozières, A., Schmitt, A., Nicolas, J., Olivry, T., Naydan, D., Moore, P., Sinke, J., Thepen, T., Bihari, I., Rutten, V., Willemse, T., Akdis, M., Blaser, K., Akdis, C., Palomares, O., Yaman, G., Azkur, A., Akkoc, T., Akdis, M., Akdis, C., Fujita, H., Soyka, M., Akdis, M., Akdis, C., Wisniewski, J., Agrawal, R., Woodfolk, J., Merryman-Simpson, A., Wood, S., Fretwell, N., Jones, P., McLaren, W., McEwan, N., Plager, D., Torres, S., Koch, S., Kita, H., Schamber, P., Schwab-Richards, R., Bauersachs, S., Mueller, R., Nikitin, A., Egorov, S., Daraselia, N., Mazo, I., Schmitz, S., Garden, O., Werling, D., Allenspach, K., Brinkhof, B., Spee, B., Rothuizen, J., Penning, L., Livak, K., Schmittgen, T., Hennino, A., Vocanson, M., Toussaint, Y., Stock, P., Kallinich, T., Akbari, O., Quarcoo, D., Gerhold, K., Wahn, U., Umetsu, D., Tarpataki, N., Terenyi, M., Nagy, S., Taszkun, I., Chabanne, L., Marchal, T., Denerolle, P., Magnol, J., Fournel, C., Monier, J., Rigal, D., Pinheiro, D., Singh, Y., Grant, C., Appleton, R., Sacchini, F., Walker, K., Hauck, V., Hügli, P., Meli, M., Rostaher, A., Fischer, N., Hofmann-Lehmann, R., Favrot, C., Beccati, M., Martini, V., Comazzi, S., Fanton, N., Cornegliani, L., Bellinghausen, I., König, B., Böttcher, I., Knop, J., Saloga, J., Marsella, R., Olivry, T., Maeda, S., Wakugawa, M., Hayashi, K., Nakamura, K., Tamaki, K., Grutta, S., Richiusa, P., Pizzolanti, G., Mattina, A., Pajno, G., Citarrella, R., Hayashiya, S., Tani, K., Morimoto, M., Hayashi, T., Hayasaki, M., Nomura, T., Une, S., Pasparakis, M., Alexopoulou, L., Episkopou, V., Kollias, G., Stanley, A., Lacy, P., Lin, Y., Shieh, C., Wang, J., Fontenot, J., Rasmussen, J., Williams, L., Dooley, J., Farr, A., Rudensky, A., Turka, L., Walsh, P., Nandakumar, S., Miller, C., Kumaraguru, U., Zorn, E., Nelson, E., Mohseni, M., Porcheray, F., Kim, H., Litsa, D., Bellucci, R., Raderschall, E., Canning, C., Soiffer, R., Frank, D., Ritz, J., Burchill, M., Yang, J., Vogtenhuber, C., Blazar, B., Farrar, M., Yao, Z., Kanno, Y., Kerenyi, M., Stephens, G., Durant, L., Watford, W., Sakaguchi, S., Wing, K., Onishi, Y., Prieto-Martin, P., Yamaguchi, T., Xie, X., Stubbington, M., Nissen, J., Andersen, K., Hebenstreit, D., Teichmann, S., Betz, A., Shevach, E., Moon, B., Kim, T., Seoh, J., Akdis, M., Akdis, C., Keppel, K., Campbell, K., Zuckermann, F., Greeley, E., Schaeffer, D., Husmann, R., Maeda, S., Tsuchida, H., Marsella, R., Zheng, S., Wang, J., Horwitz, D., Wahl, S., Vázquez, N., Chen, W., Lee, C., Link, H., Baluk, P., Homer, R., Chapoval, S., Bhandari, V., Zhang, Y., Matsuo, H., Morita, E., Koczy-Baron, E., Jochem, J., Kasperska-Zajac, A., Chen, W., Wahl, S., Nakamura, K., Kitani, A., Fuss, I., Pedersen, A., Harada, N., Nawata, H., Strober, W., Aki, S., Yoshioka, K., Okamoto, Y., Takuwa, N., Takuwa, Y., Yang, N., Zhao, B., Rasul, A., Qin, H., Li, J., Li, X., Giguere, V., Tini, M., Flock, G., Ong, E., Evans, R., Otulakowski, G., Jetten, A., Du, J., Huang, C., Zhou, B., Ziegler, S., Dzhagalov, I., Giguère, V., He, Y., Yang, L., Anderson, D., Baecher-Allan, C., Hastings, W., Bettelli, E., Oukka, M., Delerive, P., Monté, D., Dubois, G., Trottein, F., Fruchart-Najib, J., Mariani, J., Fruchart, J., Staels, B., Farez, M., Mascanfroni, I., Méndez-Huergo, S., Yeste, A., Murugaiyan, G., Garo, L., Mosnier, L., Zlokovic, B., Griffin, J., Wang, L., Bastarache, J., Wickersham, N., Fang, X., Matthay, M., Ware, L., Moxon, C., Heyderman, R., Wassmer, S., Beinsberger, J., Heemskerk, J., Cosemans, J., Rui, L., Carter-Su, C., O'Brien, K., O'Shea, J. and Carter-Su, C. Lymphocytic, cytokine and transcriptomic profiles in peripheral blood of dogs with atopic dermatitis 2016 BMC Veterinary Research
Vol. 12(1), pp. 174 
article DOI URL 
BibTeX:
@article{Majewska2016,
  author = {Majewska, Alicja and Gajewska, Małgorzata and Dembele, Kourou and Maciejewski, Henryk and Prostek, Adam and Jank, Michał and Olivry, T and DeBoer, DJ and Griffin, CE and Halliwell, RE and Hill, PB and Hillier, A and Marsella, R and Olivry, T and Carlotti, DN and Bieber, T and Nuttall, TJ and Knight, PA and McAleese, SM and Lamb, JR and Hill, PB and Schlotter, YM and Rutten, VP and Riemers, FM and Knol, EF and Willemse, T and Martinez, GJ and Nurieva, RI and Yang, XO and Dong, C and Jutel, M and Akdis, CA and Hennino, A and Jean-Decoster, C and Giordano-Labadie, F and Debeer, S and Vanbervliet, B and Rozières, A and Schmitt, AM and Nicolas, JF and Olivry, T and Naydan, DK and Moore, PF and Sinke, JD and Thepen, T and Bihari, IC and Rutten, VP and Willemse, T and Akdis, M and Blaser, K and Akdis, CA and Palomares, O and Yaman, G and Azkur, AK and Akkoc, T and Akdis, M and Akdis, CA and Fujita, H and Soyka, MB and Akdis, M and Akdis, CA and Wisniewski, J and Agrawal, R and Woodfolk, JA and Merryman-Simpson, AE and Wood, SH and Fretwell, N and Jones, PG and McLaren, WM and McEwan, NA and Plager, DA and Torres, SM and Koch, SN and Kita, H and Schamber, P and Schwab-Richards, R and Bauersachs, S and Mueller, RS and Nikitin, A and Egorov, S and Daraselia, N and Mazo, I and Schmitz, S and Garden, OA and Werling, D and Allenspach, K and Brinkhof, B and Spee, B and Rothuizen, J and Penning, LC and Livak, KJ and Schmittgen, TD and Hennino, A and Vocanson, M and Toussaint, Y and Stock, P and Kallinich, T and Akbari, O and Quarcoo, D and Gerhold, K and Wahn, U and Umetsu, DT and Tarpataki, N and Terenyi, M and Nagy, SZ and Taszkun, I and Chabanne, L and Marchal, T and Denerolle, P and Magnol, JP and Fournel, C and Monier, JC and Rigal, D and Pinheiro, D and Singh, Y and Grant, CR and Appleton, RC and Sacchini, F and Walker, KR and Hauck, V and Hügli, P and Meli, ML and Rostaher, A and Fischer, N and Hofmann-Lehmann, R and Favrot, C and Beccati, M and Martini, V and Comazzi, S and Fanton, N and Cornegliani, L and Bellinghausen, I and König, B and Böttcher, I and Knop, J and Saloga, J and Marsella, R and Olivry, T and Maeda, S and Wakugawa, M and Hayashi, K and Nakamura, K and Tamaki, KJ and Grutta, S and Richiusa, P and Pizzolanti, G and Mattina, A and Pajno, GB and Citarrella, R and Hayashiya, S and Tani, K and Morimoto, M and Hayashi, T and Hayasaki, M and Nomura, T and Une, S and Pasparakis, M and Alexopoulou, L and Episkopou, V and Kollias, G and Stanley, AC and Lacy, P and Lin, YL and Shieh, CC and Wang, JY and Fontenot, JD and Rasmussen, JP and Williams, LM and Dooley, JL and Farr, AG and Rudensky, AY and Turka, LA and Walsh, PT and Nandakumar, S and Miller, CW and Kumaraguru, U and Zorn, E and Nelson, EA and Mohseni, M and Porcheray, F and Kim, H and Litsa, D and Bellucci, R and Raderschall, E and Canning, C and Soiffer, RJ and Frank, DA and Ritz, J and Burchill, MA and Yang, J and Vogtenhuber, C and Blazar, BR and Farrar, MA and Yao, Z and Kanno, Y and Kerenyi, M and Stephens, G and Durant, L and Watford, WT and Sakaguchi, S and Wing, K and Onishi, Y and Prieto-Martin, P and Yamaguchi, T and Xie, X and Stubbington, MJ and Nissen, JK and Andersen, KG and Hebenstreit, D and Teichmann, SA and Betz, AG and Shevach, EM and Moon, BI and Kim, TH and Seoh, JY and Akdis, M and Akdis, CA and Keppel, KE and Campbell, KL and Zuckermann, FA and Greeley, EA and Schaeffer, DJ and Husmann, RJ and Maeda, S and Tsuchida, H and Marsella, R and Zheng, SG and Wang, JY and Horwitz, DA and Wahl, SM and Vázquez, N and Chen, W and Lee, CG and Link, H and Baluk, P and Homer, RJ and Chapoval, S and Bhandari, V and Zhang, Y and Matsuo, H and Morita, E and Koczy-Baron, E and Jochem, J and Kasperska-Zajac, A and Chen, W and Wahl, SM and Nakamura, K and Kitani, A and Fuss, I and Pedersen, A and Harada, N and Nawata, H and Strober, W and Aki, S and Yoshioka, K and Okamoto, Y and Takuwa, N and Takuwa, Y and Yang, N and Zhao, B and Rasul, A and Qin, H and Li, J and Li, X and Giguere, V and Tini, M and Flock, G and Ong, E and Evans, RM and Otulakowski, G and Jetten, AM and Du, J and Huang, C and Zhou, B and Ziegler, SF and Dzhagalov, I and Giguère, V and He, YW and Yang, L and Anderson, DE and Baecher-Allan, C and Hastings, WD and Bettelli, E and Oukka, M and Delerive, P and Monté, D and Dubois, G and Trottein, F and Fruchart-Najib, J and Mariani, J and Fruchart, JC and Staels, B and Farez, MF and Mascanfroni, ID and Méndez-Huergo, SP and Yeste, A and Murugaiyan, G and Garo, LP and Mosnier, LO and Zlokovic, BV and Griffin, JH and Wang, L and Bastarache, JA and Wickersham, N and Fang, X and Matthay, MA and Ware, LB and Moxon, CA and Heyderman, RS and Wassmer, SC and Beinsberger, J and Heemskerk, JW and Cosemans, JM and Rui, L and Carter-Su, C and O'Brien, KB and O'Shea, JJ and Carter-Su, C},
  title = {Lymphocytic, cytokine and transcriptomic profiles in peripheral blood of dogs with atopic dermatitis},
  journal = {BMC Veterinary Research},
  publisher = {BioMed Central},
  year = {2016},
  volume = {12},
  number = {1},
  pages = {174},
  url = {http://bmcvetres.biomedcentral.com/articles/10.1186/s12917-016-0805-6},
  doi = {http://doi.org/10.1186/s12917-016-0805-6}
}
Makoukji, J., Makhoul, N.J., Khalil, M., El-Sitt, S., Aldin, E.S., Jabbour, M., Boulos, F., Gadaleta, E., Sangaralingam, A., Chelala, C., Boustany, R.-M. and Tfayli, A. Gene expression profiling of breast cancer in Lebanese women. 2016 Scientific reports
Vol. 6, pp. 36639 
article URL 
Abstract: Breast cancer is commonest cancer in women worldwide. Elucidation of underlying biology and molecular pathways is necessary for improving therapeutic options and clinical outcomes. Molecular alterations in breast cancer are complex and involve cross-talk between multiple signaling pathways. The aim of this study is to extract a unique mRNA fingerprint of breast cancer in Lebanese women using microarray technologies. Gene-expression profiles of 94 fresh breast tissue samples (84 cancerous/10 non-tumor adjacent samples) were analyzed using GeneChip Human Genome U133 Plus 2.0 arrays. Quantitative real-time PCR was employed to validate candidate genes. Differentially expressed genes between breast cancer and non-tumor tissues were screened. Significant differences in gene expression were established for COL11A1/COL10A1/MMP1/COL6A6/DLK1/S100P/CXCL11/SOX11/LEP/ADIPOQ/OXTR/FOSL1/ACSBG1 and C21orf37. Pathways/diseases representing these genes were retrieved and linked using PANTHER(®)/Pathway Studio(®). Many of the deregulated genes are associated with extracellular matrix, inflammation, angiogenesis, metastasis, differentiation, cell proliferation and tumorigenesis. Characteristics of breast cancers in Lebanese were compared to those of women from Western populations to explain why breast cancer is more aggressive and presents a decade earlier in Lebanese victims. Delineating molecular mechanisms of breast cancer in Lebanese women led to key genes which could serve as potential biomarkers and/or novel drug targets for breast cancer.
BibTeX:
@article{Makoukji2016,
  author = {Makoukji, Joelle and Makhoul, Nadine J and Khalil, Maya and El-Sitt, Sally and Aldin, Ehab Saad and Jabbour, Mark and Boulos, Fouad and Gadaleta, Emanuela and Sangaralingam, Ajanthah and Chelala, Claude and Boustany, Rose-Mary and Tfayli, Arafat},
  title = {Gene expression profiling of breast cancer in Lebanese women.},
  journal = {Scientific reports},
  publisher = {Nature Publishing Group},
  year = {2016},
  volume = {6},
  pages = {36639},
  url = {http://www.nature.com/srep/2016/161118/srep36639/full/srep36639.html}
}
Mallmann Focus: Cervical Cancer 2016 ContentsCologne C.B. (Bochum
Vol. 39(9) 
article  
BibTeX:
@article{Mallmann2016,
  author = {Mallmann},
  title = {Focus: Cervical Cancer},
  journal = {ContentsCologne C.B. (Bochum},
  year = {2016},
  volume = {39},
  number = {9}
}
Maria K. Herndon , Nathan C. Law , Elyse M. Donaubauer , Brandon Kyriss1, M.H.-D. Forkhead box O member FOXO1 regulates the majority of follicle-stimulating hormone responsive genes in ovarian granulosa cells 2016   article URL 
Abstract: FSH promotes maturation of ovarian follicles. One pathway activated by FSH in granulosa cells (GCs) is phosphatidylinositol-3 kinase/AKT. The AKT target FOXO1 is reported to function primarily as a repressor of FSH genes, including Ccnd2 and Inha. Based on its broad functions in other tissues, we hypothesized that FOXO1 may regulate many more GC genes. We transduced GCs with empty adenovirus or constitutively active FOXO1 followed by treatment with FSH for 24 h, and conducted RNA deep sequencing. Results show that FSH regulates 3,772 genes ≥2.0-fold; 60% of these genes are activated or repressed by FOXO1. Pathway Studio Analysis revealed enrichment of genes repressed by FOXO1 in metabolism, signaling, transport, development, and activated by FOXO1 in signaling, cytoskeletal functions, and apoptosis. Gene regulation was verified by q-PCR (eight genes) and ChIP analysis (two genes). We conclude that FOXO1 regulates the majority of FSH target genes in GCs.
BibTeX:
@article{MariaK.HerndonNathanC.LawElyseM.DonaubauerBrandonKyriss12016,
  author = {Maria K. Herndon , Nathan C. Law , Elyse M. Donaubauer , Brandon Kyriss1, Mary Hunzicker-Dunn},
  title = {Forkhead box O member FOXO1 regulates the majority of follicle-stimulating hormone responsive genes in ovarian granulosa cells},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S0303720716302222}
}
Martyniuk, C.J., Doperalski, N.J., Feswick, A., Prucha, M.S., Kroll, K.J., Barber, D.S. and Denslow, N.D. Transcriptional networks associated with the immune system are disrupted by organochlorine pesticides in largemouth bass (Micropterus salmoides) ovary 2016 Aquatic Toxicology  article DOI  
Abstract: Largemouth bass (Micropterus salmoides) inhabiting Lake Apopka, Florida are exposed to high levels of persistent organochlorine pesticides (OCPs) and dietary uptake is a significant route of exposure for these apex predators. The objectives of this study were to determine the dietary effects of two organochlorine pesticides (p,p'-dichlorodiphenyldichloroethylene; p,p' DDE and methoxychlor; MXC) on the reproductive axis of largemouth bass. Reproductive bass (late vitellogenesis) were fed one of the following diets: control pellets, 125ppm p,p'-DDE, or 10ppm MXC (mg/kg) for 84 days. Due to the fact that both p,p' DDE and MXC have anti-androgenic properties, the anti-androgenic pharmaceutical flutamide was fed to a fourth group of largemouth bass (750ppm). Following a 3 month exposure, fish incorporated p,p' DDE and MXC into both muscle and ovary tissue, with the ovary incorporating 3 times more organochlorine pesticides compared to muscle. Endpoints assessed were those related to reproduction due to previous studies demonstrating that these pesticides impact the reproductive axis and we hypothesized that a dietary exposure would result in impaired reproduction. However, oocyte distribution, gonadosomatic index, plasma vitellogenin, and plasma sex steroids (17β-estradiol, E2 and testosterone, T) were not different between control animals and contaminant-fed largemouth bass. Moreover, neither p,p' DDE nor MXC affected E2 or T production in ex vivo oocyte cultures from chemical-fed largemouth bass. However, both pesticides did interfere with the normal upregulation of androgen receptor that is observed in response to human chorionic gonadotropin in ex vivo cultures, an observation that may be related to their anti-androgenic properties. Transcriptomics profiling in the ovary revealed that gene networks related to cell processes such as leukocyte cell adhesion, ossification, platelet function and inhibition, xenobiotic metabolism, fibrinolysis, and thermoregulation were altered by p,p' DDE, MXC, and flutamide. Interestingly, immune-related gene networks were suppressed by all three chemicals. The data suggest that p,p' DDE and flutamide affected more genes in common with each other than either chemical with MXC, consistent with studies suggesting that p,p' DDE is a more potent anti-androgen than MXC. These data demonstrate that reproductive health was not affected by these specific dietary treatments, but rather the immune system, which may be a significant target of organochlorine pesticides. The interaction between the reproductive and immune systems should be considered in future studies on these legacy and persistent pesticides.
BibTeX:
@article{Martyniuk2016,
  author = {Martyniuk, Christopher J. and Doperalski, Nicholas J. and Feswick, April and Prucha, Melinda S. and Kroll, Kevin J. and Barber, David S. and Denslow, Nancy D.},
  title = {Transcriptional networks associated with the immune system are disrupted by organochlorine pesticides in largemouth bass (Micropterus salmoides) ovary},
  journal = {Aquatic Toxicology},
  year = {2016},
  doi = {http://doi.org/10.1016/j.aquatox.2016.06.009}
}
Mathieu-Denoncourt, J., Martyniuk, C.J., Loughery, J.R., Yargeau, V., de Solla, S.R. and Langlois, V.S. Lethal and sublethal effects of phthalate diesters in Silurana tropicalis larvae. 2016 Environmental toxicology and chemistry / SETAC  article URL 
Abstract: Phthalates are compounds used in polymers to increase their flexibility and are now ubiquitous in the environment due to widespread use. As few studies have focused on the adverse effects of these chemicals in aquatic species, this study aimed to determine the effects of phthalate diesters in amphibians. Western clawed frog (Silurana tropicalis) tadpoles were acutely exposed to water spiked with monomethyl (MMP; 1.3 to 1,595.5 mg/L), dimethyl (DMP; 0.03 to 924.0 mg/L), or dicyclohexyl (DCHP; 0.3 to 99.3 mg/L) phthalates. As few studies have addressed the toxicity of these specific phthalates in most organisms, this study used higher concentrations of these chemicals to determine their toxicity pathways in amphibians and at the same time investigate a suite of genes known to be altered by the well-studied phthalates. Both DMP and DCHP increased larval mortality (9.1 to 924.0 mg/L DMP and 4.1 to 99.3 mg/L DCHP), increased frequency of malformations in tadpoles (0.1 to 34.1 mg/L DMP and 4.1 to 19.0 mg/L DCHP), and upregulation of cellular stress-related mRNA levels (4.1 mg/L DCHP). To characterize the molecular toxicity pathway of these phthalates in tadpoles, transcriptome analysis was conducted using a custom microarray. Parametric analysis of gene set enrichment revealed an important increase in the expression of genes related to drug metabolism and transport, liver metabolism, xenobiotic clearance, and xenobiotic metabolism after DMP and DCHP treatments, while these responses were less pronounced with MMP (the metabolite of DMP). This is one of the few studies that demonstrated complementarity between gene expression analysis and organismal effects. This article is protected by copyright. All rights reserved.
BibTeX:
@article{Mathieu-Denoncourt2016,
  author = {Mathieu-Denoncourt, Justine and Martyniuk, Christopher J and Loughery, Jennifer R and Yargeau, Viviane and de Solla, Shane R and Langlois, Valerie S},
  title = {Lethal and sublethal effects of phthalate diesters in Silurana tropicalis larvae.},
  journal = {Environmental toxicology and chemistry / SETAC},
  year = {2016},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/26924002}
}
McAuley, J., Guthke, R., Schmidtke, M., Manchanda, H., Seidel, N., Blaess, M.F., Claus, R.A., Linde, J.J., Slevogt, H., Sauerbrei, A., Guthke, R. and Schmidtke, M. Differential Biphasic Transcriptional Host Response Associated with Coevolution of Hemagglutinin Quasispecies of Influenza A Virus 2016
Vol. 7(7) 
article  
BibTeX:
@article{McAuley2016,
  author = {McAuley, Julie and Guthke, Reinhard and Schmidtke, Michaela and Manchanda, Himanshu and Seidel, Nora and Blaess, Markus F and Claus, Ralf Alexander and Linde, Joerg Jörg and Slevogt, Hortense and Sauerbrei, Andreas and Guthke, Reinhard and Schmidtke, Michaela},
  title = {Differential Biphasic Transcriptional Host Response Associated with Coevolution of Hemagglutinin Quasispecies of Influenza A Virus},
  publisher = {Frontiers},
  year = {2016},
  volume = {7},
  number = {7}
}
Mehrfarjam, Z., Esmaeili, F., Shabani, L. and Ebrahimie, E. Induction of pancreatic β cell gene expression in mesenchymal stem cells 2016 Cell Biology International
Vol. 40(5), pp. 486-500 
article DOI URL 
BibTeX:
@article{Mehrfarjam2016,
  author = {Mehrfarjam, Zahra and Esmaeili, Fariba and Shabani, Leila and Ebrahimie, Esmaeil},
  title = {Induction of pancreatic β cell gene expression in mesenchymal stem cells},
  journal = {Cell Biology International},
  year = {2016},
  volume = {40},
  number = {5},
  pages = {486--500},
  url = {http://doi.wiley.com/10.1002/cbin.10567},
  doi = {http://doi.org/10.1002/cbin.10567}
}
Mercado, A.T., Yeh, J.-M., Chin, T.Y., Chen, W.S., Chen-Yang, Y.W. and Chen, C.-Y. The Effect of Chemically-Modified Electrospun Silica Nanofiber on the mRNA and miRNA Expression Profile of Neural Stem Cell Differentiation 2016 Journal of Biomedical Materials Research Part A  article DOI URL 
BibTeX:
@article{Mercado2016,
  author = {Mercado, Augustus T. and Yeh, Jui-Ming and Chin, Ting Yu and Chen, Wen Shuo and Chen-Yang, Yui Whei and Chen, Chung-Yung},
  title = {The Effect of Chemically-Modified Electrospun Silica Nanofiber on the mRNA and miRNA Expression Profile of Neural Stem Cell Differentiation},
  journal = {Journal of Biomedical Materials Research Part A},
  year = {2016},
  url = {http://doi.wiley.com/10.1002/jbm.a.35819},
  doi = {http://doi.org/10.1002/jbm.a.35819}
}
Moghieb, A., Bramlett, H.M., Das, J.H., Yang, Z., Selig, T., Yost, R.A., Wang, M.S., Dietrich, W.D. and Wang, K.K.W. Differential neuroproteomic and systems biology analysis of spinal cord injury. 2016 Molecular & cellular proteomics : MCP, pp. M116.058115-  article URL 
Abstract: Acute spinal cord injury (SCI) is a devastating condition with many consequences and no known effective treatment. Although it is quite easy to diagnose traumatic SCI, the assessment of injury severity and projection of disease progression or recovery are often challenging, as no consensus biomarkers have been clearly identified. Here rats were subjected to experimental moderate or severe thoracic SCI. At 24h and 7d post-injury, spinal cord segment caudal to injury center versus sham samples was harvested and subjected to differential proteomic analysis. Cationic/anionic-exchange (CAX) chromatography, followed by 1D polyacrylamide gel electrophoresis (PAGE), was used to reduce protein complexity. A reverse phase liquid chromatography-tandem mass spectrometry (RPLC-MS/MS) proteomic platform was then utilized to identify proteome changes associated with SCI. 22 and 22 proteins were upregulated at 24h and 7d after SCI, respectively; while 19 and 16 proteins are down- regulated at 24h and 7d after SCI, respectively, when compared to sham control. A subset of 12 proteins were identified as candidate SCI biomarkers TF (Transferrin), FASN (Fatty acid synthase), NME1 (Nucleoside diphosphate kinase 1), STMN1 (Stathmin 1), EEF2 (Eukaryotic translation elongation factor 2), CTSD (Cathepsin D), ANXA1 (Annexin A1), ANXA2 (Annexin A2), PGM1 (Phosphoglucomutase 1), PEA15 (Phosphoprotein enriched in astrocytes 15), GOT2 (Glutamic-oxaloacetic transaminase 2) and TPI-1 (Triosephosphate isomerase 1), data are available via ProteomeXchange with identifierPXD003473. In addition, Transferrin, Cathepsin D, and TPI-1 and PEA15 were further verified in rat spinal cord tissue and/or CSF samples after SCI and in human CSF samples from moderate/severe SCI patients. Lastly, a systems biology approach was utilized to determine the critical biochemical pathways and interactome in the pathogenesis of SCI. Thus, SCI candidate biomarkers identified can be used to correlate with disease progression or to identify potential SCI therapeutic targets.
BibTeX:
@article{Moghieb2016,
  author = {Moghieb, Ahmed and Bramlett, Helen M and Das, Jyotirmoy H and Yang, Zhihui and Selig, Tyler and Yost, Richard A and Wang, Michael S and Dietrich, W Dalton and Wang, Kevin K W},
  title = {Differential neuroproteomic and systems biology analysis of spinal cord injury.},
  journal = {Molecular & cellular proteomics : MCP},
  year = {2016},
  pages = {M116.058115--},
  url = {http://www.mcponline.org/content/early/2016/05/05/mcp.M116.058115.abstract}
}
Mullen, M. and Gonzalez-Perez, R. Leptin-Induced JAK/STAT Signaling and Cancer Growth 2016 Vaccines
Vol. 4(3), pp. 26 
article DOI URL 
Abstract: Growth factor and cytokine signaling can influence the development of several cancer types. One of the key players in the development of cancer is the Janus kinas (JAK) signal transducer of activators of transcription (STAT) signaling pathway. The majority of growth factors and cytokine interactions with their membrane-bound receptors trigger JAK-STAT activation. The influential relationship between obesity and cancer is a fact. However, there is a complex sequence of events contributing to the regulation of this mechanism to promote tumor growth, yet to be fully elucidated. The JAK-STAT pathway is influenced by obesity-associated changes that have been shown to impact cancer growth and progression. This intricate process is highly regulated by a vast array of adipokines and cytokines that exert their pleiotropic effects on cancer cells to enhance metastasis to distant target sites. Leptin is a cytokine, or more precise, an adipokine secreted mainly by adipose tissue that requires JAK-STAT activation to exert its biological functions. Leptin is the central regulator of energy balance and appetite. Leptin binding to its receptor OB-R in turn activates JAK-STAT, which induces proliferation, angiogenesis, and anti-apoptotic events in normal cells and malignant cells expressing the receptor. Leptin also induces crosstalk with Notch and IL-1 (NILCO), which involves other angiogenic factors promoting tumor growth. Therefore, the existence of multiple novel classes of therapeutics that target the JAK/STAT pathway has significant clinical implications. Then, the identification of the signaling networks and factors that regulate the obesity-cancer link to which potential pharmacologic interventions can be implemented to inhibit tumor growth and metastasis. In this review, we will discuss the specific relationship between leptin-JAK-STAT signaling and cancer.
BibTeX:
@article{Mullen2016,
  author = {Mullen, McKay and Gonzalez-Perez, Ruben},
  title = {Leptin-Induced JAK/STAT Signaling and Cancer Growth},
  journal = {Vaccines},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2016},
  volume = {4},
  number = {3},
  pages = {26},
  url = {http://www.mdpi.com/2076-393X/4/3/26},
  doi = {http://doi.org/10.3390/vaccines4030026}
}
Ortea, I., O'Connor, G. and Maquet, A. Review on proteomics for food authentication 2016 Journal of Proteomics  article DOI  
Abstract: Consumers have the right to know what is in the food they are eating. Accordingly, European and global food regulations require that the provenance of the food can be guaranteed from farm to fork. Many different instrumental techniques have been proposed for food authentication. Although traditional methods are still being used, new approaches such as genomics, proteomics, and metabolomics are helping to complement existing methodologies for verifying the claims made about certain food products. During the last decade, proteomics (the large-scale analysis of proteins in a particular biological system at a particular time) has been applied to different research areas within food technology. Since proteins can be used as markers for many properties of a food, even indicating processes to which the food has been subjected, they can provide further evidence of the foods labeling claim. This review is a comprehensive and updated overview of the applications, drawbacks, advantages, and challenges of proteomics for food authentication in the assessment of the foods compliance with labeling regulations and policies.

SIGNIFICANCE
This review paper provides a comprehensive and critical overview of the application of proteomics approaches to determine the authenticity of several food products updating the performances and current limitations of the applied techniques in both laboratory and industrial environments.
BibTeX:
@article{Ortea2016,
  author = {Ortea, Ignacio and O'Connor, Gavin and Maquet, Alain},
  title = {Review on proteomics for food authentication},
  journal = {Journal of Proteomics},
  year = {2016},
  doi = {http://doi.org/10.1016/j.jprot.2016.06.033}
}
Pang, Myung-geol (Seoul, K. and Kwon, Woo-sung (Seoul, K. METHOD OF PREDICTING ANIMAL LITTER SIZE USING PROTEIN BIOMARKERS RELATED WITH FERTILITY, AND METHOD OF PREDICTING ANIMAL SPERM QUALITY AND LITTER SIZE USING CHLORTETRACYCLINE STAINING 2016   misc URL 
Abstract: The present invention relates to a method of predicting animal litter size using a fertility-related protein marker, and more particularly, to the discovery of a sperm marker that is expressed differently depending on animal fertility, a marker composition for predicting litter size, which comprises an antibody that binds specifically to the marker, and a method of predicting animal litter size using the marker composition. Moreover, the present invention relates to a method of predicting animal semen quality and litter size by chlortetracycline staining, and more particularly, to a method of predicting of animal litter size by measuring the motility, motion kinematics or capacitation status of sperm. When the animal sperm-derived protein marker according to the present invention is used, the litter size of individuals can be predicted by analyzing a protein that is expressed differently depending on litter size. When the method of animal semen quality and litter size by chlortetracycline staining is used, the fertility of sperm and the litter size of individuals can be predicted. According to the present invention, superior species having high sperm fertility and high litter size can be selected based on information provided by the method. Thus, the present invention is highly useful for the sustainable production of animals.

BibTeX:
@misc{PangMyung-geolSeoul2016,
  author = {Pang, Myung-geol (Seoul, KR) and Kwon, Woo-sung (Seoul, KR)},
  title = {METHOD OF PREDICTING ANIMAL LITTER SIZE USING PROTEIN BIOMARKERS RELATED WITH FERTILITY, AND METHOD OF PREDICTING ANIMAL SPERM QUALITY AND LITTER SIZE USING CHLORTETRACYCLINE STAINING},
  year = {2016},
  url = {http://www.freepatentsonline.com/y2016/0154002.html}
}
Pashaiasl, M., Ebrahimi, M. and Ebrahimie, E. Identification of the key regulating genes of diminished ovarian reserve (DOR) by network and gene ontology analysis 2016 Molecular Biology Reports, pp. 1-15  article DOI URL 
BibTeX:
@article{Pashaiasl2016,
  author = {Pashaiasl, Maryam and Ebrahimi, Mansour and Ebrahimie, Esmaeil},
  title = {Identification of the key regulating genes of diminished ovarian reserve (DOR) by network and gene ontology analysis},
  journal = {Molecular Biology Reports},
  publisher = {Springer Netherlands},
  year = {2016},
  pages = {1--15},
  url = {http://link.springer.com/10.1007/s11033-016-4025-8},
  doi = {http://doi.org/10.1007/s11033-016-4025-8}
}
Paullin, T. Gene Expression Profiling and the Role of HSF1 in Ovarian Cancer 3D Spheroid Models 2016   article URL 
BibTeX:
@article{Paullin2016,
  author = {Paullin, Trillitye},
  title = {Gene Expression Profiling and the Role of HSF1 in Ovarian Cancer 3D Spheroid Models},
  year = {2016},
  url = {http://scholarcommons.usf.edu/etd http://scholarcommons.usf.edu/etd/6563}
}
Pawlowski, K., Leroux, C., Faulconnier, Y., Boby, C., de la Foye, A., Durand, D. and Pires, J.A.A. 0129 Liver transcriptome modifications by nutrient restriction in early lactation Holstein cows challenged with intramammary lipopolysaccharide. 2016 Journal of Animal Science
Vol. 94(supplement5), pp. 60 
article DOI URL 
BibTeX:
@article{Pawlowski2016,
  author = {Pawlowski, K. and Leroux, C. and Faulconnier, Y. and Boby, C. and de la Foye, A. and Durand, D. and Pires, J. A. A.},
  title = {0129 Liver transcriptome modifications by nutrient restriction in early lactation Holstein cows challenged with intramammary lipopolysaccharide.},
  journal = {Journal of Animal Science},
  publisher = {American Society of Animal Science},
  year = {2016},
  volume = {94},
  number = {supplement5},
  pages = {60},
  url = {https://dl.sciencesocieties.org/publications/jas/abstracts/94/supplement5/60a},
  doi = {http://doi.org/10.2527/jam2016-0129}
}
Peng Zhou, Benjamin H Lehrman, Z.H. Sparse Representation based Genetic Biomarker Evaluation for Congenital Heart Defects 2016 Med One
Vol. 1(4), pp. 3 
article DOI URL 
Abstract: Background: Congenital heart defects (CHD) are the most common type of birth defect, affecting approximately 8 out of every 1,000 newborns. Hundreds of genes have been reported as CHD candidate genes. Nevertheless, each patient/patient group may demonstrate unique etiologic characteristics that need personalized treatment. Methods: We proposed a sparse representation based variable selection (SRVS) approach to select disease-related genetic markers from a huge disease candidate gene pool acquired from ResNet relation database. The proposed approach has been applied to evaluate 167 CHD candidate genes, followed by validation on a microarray expression data set. Pathway enrichment analysis (PEA), sub-network enrichment analysis (SNEA) and network connectivity analysis (NCA) were conducted to study the functional profile of the variables selected by SRVS and compare them with previous reported genetic markers. Results: A significant high disease predication accuracy of 81.40 % was acquired (permutation p-value textless 0.0002) using the top 24 SRVS selected genes, which were enriched within multiple pathways and sub-networks that were previously implicated with CHD. In contrast, using the most frequently reported genes out of the 167 CHD candidate genes, the highest accuracy of 69.77 % was reached with permutation p-value = 0.017. Additionally, enrichment analysis and NCA showed that the top genes selected by the proposed SRVS approach were strongly related to the frequently reported CHD genes, although a functional difference was present. Conclusion: Our study suggests that SRVS is an effective method in data driven variable selection for CHD. Furthermore, frequently reported CHD candidate genes might not be the best biomarkers for a specific CHD patient/ patient group. Key Words: Congenital heart defects; Sparse Representation; Variables selection; ResNet Database
BibTeX:
@article{PengZhouBenjaminHLehrman2016,
  author = {Peng Zhou, Benjamin H Lehrman, Zheng Hongping},
  title = {Sparse Representation based Genetic Biomarker Evaluation for Congenital Heart Defects},
  journal = {Med One},
  year = {2016},
  volume = {1},
  number = {4},
  pages = {3},
  url = {http://mo.qingres.com/UpLoad/PdfFile/Mo856.pdf},
  doi = {http://doi.org/10.20900/mo.20160016}
}
Petitot, F., Frelon, S., Chambon, C., Paquet, F. and Guipaud, O. Proteome changes in rat serum after a chronic ingestion of enriched uranium: toward a biological signature of internal contamination and radiological effect 2016 Toxicology Letters  article DOI  
Abstract: The civilian and military use of uranium results in an increased risk of human exposure. The toxicity of uranium results from both its chemical and radiological properties that vary with isotopic composition. Validated biomarkers of health effects associated with exposure to uranium are neither sensitive nor specific to uranium radiotoxicity and/or radiological effect. This study aimed at investigating if serum proteins could be useful as biomarkers of both uranium exposure and radiological effect. Male Sprague-Dawley rats were chronically exposed through drinking water to low levels (40mg/L, corresponding to 1mg of uranium per animal per day) of either 4% 235U-enriched uranium (EU) or 12% EU during 6 weeks. A proteomics approach based on two-dimensional electrophoresis (2D-DIGE) and mass spectrometry (MS) was used to establish protein expression profiles that could be relevant for discriminating between groups, and to identify some differentially expressed proteins following uranium ingestion. It demonstrated that the expressions of 174 protein spots over 1045 quantified spots were altered after uranium exposure (ptextless0.05). Using both inferential and non-supervised multivariate statistics, we show sets of spots features that lead to a clear discrimination between controls and EU exposed groups on the one hand (21 spots), and between 4% EU and 12% EU on the other hand (7 spots), showing that investigation of the serum proteome may possibly be of relevance to address both uranium contamination and radiological effect. Finally, using bioinformatics tools, pathway analyses of differentially expressed MS-identified proteins find that acute phase, inflammatory and immune responses as well as oxidative stress are likely involved in the response to contamination, suggesting a physiological perturbation, but that does not necessarily lead to a toxic effect.
BibTeX:
@article{Petitot2016,
  author = {Petitot, F. and Frelon, S. and Chambon, C. and Paquet, F. and Guipaud, O.},
  title = {Proteome changes in rat serum after a chronic ingestion of enriched uranium: toward a biological signature of internal contamination and radiological effect},
  journal = {Toxicology Letters},
  year = {2016},
  doi = {http://doi.org/10.1016/j.toxlet.2016.05.026}
}
Petri, V., Hayman, G.T., Tutaj, M., Smith, J.R., Laulederkind, S., Wang, S.-J., Nigam, R., De Pons, J., Shimoyama, M. and Dwinell, M.R. Disease, Models, Variants and Altered Pathways—Journeying RGD Through the Magnifying Glass 2016 Computational and Structural Biotechnology Journal
Vol. 14, pp. 35-48 
article URL 
Abstract: Understanding the pathogenesis of disease is instrumental in delineating its progression mechanisms and for envisioning ways to counteract it. In the process, animal models represent invaluable tools for identifying disease-related loci and their genetic components. Amongst them, the laboratory rat is used extensively in the study of many conditions and disorders. The Rat Genome Database (RGD—http://rgd.mcw.edu) has been established to house rat genetic, genomic and phenotypic data. Since its inception, it has continually expanded the depth and breadth of its content. Currently, in addition to rat genes, QTLs and strains, RGD houses mouse and human genes and QTLs and offers pertinent associated data, acquired through manual literature curation and imported via pipelines. A collection of controlled vocabularies and ontologies is employed for the standardized extraction and provision of biological data. The vocabularies/ontologies allow the capture of disease and phenotype associations of rat strains and QTLs, as well as disease and pathway associations of rat, human and mouse genes. A suite of tools enables the retrieval, manipulation, viewing and analysis of data. Genes associated with particular conditions or with altered networks underlying disease pathways can be retrieved. Genetic variants in humans or in sequenced rat strains can be searched and compared. Lists of rat strains and species-specific genes and QTLs can be generated for selected ontology terms and then analyzed, downloaded or sent to other tools. From many entry points, data can be accessed and results retrieved. To illustrate, diabetes is used as a case study to initiate and embark upon an exploratory journey.
BibTeX:
@article{Petri2016,
  author = {Petri, Victoria and Hayman, G. Thomas and Tutaj, Marek and Smith, Jennifer R. and Laulederkind, Stan and Wang, Shur-Jen and Nigam, Rajni and De Pons, Jeff and Shimoyama, Mary and Dwinell, Melinda R.},
  title = {Disease, Models, Variants and Altered Pathways—Journeying RGD Through the Magnifying Glass},
  journal = {Computational and Structural Biotechnology Journal},
  year = {2016},
  volume = {14},
  pages = {35--48},
  url = {http://www.sciencedirect.com/science/article/pii/S2001037015000537}
}
Qu, Y., Elsasser, T.H., Garcia, M., Scholte, C.M., Connor, E.E., Newbold, J.R. and Moyes, K.M. 0127 The effects of short-term feeding of tocopherol mix (α-, β-, γ-, and δ) on blood neutrophil function and immunometabolic-related gene expression in lactating dairy cows. 2016 Journal of Animal Science
Vol. 94(supplement5), pp. 59 
article DOI URL 
BibTeX:
@article{Qu2016,
  author = {Qu, Y. and Elsasser, T. H. and Garcia, M. and Scholte, C. M. and Connor, E. E. and Newbold, J. R. and Moyes, K. M.},
  title = {0127 The effects of short-term feeding of tocopherol mix (α-, β-, γ-, and δ) on blood neutrophil function and immunometabolic-related gene expression in lactating dairy cows.},
  journal = {Journal of Animal Science},
  publisher = {American Society of Animal Science},
  year = {2016},
  volume = {94},
  number = {supplement5},
  pages = {59},
  url = {https://dl.sciencesocieties.org/publications/jas/abstracts/94/supplement5/59a},
  doi = {http://doi.org/10.2527/jam2016-0127}
}
Quillen, E.E., Blangero, J. and Almasy, L. A variance component method for integrated pathway analysis of gene expression data. 2016 BMC proceedings
Vol. 10(Suppl 7), pp. 337-342 
article URL 
Abstract: BACKGROUND: The application of pathway and gene-set based analyses to high-throughput data is increasingly common and represents an effort to understand underlying biology where single-gene or single-marker analyses have failed. Many such analyses rely on the a priori identification of genes associated with the trait of interest. In contrast, this variance-component-based approach creates a similarity matrix of individuals based on the expression of genes in each pathway.

METHODS: We compared 16 methods of calculating similarity for positive control matrices based on probes for the genes used to model the simulated Genetic Analysis Workshop phenotypes.

RESULTS: A simple correlation matrix outperforms the other methods by identifying pathways associated with the simulated phenotypes at nearly twice the rate expected based on the associations of the component transcripts and an approximate false-positive rate of 0.05.

CONCLUSIONS: This method has a number of additional advantages compared to single-transcript and pathway overrepresentation analyses, including the ability to estimate the proportion of variation explained by each pathway and the logistical advantage of only calculating the distance matrices once for each messenger RNA data set regardless of the number of phenotypes. Additionally, it offers a significant reduction in the multiple testing burden over individual consideration of each probe.
BibTeX:
@article{Quillen2016,
  author = {Quillen, Ellen E and Blangero, John and Almasy, Laura},
  title = {A variance component method for integrated pathway analysis of gene expression data.},
  journal = {BMC proceedings},
  year = {2016},
  volume = {10},
  number = {Suppl 7},
  pages = {337--342},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=5133490&tool=pmcentrez&rendertype=abstract}
}
Rahman, M.S., Kwon, W.-S., Yoon, S.-J., Park, Y.-J., Ryu, B.-Y. and Pang, M.-G. A novel approach to assessing bisphenol-A hazards using an in vitro model system. 2016 BMC genomics
Vol. 17, pp. 577 
article URL 
Abstract: BACKGROUND: Although the toxicological impacts of the xenoestrogen bisphenol-A (BPA) have been studied extensively, but the mechanism of action is poorly understood. Eventually, no standard method exists for evaluating the possible health hazards of BPA exposure. Considering mice spermatozoa as a potential in vitro model, we investigated the effects of BPA exposure (0.0001, 0.01, 1, and 100 μM for 6 h) on spermatozoa and the related mechanisms of action. The same doses were also employed to evaluate protein profiles of spermatozoa as a means to monitor their functional affiliation to diseases.

RESULTS: Our results demonstrated that high concentrations of BPA negatively affect sperm motility, viability, mitochondrial functions, and intracellular ATP levels by activating the mitogen-activated protein kinase, phosphatidylinositol 3-kinase, and protein kinase-A pathways. Moreover, short-term exposure of spermatozoa to high concentrations of BPA induced differential expressions of 24 proteins. These effects appeared to be caused by protein degradation and phosphorylation in spermatozoa. Proteins differentially expressed in spermatozoa from BPA treatment groups are putatively involved in the pathogenesis of several diseases, mainly cancer, carcinoma, neoplasm, and infertility.

CONCLUSIONS: Based on these results, we propose that BPA adversely affects sperm function by the activation of several kinase pathways in spermatozoa. In addition, BPA-induced changes in the sperm proteome might be partly responsible for the observed effects in spermatozoa, subsequently involve in the pathogenesis of many diseases. Therefore, we anticipated that current strategy might broadly consider for the health hazards assessment of other toxicological agents.
BibTeX:
@article{Rahman2016,
  author = {Rahman, Md Saidur and Kwon, Woo-Sung and Yoon, Sung-Jae and Park, Yoo-Jin and Ryu, Buom-Yong and Pang, Myung-Geol},
  title = {A novel approach to assessing bisphenol-A hazards using an in vitro model system.},
  journal = {BMC genomics},
  year = {2016},
  volume = {17},
  pages = {577},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4977886&tool=pmcentrez&rendertype=abstract}
}
Reins, R.Y., Mesmar, F., Williams, C. and McDermott, A.M. Vitamin D Induces Global Gene Transcription in Human Corneal Epithelial Cells: Implications for Corneal Inflammation. 2016 Investigative ophthalmology & visual science
Vol. 57(6), pp. 2689-98 
article URL 
Abstract: PURPOSE: Our previous studies show that human corneal epithelial cells (HCEC) have a functional vitamin D receptor (VDR) and respond to vitamin D by dampening TLR-induced inflammation. Here, we further examined the timing of the cytokine response to combined vitamin D-TLR treatment and used genome-wide microarray analysis to examine the effect of vitamin D on corneal gene expression.

METHODS: Telomerase-immortalized HCEC (hTCEpi) were stimulated with polyinosinic-polycytidylic acid (poly[I:C]) and 1,25-dihydroxyvitamin D3 (1,25D3) for 2 to 24 hours and interleukin (IL)-8 expression was examined by quantitative (q)PCR and ELISA. Telomerase-immortalized HCEC and SV40-HCEC were treated with 1,25D3 and used in genome-wide microarray analysis. Expression of target genes was validated using qPCR in both cell lines and primary HCEC. For confirmation of IκBα protein, hTCEpi were treated with 1,25D3 for 24 hours and cell lysates used in an ELISA.

RESULTS: Treatment with 1,25D3 increased poly(I:C)-induced IL-8 mRNA and protein expression after 2 to 6 hours. However, when cells were pretreated with 1,25D3 for 24 hours, 1,25D3 decreased cytokine expression. For microarray analysis, 308 genes were differentially expressed by 1,25D3 treatment in hTCEpi, and 69 genes in SV40s. Quantitative (q)PCR confirmed the vitamin D-mediated upregulation of target genes, including nuclear factor of κ light polypeptide gene enhancer in B-cells inhibitor, α (IκBα). In addition to increased transcript levels, IκBα protein was increased by 28% following 24 hours of vitamin D treatment.

CONCLUSIONS: Microarray analysis demonstrates that vitamin D regulates numerous genes in HCEC and influences TLR signaling through upregulation of IκBα. These findings are important in dissecting the role of vitamin D at the ocular surface and highlight the need for further research into the functions of vitamin D and its influence on corneal gene expression.
BibTeX:
@article{Reins2016,
  author = {Reins, Rose Y and Mesmar, Fahmi and Williams, Cecilia and McDermott, Alison M},
  title = {Vitamin D Induces Global Gene Transcription in Human Corneal Epithelial Cells: Implications for Corneal Inflammation.},
  journal = {Investigative ophthalmology & visual science},
  publisher = {The Association for Research in Vision and Ophthalmology},
  year = {2016},
  volume = {57},
  number = {6},
  pages = {2689--98},
  url = {http://iovs.arvojournals.org/article.aspx?articleid=2524810}
}
Rengaraj, D., Truong, A.D., Lee, S.-H., Lillehoj, H.S. and Hong, Y.H. Expression analysis of cytosolic DNA-sensing pathway genes in the intestinal mucosal layer of necrotic enteritis-induced chicken 2016 Veterinary Immunology and Immunopathology
Vol. 170, pp. 1-12 
article URL 
Abstract: Necrotic enteritis (NE) is a serious problem to the poultry farms, which report NE outbreaks more than once per year, as a result of the inappropriate use of antibiotics in the feed. The NE affected bird die rapidly as a result of various pathophysiological complications in the intestine and immune system. Also, several studies have reported that the genes exclusively related to intestine and immune functions are significantly altered in response to NE. In this study, NE was induced in two genetically disparate chicken lines that are resistant (line 6.3) and sensitive (line 7.2) to avian leukosis and Marek's disease. The intestinal mucosal layer was collected from NE-induced and control chickens, and subjected to RNA-sequencing analysis. The involvement of differentially expressed genes in the intestinal mucosal layer of line 6.3 and 7.2 with the immune system-related pathways was investigated. Among the identified immune system-related pathways, a candidate pathway known as chicken cytosolic DNA-sensing pathway (CDS pathway) was selected for further investigation. RNA-sequencing and pathway analysis identified a total of 21 genes that were involved in CDS pathway and differentially expressed in the intestinal mucosal layer of lines 6.3 and 7.2. The expression of CDS pathway genes was further confirmed by real-time qPCR. In the results, a majority of the CDS pathway genes were significantly altered in the NE-induced intestinal mucosal layer from lines 6.3 and 7.2. In conclusion, our study indicate that NE seriously affects several genes involved in innate immune defense and foreign DNA sensing mechanisms in the chicken intestinal mucosal layer. Identifying the immune genes affected by NE could be an important evidence for the protective immune response to NE-causative pathogens.
BibTeX:
@article{Rengaraj2016,
  author = {Rengaraj, Deivendran and Truong, Anh Duc and Lee, Sung-Hyen and Lillehoj, Hyun S. and Hong, Yeong Ho},
  title = {Expression analysis of cytosolic DNA-sensing pathway genes in the intestinal mucosal layer of necrotic enteritis-induced chicken},
  journal = {Veterinary Immunology and Immunopathology},
  year = {2016},
  volume = {170},
  pages = {1--12},
  url = {http://www.sciencedirect.com/science/article/pii/S0165242715300337}
}
Rengaraj, D. Annotation of the Y chromosome-encoded proteins in human, chimpanzee, and mouse 2016 , pp. 4-5  misc  
Abstract: The Y chromosome is a type of sex chromosome existing primarily in male mammalian species. The Y chromosome passes through the male gamete and determines male sex in humans, non-human primates, and other mammals. The mammalian Y chromosome varies from the X chromosome and the rest of the chromosomes primarily by size and its male sex-determining/spermatogenesis function. In the Y chromosome, male sex-determining function is exclusively located on the short arm, while the spermatogenesis function is distributed widely on the short and long arm. Deletions or mutations particularly in the male-specific region of Y chromosome (MSY) may cause male infertility. During the last few decades, researchers put forth an enormous effort to discover Y chromosome specific genes, and their encoded RNAs and proteins in humans, primates, and rodents. As a result, most of the genes and encoded proteins responsible for male-sex determination, testis development, and spermatogenesis have been discovered in humans, however not well established in non-human primates and rodents. Also, there might be a percent of proteins missing in human Y chromosome. The aim of this study is to annotate the proteins that encoded on the Y chromosome of humans, chimpanzee, and mouse using extensive bioinformatics tools. The human (annotation release 107), chimpanzee (annotation release 103), and mouse (annotation release 105) proteins were first retrieved from the National Center for Biotechnology Information (NCBI) eukaryotic genome annotation resource database. Then, the annotated human proteins (66 proteins) were compared with the core databases of human proteome project such as neXtProt, PeptideAtlas, and the Human Protein Atlas. The X-homologous of human Y chromosome-encoded proteins were searched using the NCBI Protein BLAST program. The cellular pathways and protein-protein interactions involving human Y chromosome-encoded proteins were searched using the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway mapping database, the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, and the Pathway Studio software. Finally, the human Y chromosome-encoded protein homologs/orthologs in chimpanzee and mouse were analyzed using the NCBI bl2seq program. This analysis resulted a significant number of homologous/orthologous proteins between human, chimpanzee and mouse. Our findings provide the scientific community with updated information on the Y chromosome-encoded proteins in humans, chimpanzee, and mouse.
BibTeX:
@misc{Rengaraj2016a,
  author = {Rengaraj, Deivendran},
  title = {Annotation of the Y chromosome-encoded proteins in human, chimpanzee, and mouse},
  year = {2016},
  pages = {4--5}
}
Riwaldt, S., Bauer, J., Wehland, M., Slumstrup, L., Kopp, S., Warnke, E., Dittrich, A., Magnusson, N., Pietsch, J., Corydon, T., Infanger, M. and Grimm, D. Pathways Regulating Spheroid Formation of Human Follicular Thyroid Cancer Cells under Simulated Microgravity Conditions: A Genetic Approach 2016 International Journal of Molecular Sciences
Vol. 17(4), pp. 528 
article URL 
Abstract: Microgravity induces three-dimensional (3D) growth in numerous cell types. Despite substantial efforts to clarify the underlying mechanisms for spheroid formation, the precise molecular pathways are still not known. The principal aim of this paper is to compare static 1g-control cells with spheroid forming (MCS) and spheroid non-forming (AD) thyroid cancer cells cultured in the same flask under simulated microgravity conditions. We investigated the morphology and gene expression patterns in human follicular thyroid cancer cells (UCLA RO82-W-1 cell line) after a 24 h-exposure on the Random Positioning Machine (RPM) and focused on 3D growth signaling processes. After 24 h, spheroid formation was observed in RPM-cultures together with alterations in the F-actin cytoskeleton. qPCR indicated more changes in gene expression in MCS than in AD cells. Of the 24 genes analyzed VEGFA, VEGFD, MSN, and MMP3 were upregulated in MCS compared to 1g-controls, whereas ACTB, ACTA2, KRT8, TUBB, EZR, RDX, PRKCA, CAV1, MMP9, PAI1, CTGF, MCP1 were downregulated. A pathway analysis revealed that the upregulated genes code for proteins, which promote 3D growth (angiogenesis) and prevent excessive accumulation of extracellular proteins, while genes coding for structural proteins are downregulated. Pathways regulating the strength/rigidity of cytoskeletal proteins, the amount of extracellular proteins, and 3D growth may be involved in MCS formation.
BibTeX:
@article{Riwaldt2016,
  author = {Riwaldt, Stefan and Bauer, Johann and Wehland, Markus and Slumstrup, Lasse and Kopp, Sascha and Warnke, Elisabeth and Dittrich, Anita and Magnusson, Nils and Pietsch, Jessica and Corydon, Thomas and Infanger, Manfred and Grimm, Daniela},
  title = {Pathways Regulating Spheroid Formation of Human Follicular Thyroid Cancer Cells under Simulated Microgravity Conditions: A Genetic Approach},
  journal = {International Journal of Molecular Sciences},
  publisher = {Multidisciplinary Digital Publishing Institute},
  year = {2016},
  volume = {17},
  number = {4},
  pages = {528},
  url = {http://www.mdpi.com/1422-0067/17/4/528/htm}
}
Sallin, P. and Jaźwiʼnska, A. Acute stress is detrimental to heart regeneration in zebrafish. 2016 Open biology
Vol. 6(3), pp. 160012- 
article URL 
Abstract: Psychological stress is one of the factors associated with human cardiovascular disease. Here, we demonstrate that acute perceived stress impairs the natural capacity of heart regeneration in zebrafish. Beside physical and chemical disturbances, intermittent crowding triggered an increase in cortisol secretion and blocked the replacement of fibrotic tissue with new myocardium. Pharmacological simulation of stress by pulse treatment with dexamethasone/adrenaline reproduced the regeneration failure, while inhibition of the stress response with anxiolytic drugs partially rescued the regenerative process. Impaired heart regeneration in stressed animals was associated with a reduced cardiomyocyte proliferation and with the downregulation of several genes, includingigfbp1b, a modulator of IGF signalling. Notably, daily stress induced a decrease in Igf1r phosphorylation. As cardiomyocyte proliferation was decreased in response to IGF-1 receptor inhibition, we propose that the stress-induced cardiac regenerative failure is partially caused by the attenuation of IGF signalling. These findings indicate that the natural regenerative ability of the zebrafish heart is vulnerable to the systemic paracrine stress response.
BibTeX:
@article{Sallin2016,
  author = {Sallin, Pauline and Jaźwiʼnska, Anna},
  title = {Acute stress is detrimental to heart regeneration in zebrafish.},
  journal = {Open biology},
  year = {2016},
  volume = {6},
  number = {3},
  pages = {160012--},
  url = {http://rsob.royalsocietypublishing.org/content/6/3/160012}
}
Samanta, L., Swain, N., Ayaz, A., Venugopal, V. and Agarwal, A. Post-Translational Modifications in sperm Proteome: The Chemistry of Proteome diversifications in the Pathophysiology of male factor infertility. 2016 Biochimica et biophysica acta
Vol. 1860(7), pp. 1450-1465 
article URL 
Abstract: BACKGROUND: The spermatozoa undergo a series of changes in the epididymis to mature after their release from the testis and subsequently in the female reproductive tract after ejaculation to get capacitated and achieve fertilization potential. Despite having a silenced protein synthesis machinery, the dynamic change in protein profile of the spermatozoa is attributed either to acquisition of new proteins via vescicular transport or to several post-translational modifications (PTMs) occurring on the already expressed protein complement.

SCOPE OF REVIEW: In this review emphasis is given on the PTMs already reported on the human sperm proteins under normal and pathologic conditions with particular reference to sperm function such as motility and fertilization. An attempt has been made to summarize different protocols and methods used for analysis of PTMs on sperm proteins and the newer trends those were emerging.

MAJOR CONCLUSIONS: Deciphering the differential occurrence of PTM on protein at ultrastructural level would give us a better insight of structure-function relationship of the particular protein. Protein with multiple PTMs could be used to generate the complex interaction network involved in a physiological function of a sperm. It can be speculated that crosstalk between different PTMs occurring either on same/ other proteins actually regulate the protein stability and activity both in physiological and pathological states.

GENERAL SIGNIFICANCE: The analytical prospective of various PTMs reported in human spermatozoa and their relevance to sperm function particularly in various pathophysiological states, would pave way for development of biomarkers for diagnosis, prognosis and therapeutic intervention of male infertility.
BibTeX:
@article{Samanta2016,
  author = {Samanta, Luna and Swain, Nirlipta and Ayaz, Ahmet and Venugopal, Vijay and Agarwal, Ashok},
  title = {Post-Translational Modifications in sperm Proteome: The Chemistry of Proteome diversifications in the Pathophysiology of male factor infertility.},
  journal = {Biochimica et biophysica acta},
  year = {2016},
  volume = {1860},
  number = {7},
  pages = {1450--1465},
  url = {http://www.sciencedirect.com/science/article/pii/S0304416516300927}
}
Sánchez Garayzar, A.B., Bahamonde, P.A., Martyniuk, C.J., Betancourt, M. and Munkittrick, K.R. Hepatic gene expression profiling in zebrafish (Danio rerio) exposed to the fungicide chlorothalonil 2016 Comparative Biochemistry and Physiology Part D: Genomics and Proteomics  article URL 
Abstract: Chlorothalonil (tetrachloroisophtalonitrile) is a fungicide that is widely used on agricultural crops around the world and as such, it is a ubiquitous aquatic contaminant. Despite high usage, the effects of this fungicide on non-target aquatic organisms have not been fully investigated. The aim of the present study was to (1) determine the effects of chlorothalonil toxicity on adult male zebrafish (Danio rerio) and (2) characterize the effects of chlorothalonil on gene expression patterns in the liver using two different concentrations of the fungicide, 0.007mg/L (environmentally-relevant) and 0.035mg/L (sublethal). These concentrations were selected from range-finding experiments that showed that zebrafish survival was significantly different from control animals at concentrations higher than 0.035mg/L but not below. Male zebrafish in both treatments of chlorothalonil showed a decrease in liversomatic index. A commercial Danio rerio microarray (4x44k) was used to determine gene expression profiles in male zebrafish liver following a 96h toxicological assay. Microarray analysis revealed that males exposed to both 0.007mg/L or 0.035mg/L of chlorothalonil showed increased transcriptional sub-networks related to cell division and DNA damage and decreased expression of gene networks associated with reproduction, immunity, and xenobiotic clearance. This study improves knowledge regarding whole animal exposures to chlorothalonil and identifies molecular signaling cascades that are sensitive to this fungicide in the fish liver.
BibTeX:
@article{SanchezGarayzar2016,
  author = {Sánchez Garayzar, Anny B. and Bahamonde, Paulina A. and Martyniuk, Christopher J. and Betancourt, Miguel and Munkittrick, Kelly R.},
  title = {Hepatic gene expression profiling in zebrafish (Danio rerio) exposed to the fungicide chlorothalonil},
  journal = {Comparative Biochemistry and Physiology Part D: Genomics and Proteomics},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S1744117X16300326}
}
Sarkar, D. and Saha, S. Computational Proteomics 2016 Systems Biology Application in Synthetic Biology, pp. 11-20  incollection DOI URL 
BibTeX:
@incollection{Sarkar2016,
  author = {Sarkar, Debasree and Saha, Sudipto},
  title = {Computational Proteomics},
  booktitle = {Systems Biology Application in Synthetic Biology},
  publisher = {Springer India},
  year = {2016},
  pages = {11--20},
  url = {http://link.springer.com/10.1007/978-81-322-2809-72},
  doi = {http://doi.org/10.1007/978-81-322-2809-7_2}
}
Sasagawa, S., Nishimura, Y., Okabe, S., Murakami, S., Ashikawa, Y., Yuge, M., Kawaguchi, K., Kawase, R., Okamoto, R., Ito, M. and Tanaka, T. Downregulation of GSTK1 Is a Common Mechanism Underlying Hypertrophic Cardiomyopathy. 2016 Frontiers in pharmacology
Vol. 7, pp. 162 
article URL 
Abstract: Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy and is associated with a number of potential outcomes, including impaired diastolic function, heart failure, and sudden cardiac death. Various etiologies have been described for HCM, including pressure overload and mutations in sarcomeric and non-sarcomeric genes. However, the molecular pathogenesis of HCM remains incompletely understood. In this study, we performed comparative transcriptome analysis to identify dysregulated genes common to five mouse HCM models of differing etiology: (i) mutation of myosin heavy chain 6, (ii) mutation of tropomyosin 1, (iii) expressing human phospholamban on a null background, (iv) knockout of frataxin, and (v) transverse aortic constriction. Gene-by-gene comparison identified five genes dysregulated in all five HCM models. Glutathione S-transferase kappa 1 (Gstk1) was significantly downregulated in the five models, whereas myosin heavy chain 7 (Myh7), connective tissue growth factor (Ctgf), periostin (Postn), and reticulon 4 (Rtn4) were significantly upregulated. Gene ontology comparison revealed that 51 cellular processes were significantly enriched in genes dysregulated in each transcriptome dataset. Among them, six processes (oxidative stress, aging, contraction, developmental process, cell differentiation, and cell proliferation) were related to four of the five genes dysregulated in all HCM models. GSTK1 was related to oxidative stress only, whereas the other four genes were related to all six cell processes except MYH7 for oxidative stress. Gene-gene functional interaction network analysis suggested correlative expression of GSTK1, MYH7, and actin alpha 2 (ACTA2). To investigate the implications of Gstk1 downregulation for cardiac function, we knocked out gstk1 in zebrafish using the clustered regularly interspaced short palindromic repeats/Cas9 system. We found that expression of the zebrafish homologs of MYH7, ACTA2, and actin alpha 1 were increased in the gstk1-knockout zebrafish. In vivo imaging of zebrafish expressing a fluorescent protein in cardiomyocytes showed that gstk1 deletion significantly decreased the end diastolic volume and, to a lesser extent, end systolic volume. These results suggest that downregulation of GSTK1 may be a common mechanism underlying HCM of various etiologies, possibly through increasing oxidative stress and the expression of sarcomere genes.
BibTeX:
@article{Sasagawa2016,
  author = {Sasagawa, Shota and Nishimura, Yuhei and Okabe, Shiko and Murakami, Soichiro and Ashikawa, Yoshifumi and Yuge, Mizuki and Kawaguchi, Koki and Kawase, Reiko and Okamoto, Ryuji and Ito, Masaaki and Tanaka, Toshio},
  title = {Downregulation of GSTK1 Is a Common Mechanism Underlying Hypertrophic Cardiomyopathy.},
  journal = {Frontiers in pharmacology},
  year = {2016},
  volume = {7},
  pages = {162},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4905960&tool=pmcentrez&rendertype=abstract}
}
Sheng, N., Zhou, X., Zheng, F., Pan, Y., Guo, X., Guo, Y., Sun, Y. and Dai, J. Comparative hepatotoxicity of 6:2 fluorotelomer carboxylic acid and 6:2 fluorotelomer sulfonic acid, two fluorinated alternatives to long-chain perfluoroalkyl acids, on adult male mice 2016 Archives of Toxicology, pp. 1-11  article DOI URL 
BibTeX:
@article{Sheng2016,
  author = {Sheng, Nan and Zhou, Xiujuan and Zheng, Fei and Pan, Yitao and Guo, Xuejiang and Guo, Yong and Sun, Yan and Dai, Jiayin},
  title = {Comparative hepatotoxicity of 6:2 fluorotelomer carboxylic acid and 6:2 fluorotelomer sulfonic acid, two fluorinated alternatives to long-chain perfluoroalkyl acids, on adult male mice},
  journal = {Archives of Toxicology},
  publisher = {Springer Berlin Heidelberg},
  year = {2016},
  pages = {1--11},
  url = {http://link.springer.com/10.1007/s00204-016-1917-2},
  doi = {http://doi.org/10.1007/s00204-016-1917-2}
}
Shin, G.H., Kang, B.-C. and Jang, D.J. Metabolic Pathways Associated with Kimchi, a Traditional Korean Food, Based on In Silico Modeling of Published Data 2016 Genomics & Informatics
Vol. 14(4), pp. 222 
article URL 
BibTeX:
@article{Shin2016,
  author = {Shin, Ga Hee and Kang, Byeong-Chul and Jang, Dai Ja},
  title = {Metabolic Pathways Associated with Kimchi, a Traditional Korean Food, Based on In Silico Modeling of Published Data},
  journal = {Genomics & Informatics},
  year = {2016},
  volume = {14},
  number = {4},
  pages = {222},
  url = {https://synapse.koreamed.org/search.php?where=aview&id=10.5808/GI.2016.14.4.222&code=0117GNI&vmode=FULL}
}
Silberstein, E., Ulitzky, L., Lima, L.A., Cehan, N., Teixeira-Carvalho, A., Roingeard, P. and Taylor, D.R. HCV-Mediated Apoptosis of Hepatocytes in Culture and Viral Pathogenesis. 2016 PloS one
Vol. 11(6), pp. e0155708 
article URL 
Abstract: Chronic Hepatitis C Virus (HCV) infection is associated with progressive liver injury and subsequent development of fibrosis and cirrhosis. The death of hepatocytes results in the release of cytokines that induce inflammatory and fibrotic responses. The mechanism of liver damage is still under investigation but both apoptosis and immune-mediated processes may play roles. By observing the changes in gene expression patterns in HCV-infected cells, both markers and the causes of HCV-associated liver injury may be elucidated. HCV genotype 1b virus from persistently infected VeroE6 cells induced a strong cytopathic effect when used to infect Huh7.5 hepatoma cells. To determine if this cytopathic effect was a result of apoptosis, ultrastructural changes were observed by electron microscopy and markers of programmed cell death were surveyed. Screening of a human PCR array demonstrated a gene expression profile that contained upregulated markers of apoptosis, including tumor necrosis factor, caspases and caspase activators, Fas, Bcl2-interacting killer (BIK) and tumor suppressor protein, p53, as a result of HCV genotype 1b infection. The genes identified in this study should provide new insights into understanding viral pathogenesis in liver cells and may possibly help to identify novel antiviral and antifibrotic targets.
BibTeX:
@article{Silberstein2016,
  author = {Silberstein, Erica and Ulitzky, Laura and Lima, Livia Alves and Cehan, Nicoleta and Teixeira-Carvalho, Andréa and Roingeard, Philippe and Taylor, Deborah R},
  title = {HCV-Mediated Apoptosis of Hepatocytes in Culture and Viral Pathogenesis.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {6},
  pages = {e0155708},
  url = {http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0155708}
}
Smith, L.C., Clark, J.C., Bisesi, J.H., Ferguson, P.L. and Sabo-Attwood, T. Differential recruitment of co-regulatory proteins to the human estrogen receptor 1 in response to xenoestrogens 2016 Comparative Biochemistry and Physiology Part D: Genomics and Proteomics  article URL 
Abstract: The diverse biological effects of xenoestrogens may be explained by their ability to differentially recruit co-regulatory proteins to the estrogen receptor (ER). We employed high-throughput receptor affinity binding and co-regulatory protein recruitment screening assays based on fluorescence polarization and time resolved florescence resonance energy transfer (TR-FRET), respectively, to assess xenoestrogen-specific binding and co-regulatory protein recruitment to the ER. Then we used a functional proteomic assay based on co-immunoprecipitation of ER-bound proteins to isolate and identify intact co-regulatory proteins recruited to a ligand-activated ER. Through these approaches, we revealed differential binding affinity of bisphenol-A (BPA) and genistein (GEN) to the human ERα (ESR1) and ligand-dependent recruitment of SRC-1 and SRC-3 peptides. Recruitment profiles were variable for each ligand and in some cases were distinct compared to 17β-estradiol (E2). For example, E2 and GEN recruited both SRC-1 and -3 peptides whereas BPA recruited only SRC-1 peptides. Results of the functional proteomic assay showed differential recruitment between ligands where E2 recruited the greatest number of proteins followed by BPA then GEN. A number of proteins share previously identified relationships with ESR1 as determined by STRING analysis. Although there was limited overlap in proteins identified between treatments, all ligands recruited proteins involved in cell growth as determined by subnetwork enrichment analysis (p textless 0.05). A comparative, in silico analysis revealed that fewer interactions exist between zebrafish (Danio rerio) esr1 and zebrafish orthologs of proteins identified in our functional proteomic analysis. Taken together these results identify recruitment of known and previously unknown co-regulatory proteins to ESR1 and highlight new methods to assay recruitment of low abundant and intact, endogenous co-regulatory proteins to ESR1 or other nuclear receptors, in both human and aquatic species.
BibTeX:
@article{Smith2016,
  author = {Smith, L. Cody and Clark, Jessica C. and Bisesi, Joseph H. and Ferguson, P. Lee and Sabo-Attwood, Tara},
  title = {Differential recruitment of co-regulatory proteins to the human estrogen receptor 1 in response to xenoestrogens},
  journal = {Comparative Biochemistry and Physiology Part D: Genomics and Proteomics},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S1744117X16300235}
}
Sobkowiak, A., Joʼnczyk, M., Adamczyk, J., Szczepanik, J., Solecka, D., Kuciara, I., Hetmaʼnczyk, K., Trzcinska-Danielewicz, J., Grzybowski, M., Skoneczny, M., Fronk, J. and Sowiʼnski, P. Molecular foundations of chilling-tolerance of modern maize. 2016 BMC genomics
Vol. 17(1), pp. 125 
article URL 
Abstract: BACKGROUND: Recent progress in selective breeding of maize (Zea mays L.) towards adaptation to temperate climate has allowed the production of inbred lines withstanding cold springs with temperatures below 8 °C or even close to 0 °C, indicating that despite its tropical origins maize is not inherently cold-sensitive.

RESULTS: Here we studied the acclimatory response of three maize inbred lines of contrasting cold-sensitivity selected basing on multi-year routine field data. The field observations were confirmed in the growth chamber. Under controlled conditions the damage to the photosynthetic apparatus due to severe cold treatment was the least in the cold-tolerant line provided that it had been subjected to prior moderate chilling, i.e., acclimation. The cold-sensitive lines performed equally poorly with or without acclimation. To uncover the molecular basis of the attained cold-acclimatability we performed comparative transcriptome profiling of the response of the lines to the cold during acclimation phase by means of microarrays with a statistical and bioinformatic data analysis.

CONCLUSIONS: The analyses indicated three mechanisms likely responsible for the cold-tolerance: acclimation-dependent modification of the photosynthetic apparatus, cell wall properties, and developmental processes. Those conclusions supported the observed acclimation of photosynthesis to severe cold at moderate chilling and were further confirmed by experimentally showing specific modification of cell wall properties and repression of selected miRNA species, general regulators of development, in the cold-tolerant line subjected to cold stress.
BibTeX:
@article{Sobkowiak2016,
  author = {Sobkowiak, Alicja and Joʼnczyk, Maciej and Adamczyk, Józef and Szczepanik, Jarosław and Solecka, Danuta and Kuciara, Iwona and Hetmaʼnczyk, Katarzyna and Trzcinska-Danielewicz, Joanna and Grzybowski, Marcin and Skoneczny, Marek and Fronk, Jan and Sowiʼnski, Paweł},
  title = {Molecular foundations of chilling-tolerance of modern maize.},
  journal = {BMC genomics},
  year = {2016},
  volume = {17},
  number = {1},
  pages = {125},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4761173&tool=pmcentrez&rendertype=abstract}
}
Soueid, J., Kourtian, S., Makhoul, N.J., Makoukji, J., Haddad, S., Ghanem, S.S., Kobeissy, F. and Boustany, R.-M. RYR2, PTDSS1 and AREG genes are implicated in a Lebanese population-based study of copy number variation in autism. 2016 Scientific reports
Vol. 6, pp. 19088 
article URL 
Abstract: Autism Spectrum Disorders (ASDs) are a group of neurodevelopmental disorders characterized by ritualistic-repetitive behaviors and impaired verbal and non-verbal communication. Objectives were to determine the contribution of genetic variation to ASDs in the Lebanese. Affymetrix Cytogenetics Whole-Genome 2.7 M and CytoScan(™) HD Arrays were used to detect CNVs in 41 Lebanese autistic children and 35 non-autistic, developmentally delayed and intellectually disabled patients. 33 normal participants were used as controls. 16 de novo CNVs and 57 inherited CNVs, including recognized pathogenic 16p11.2 duplications and 2p16.3 deletions were identified. A duplication at 1q43 classified as likely pathogenic encompasses RYR2 as a potential ASD candidate gene. This previously identified CNV has been classified as both pathogenic, and, of uncertain significance. A duplication of unknown significance at 10q11.22, proposed as a modulator for phenotypic disease expression in Rett syndrome, was also identified. The novel potential autism susceptibility genes PTDSS1 and AREG were uncovered and warrant further genetic and functional analyses. Previously described and novel genetic targets in ASD were identified in Lebanese families with autism. These findings may lead to improved diagnosis of ASDs and informed genetic counseling, and may also lead to untapped therapeutic targets applicable to Lebanese and non-Lebanese patients.
BibTeX:
@article{Soueid2016,
  author = {Soueid, Jihane and Kourtian, Silva and Makhoul, Nadine J and Makoukji, Joelle and Haddad, Sariah and Ghanem, Simona S and Kobeissy, Firas and Boustany, Rose-Mary},
  title = {RYR2, PTDSS1 and AREG genes are implicated in a Lebanese population-based study of copy number variation in autism.},
  journal = {Scientific reports},
  publisher = {Nature Publishing Group},
  year = {2016},
  volume = {6},
  pages = {19088},
  url = {http://www.nature.com/srep/2016/160108/srep19088/full/srep19088.html}
}
Suo, T., Wang, H. and Li, Z. Application of Proteomics in Research on Traditional Chinese Medicine 2016 Expert Review of Proteomics, pp. 14789450.2016.1220837  article DOI URL 
Abstract: AbstractIntroduction: Traditional Chinese medicine (TCM) is a widely used complementary alternative medicine approach. Although many aspects of its effectiveness have been approved clinically, rigorous scientific techniques are highly required to translate the promises from TCM into powerful modern therapies. In this respect, proteomics is useful because of its ability to unveil the underlying target proteins and/or protein biomarkers.Areas covered: In this review, we summarize the recent interplay between proteomics and research on TCM, ranging from exploration of the medicinal materials to the biological basis of TCM concepts, and from pathological studies to pharmacological investigations. We show that proteomic analyses provide preliminary biological evidence of the promises in TCM, and the integration of proteomics with other omics and bioinformatics offers a comprehensive methodology to address the complications of TCM.Expert Commentary: Currently, only limited information can be obtained regarding ...
BibTeX:
@article{Suo2016,
  author = {Suo, Tongchuan and Wang, Haixia and Li, Zheng},
  title = {Application of Proteomics in Research on Traditional Chinese Medicine},
  journal = {Expert Review of Proteomics},
  publisher = {Taylor & Francis},
  year = {2016},
  pages = {14789450.2016.1220837},
  url = {http://www.tandfonline.com/doi/full/10.1080/14789450.2016.1220837},
  doi = {http://doi.org/10.1080/14789450.2016.1220837}
}
Tallam, A., Perumal, T.M., Antony, P.M., Jäger, C., Fritz, J.V., Vallar, L., Balling, R., Del Sol, A. and Michelucci, A. Gene Regulatory Network Inference of Immunoresponsive Gene 1 (IRG1) Identifies Interferon Regulatory Factor 1 (IRF1) as Its Transcriptional Regulator in Mammalian Macrophages. 2016 PloS one
Vol. 11(2), pp. e0149050 
article URL 
Abstract: Immunoresponsive gene 1 (IRG1) is one of the highest induced genes in macrophages under pro-inflammatory conditions. Its function has been recently described: it codes for immune-responsive gene 1 protein/cis-aconitic acid decarboxylase (IRG1/CAD), an enzyme catalysing the production of itaconic acid from cis-aconitic acid, a tricarboxylic acid (TCA) cycle intermediate. Itaconic acid possesses specific antimicrobial properties inhibiting isocitrate lyase, the first enzyme of the glyoxylate shunt, an anaplerotic pathway that bypasses the TCA cycle and enables bacteria to survive on limited carbon conditions. To elucidate the mechanisms underlying itaconic acid production through IRG1 induction in macrophages, we examined the transcriptional regulation of IRG1. To this end, we studied IRG1 expression in human immune cells under different inflammatory stimuli, such as TNFα and IFNγ, in addition to lipopolysaccharides. Under these conditions, as previously shown in mouse macrophages, IRG1/CAD accumulates in mitochondria. Furthermore, using literature information and transcription factor prediction models, we re-constructed raw gene regulatory networks (GRNs) for IRG1 in mouse and human macrophages. We further implemented a contextualization algorithm that relies on genome-wide gene expression data to infer putative cell type-specific gene regulatory interactions in mouse and human macrophages, which allowed us to predict potential transcriptional regulators of IRG1. Among the computationally identified regulators, siRNA-mediated gene silencing of interferon regulatory factor 1 (IRF1) in macrophages significantly decreased the expression of IRG1/CAD at the gene and protein level, which correlated with a reduced production of itaconic acid. Using a synergistic approach of both computational and experimental methods, we here shed more light on the transcriptional machinery of IRG1 expression and could pave the way to therapeutic approaches targeting itaconic acid levels.
BibTeX:
@article{Tallam2016,
  author = {Tallam, Aravind and Perumal, Thaneer M and Antony, Paul M and Jäger, Christian and Fritz, Joëlle V and Vallar, Laurent and Balling, Rudi and Del Sol, Antonio and Michelucci, Alessandro},
  title = {Gene Regulatory Network Inference of Immunoresponsive Gene 1 (IRG1) Identifies Interferon Regulatory Factor 1 (IRF1) as Its Transcriptional Regulator in Mammalian Macrophages.},
  journal = {PloS one},
  year = {2016},
  volume = {11},
  number = {2},
  pages = {e0149050},
  url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4752512&tool=pmcentrez&rendertype=abstract}
}
Uppu, S., Krishna, A. and Gopalan, R. A review of machine learning and statistical approaches for detecting SNP interactions in high-dimensional genomic data 2016 IEEE/ACM Transactions on Computational Biology and Bioinformatics, pp. 1-1  article DOI URL 
BibTeX:
@article{Uppu2016,
  author = {Uppu, Suneetha and Krishna, Aneesh and Gopalan, Raj},
  title = {A review of machine learning and statistical approaches for detecting SNP interactions in high-dimensional genomic data},
  journal = {IEEE/ACM Transactions on Computational Biology and Bioinformatics},
  year = {2016},
  pages = {1--1},
  url = {http://ieeexplore.ieee.org/document/7765022/},
  doi = {http://doi.org/10.1109/TCBB.2016.2635125}
}
Völgyi, K., Udvari, E.B., Szabó, É.R., Györffy, B.A., Hunyadi-Gulyás, É., Medzihradszky, K., Juhász, G., Kékesi, K.A. and Dobolyi, Á. Maternal alterations in the proteome of the medial prefrontal cortex in rat 2016 Journal of Proteomics  article DOI URL 
Abstract: Proteomic differences between rat dams and control mothers deprived of their pups immediately after delivery were investigated in the medial prefrontal cortex (mPFC). A 2-D DIGE minimal dye technique combined with LC–MS/MS identified 32 different proteins that showed significant changes in expression in the mPFC, of which, 25 were upregulated and 7 were downregulated in dams. The identity of one significantly increased protein, the small heat-shock protein alpha-crystallin B chain (Cryab), was confirmed via Western blot analysis. Alpha-crystallin B chain was distributed in scattered cells in the mPFC, as demonstrated by immunohistochemistry. Furthermore, it was found to be localized in parvalbumin-containing neurons using double labeling. The elevation of its mRNA level in rat dams was also demonstrated via RT-PCR. The functional classification of the altered proteins was conducted using the UniProt and Gene Ontology protein databases. The identified proteins predominantly participate in synaptic transport and plasticity, neuron development, oxidative stress and apoptosis, and cytoskeleton organization. A common regulator and target analysis of these proteins determined using the Elsevier Pathway Studio Platform suggests that protein level changes associated with pup nursing are driven by growth factors and cytokines, while the MAP kinase pathway was identified as a common target. A high proportion of the proteins that were found to be altered in the mPFC are associated with depression.

BIOLOGICAL SIGNIFICANCE
The behavior and emotional state of females change robustly when they become mothers. The brain, which governs these changes, may also undergo molecular alterations in mothers. As no proteomics approaches have been applied regarding maternal changes in the brain, we addressed this issue in the mPFC as this brain area is the uppermost cortical center of maternal control and the associated mood changes. The high number of protein-level alterations found between mothers taking care of their litter and those without pups indicates that pup nursing is associated with cortical protein-level changes. Alterations in proteins participating in synaptic transport, plasticity and neuron development suggest neuroplastic changes in the maternal brain. In turn, the relatively high number of altered proteins in the mPFC associated with depression suggests that the physiological effects of the protein-level alterations in the maternal mPFC could promote the incidence of postpartum depression. Cryab, a protein confirmed to be increased during maternal behaviors, was selectively found in parvalbumin cells, which, as fast-spiking interneurons, are associated with depression. The function of Cryab should be further investigated to establish whether it can be used to identify drug targets for future drug development.
BibTeX:
@article{Volgyi2016,
  author = {Völgyi, Katalin and Udvari, Edina Brigitta and Szabó, Éva Rebeka and Györffy, Balázs András and Hunyadi-Gulyás, Éva and Medzihradszky, Katalin and Juhász, Gábor and Kékesi, Katalin Adrienna and Dobolyi, Árpád},
  title = {Maternal alterations in the proteome of the medial prefrontal cortex in rat},
  journal = {Journal of Proteomics},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S1874391916302068},
  doi = {http://doi.org/10.1016/j.jprot.2016.05.013}
}
Wang, L., Xu, W., Cao, L., Tian, T., Yang, M., Li, Z., Ping, F. and Fan, W. Differential Expression of Proteins Associated with the Hair Follicle Cycle - Proteomics and Bioinformatics Analyses. 2016 PloS one
Vol. 11(1), pp. e0146791 
article URL 
Abstract: Hair follicle cycling can be divided into the following three stages: anagen, catagen, and telogen. The molecular signals that orchestrate the follicular transition between phases are still unknown. To better understand the detailed protein networks controlling this process, proteomics and bioinformatics analyses were performed to construct comparative protein profiles of mouse skin at specific time points (0, 8, and 20 days). Ninety-five differentially expressed protein spots were identified by MALDI-TOF/TOF as 44 proteins, which were found to change during hair follicle cycle transition. Proteomics analysis revealed that these changes in protein expression are involved in Ca2+-regulated biological processes, migration, and regulation of signal transduction, among other processes. Subsequently, three proteins were selected to validate the reliability of expression patterns using western blotting. Cluster analysis revealed three expression patterns, and each pattern correlated with specific cell processes that occur during the hair cycle. Furthermore, bioinformatics analysis indicated that the differentially expressed proteins impacted multiple biological networks, after which detailed functional analyses were performed. Taken together, the above data may provide insight into the three stages of mouse hair follicle morphogenesis and provide a solid basis for potential therapeutic molecular targets for this hair disease.
BibTeX:
@article{Wang2016,
  author = {Wang, Lei and Xu, Wenrong and Cao, Lei and Tian, Tian and Yang, Mifang and Li, Zhongming and Ping, Fengfeng and Fan, Weixin},
  title = {Differential Expression of Proteins Associated with the Hair Follicle Cycle - Proteomics and Bioinformatics Analyses.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {1},
  pages = {e0146791},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146791}
}
Wang, C., Zhao, D., Shah, S.Z.A., Yang, W., Li, C. and Yang, L. Proteome Analysis of Potential Synaptic Vesicle Cycle Biomarkers in the Cerebrospinal Fluid of Patients with Sporadic Creutzfeldt–Jakob Disease 2016 Molecular Neurobiology, pp. 1-15  article DOI URL 
BibTeX:
@article{Wang2016a,
  author = {Wang, Chunyu and Zhao, Deming and Shah, Syed Zahid Ali and Yang, Wei and Li, Chaosi and Yang, Lifeng},
  title = {Proteome Analysis of Potential Synaptic Vesicle Cycle Biomarkers in the Cerebrospinal Fluid of Patients with Sporadic Creutzfeldt–Jakob Disease},
  journal = {Molecular Neurobiology},
  publisher = {Springer US},
  year = {2016},
  pages = {1--15},
  url = {http://link.springer.com/10.1007/s12035-016-0029-6},
  doi = {http://doi.org/10.1007/s12035-016-0029-6}
}
Wang, L., Guo, Y., Liu, W., Zhao, W., Song, G., Zhou, T., Huang, H., Guo, X. and Sun, F. Proteomic Analysis of Pachytene Spermatocytes of Sterile Hybrid Male Mice 2016 Biology of Reproduction, pp. biolreprod.116.138644  article DOI URL 
BibTeX:
@article{Wang2016b,
  author = {Wang, L. and Guo, Y. and Liu, W. and Zhao, W. and Song, G. and Zhou, T. and Huang, H. and Guo, X. and Sun, F.},
  title = {Proteomic Analysis of Pachytene Spermatocytes of Sterile Hybrid Male Mice},
  journal = {Biology of Reproduction},
  publisher = {Society for the Study of Reproduction},
  year = {2016},
  pages = {biolreprod.116.138644},
  url = {http://www.biolreprod.org/cgi/doi/10.1095/biolreprod.116.138644},
  doi = {http://doi.org/10.1095/biolreprod.116.138644}
}
Wang, X., Zhou, P., Buggs, S. and Teng, S. Genetic Biomarker Selection for Obsessive-Compulsive Disorder Genetic Biomarker Selection for Obsessive-Compulsive Disorder by Sparse Representation Based Variable Selection Method 2016 JPBS 2016
Vol. 11(4) 
article DOI  
Abstract: Background: Obsessive-compulsive disorder (OCD) is a debilitating neuropsychiatric condition estimated to afflict 1-3 % of the world population. Dozens of OCD candidate genes have been reported by an increased number of articles. Nevertheless, each patient/patient group may demonstrate unique etiologic characteristics that need personalized treatment.
BibTeX:
@article{Wang2016c,
  author = {Wang, Xuemin and Zhou, Peng and Buggs, Stephanie and Teng, Shaolei},
  title = {Genetic Biomarker Selection for Obsessive-Compulsive Disorder Genetic Biomarker Selection for Obsessive-Compulsive Disorder by Sparse Representation Based Variable Selection Method},
  journal = {JPBS 2016},
  year = {2016},
  volume = {11},
  number = {4},
  doi = {http://doi.org/10.20900/jpbs.20160015}
}
Xing, L., Martyniuk, C.J., Esau, C., Da Fonte, D.F. and Trudeau, V.L. Proteomic profiling reveals dopaminergic regulation of progenitor cell functions of goldfish radial glial cells in vitro 2016 Journal of Proteomics  article URL 
Abstract: Radial glial cells (RGCs) are stem-like cells found in the developing and adult central nervous system. They function as both a scaffold to guide neuron migration and as progenitor cells that support neurogenesis. Our previous study revealed a close anatomical relationship between dopamine neurons and RGCs in the telencephalon of female goldfish. In this study, label-free proteomics was used to identify the proteins in a primary RGC culture and to determine the proteome response to the selective dopamine D1 receptor agonist SKF 38393 (10μM), in order to better understand dopaminergic regulation of RGCs. A total of 689 unique proteins were identified in the RGCs and these were classified into biological and pathological pathways. Proteins such as nucleolin (6.9-fold) and ependymin related protein 1 (4.9-fold) were increased in abundance while proteins triosephosphate isomerase (10-fold) and phosphoglycerate dehydrogenase (5-fold) were decreased in abundance. Pathway analysis revealed that proteins that consistently changed in abundance across biological replicates were related to small molecules such as ATP, lipids and steroids, hormones, glucose, cyclic AMP and Ca2+. Sub-network enrichment analysis suggested that estrogen receptor signaling, among other transcription factors, is regulated by D1 receptor activation. This suggests that these signaling pathways are correlated to dopaminergic regulation of radial glial cell functions. Most proteins down-regulated by SKF 38393 were involved in cell cycle/proliferation, growth, death, and survival, which suggests that dopamine inhibits the progenitor-related processes of radial glial cells. Examples of differently expressed proteins including triosephosphate isomerase, nucleolin, phosphoglycerate dehydrogenase and capping protein (actin filament) muscle Z-line beta were validated by qPCR and western blot, which were consistent with MS/MS data in the direction of change. This is the first study to characterize the RGC proteome on a large scale in a vertebrate species. These data provide novel insight into glial protein networks that are associated with neuroendocrine function and neurogenesis in the teleost brain.

BIOLOGICAL SIGNIFICANCE
While the role of radial glial cells in organizing brain structure and neurogenesis has been well studied, protein profiling experiments in this unique cell type has not been conducted. This study is the first to profile the proteome of goldfish radial glial cells in culture and to study the regulation of progenitor functions of radial glial cells by the neurotransmitter dopamine. This study provides the foundation for molecular network analysis in fish radial glial cells, and identifies cellular processes and signaling pathways in these cells with roles in neurogenesis and neuroendocrine function. Lastly, this study begins to characterize signatures and biomarkers for specific neuroendocrine and neurogenesis disruptors.
BibTeX:
@article{Xing2016,
  author = {Xing, Lei and Martyniuk, Christopher J. and Esau, Crystal and Da Fonte, Dillon F. and Trudeau, Vance L.},
  title = {Proteomic profiling reveals dopaminergic regulation of progenitor cell functions of goldfish radial glial cells in vitro},
  journal = {Journal of Proteomics},
  year = {2016},
  url = {http://www.sciencedirect.com/science/article/pii/S1874391916301889}
}
Yi, D., Hou, Y., Wang, L., Zhao, D., Ding, B., Wu, T., Chen, H., Liu, Y., Kang, P. and Wu, G. Gene expression profiles in the intestine of lipopolysaccharide-challenged piglets 2016 Frontiers In Bioscience: Landmark
Vol. 21(1-1) 
article  
BibTeX:
@article{Yi2016,
  author = {Yi, Dan and Hou, Yongqing and Wang, Lei and Zhao, Di and Ding, Binying and Wu, Tao and Chen, Hongbo and Liu, Yulan and Kang, Ping and Wu, Guoyao},
  title = {Gene expression profiles in the intestine of lipopolysaccharide-challenged piglets},
  journal = {Frontiers In Bioscience: Landmark},
  year = {2016},
  volume = {21},
  number = {1-1}
}
Yoon, S.-J., Rahman, M.S., Kwon, W.-S., Park, Y.-J. and Pang, M.-G. Addition of Cryoprotectant Significantly Alters the Epididymal Sperm Proteome. 2016 PloS one
Vol. 11(3), pp. e0152690 
article URL 
Abstract: Although cryopreservation has been developed and optimized over the past decades, it causes various stresses, including cold shock, osmotic stress, and ice crystal formation, thereby reducing fertility. During cryopreservation, addition of cryoprotective agent (CPA) is crucial for protecting spermatozoa from freezing damage. However, the intrinsic toxicity and osmotic stress induced by CPA cause damage to spermatozoa. To identify the effects of CPA addition during cryopreservation, we assessed the motility (%), motion kinematics, capacitation status, and viability of epididymal spermatozoa using computer-assisted sperm analysis and Hoechst 33258/chlortetracycline fluorescence staining. Moreover, the effects of CPA addition were also demonstrated at the proteome level using two-dimensional electrophoresis. Our results demonstrated that CPA addition significantly reduced sperm motility (%), curvilinear velocity, viability (%), and non-capacitated spermatozoa, whereas straightness and acrosome-reacted spermatozoa increased significantly (p textless 0.05). Ten proteins were differentially expressed (two decreased and eight increased) (textgreater3 fold, p textless 0.05) after CPA, whereas NADH dehydrogenase flavoprotein 2, f-actin-capping protein subunit beta, superoxide dismutase 2, and outer dense fiber protein 2 were associated with several important signaling pathways (p textless 0.05). The present study provides a mechanistic basis for specific cryostresses and potential markers of CPA-induced stress. Therefore, these might provide information about the development of safe biomaterials for cryopreservation and basic ground for sperm cryopreservation.
BibTeX:
@article{Yoon2016,
  author = {Yoon, Sung-Jae and Rahman, Md Saidur and Kwon, Woo-Sung and Park, Yoo-Jin and Pang, Myung-Geol},
  title = {Addition of Cryoprotectant Significantly Alters the Epididymal Sperm Proteome.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {3},
  pages = {e0152690},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0152690}
}
Yun-Jungchoi1, Kiholee2, Woo-Jinpark1, Chankyupark1, D.-N., Jeongtaedo1, Hyuksong1, S.-K., Kwang-Wookpark6, Brown3, A., Samuel3, M., Murphy3, C., Prather3, R. and Jin-Hoikim Partiallossofinterleukin2receptorgammafunctionin pigsprovidesmechanisticinsightsforthestudyofhuman immunodeficiencysyndrome 2016   article DOI  
Abstract: See, stats, and : https : / / www . researchgate . net / publication / 305641068 Partial function for syndrome Article DOI : 10 . 18632 / oncotarget . 10812 READS 38 14 , including : Yunjung Konkuk 50 SEE Kiho Virginia 63 SEE Kwang- WookSunchon22,939SEECliftonUniversity89,252SEEAll-text,letting.Available:Jin-HoiRetrieved:01Oncotarget1www.impactjournals.com/oncotargetABSTRACTInthisstudy,wedescribedthephenotypeofmonoallelicinterleukin2receptorgammaknockout(mIL2RG+/Δ69-368KO)pigs.Approximately80%ofmIL2RG+/Δ69-368KOpigs(8/10)wereathymic,whereas20%(2/10)presentedarudimentarythymus.ThebodyweightofIL2RG+/Δ69-368KOpigsdevelopednormally.ImmunologicalanalysisshowedthatmIL2RG+/Δ69-368KOpigspossessedCD25+CD44-orCD25-CD44+cells,whereassingle(CD4orCD8)ordouble(CD4/8)positivecellswerelackinginmIL2RG+/Δ69-368KOpigs.CD3+cellsinthethymusofmIL2RG+/Δ69-368KOpigscontainedmainlyCD44+cellsand/orCD25+cells,whichincludedFOXP3+cells.TheseobservationsdemonstratedthatTcellsfrommIL2RG+/Δ69-368KOpigswereabletodeveloptotheDN3stage,butfailedtotransitiontowardtheDN4stage.Whole-transcriptomeanalysisofthymusandspleen,andsubsequentpathwayanalysisrevealedthatasubsetofgenesdifferentiallyexpressedfollowingthelossofIL2RGmightberesponsibleforbothimpairedT-cellreceptorandcytokine-mediatedsignalling.However,comparativeanalysisoftwomIL2RG+/Δ69-368
BibTeX:
@article{Yun-Jungchoi12016,
  author = {Yun-Jungchoi1 and Kiholee2 and Woo-Jinpark1 and Chankyupark1, Deug-Namkwon1 and Jeongtaedo1 and Hyuksong1, Seong-Keuncho5 and Kwang-Wookpark6 and Brown3, Alanan and Samuel3, Melissas and Murphy3, Cliftonn and Prather3, Randalls and Jin-Hoikim},
  title = {Partiallossofinterleukin2receptorgammafunctionin pigsprovidesmechanisticinsightsforthestudyofhuman immunodeficiencysyndrome},
  year = {2016},
  doi = {http://doi.org/10.18632/oncotarget.10812}
}
Zhang, L., Hapon, M.B., Goyeneche, A.A., Srinivasan, R., Gamarra-Luques, C.D., Callegari, E.A., Drappeau, D.D., Terpstra, E.J., Pan, B., Knapp, J.R., Chien, J., Wang, X., Eyster, K.M. and Telleria, C.M. Mifepristone increases mRNA translation rate, triggers the unfolded protein response, increases autophagic flux, and kills ovarian cancer cells in combination with proteasome or lysosome inhibitors 2016 Molecular Oncology  article URL 
BibTeX:
@article{Zhang2016,
  author = {Zhang, Lei and Hapon, Maria B. and Goyeneche, Alicia A. and Srinivasan, Rekha and Gamarra-Luques, Carlos D. and Callegari, Eduardo A. and Drappeau, Donis D. and Terpstra, Erin J. and Pan, Bo and Knapp, Jennifer R. and Chien, Jeremy and Wang, Xuejun and Eyster, Kathleen M. and Telleria, Carlos M.},
  title = {Mifepristone increases mRNA translation rate, triggers the unfolded protein response, increases autophagic flux, and kills ovarian cancer cells in combination with proteasome or lysosome inhibitors},
  journal = {Molecular Oncology},
  publisher = {Elsevier},
  year = {2016},
  url = {http://www.moloncol.org/article/S1574789116300357/fulltext}
}
Zhiyong Zhang, Weiyue Feng, Y.Z. Toxicology of Nanomaterials 2016   book URL 
Abstract: The network analysis can be carried out by pathway studio (Pathway Studio v9. 0 program, Ariadne Genomics, Inc.).
BibTeX:
@book{ZhiyongZhangWeiyueFeng2016,
  author = {Zhiyong Zhang, Weiyue Feng, Yuliang Zhao},
  title = {Toxicology of Nanomaterials},
  year = {2016},
  url = {https://books.google.com/books?hl=en&lr=langen&id=uxvqDAAAQBAJ&oi=fnd&pg=PA287&dq=Pathway+Studio&ots=OdGen51COr&sig=NdoZ7PAM3zJ7Gwa1prBAHwbaVHUv=onepage&q=Pathway Studio&f=false}
}
Zhou, P., Wang, Y., Cao, H. and Manor, L.C. Literature Data Mining and Enrichment Analysis Reveal Med One Literature Data Mining and Enrichment Analysis Reveal A Genetic Network of 423 Genes for Renal Cancer 2016
Vol. 1111(3310) 
article DOI  
Abstract: Background: Renal cancer (RC) is a type of cancer that starts in the cells of the kidneys. Around 208,500 new cases of renal cancer worldwide are diagnosed yearly, accounting for just under 2% of all cancers. People who have a family history of RC have an increased risk of developing the disease. Recent years, an increased number of researches have been reported hundreds of genes related to the development of the disease. However, no systemic study has summarized these findings and has provided an objective view of these genes reportedly associated with RC. Methods: We conducted a literature data mining (LDM) of over 1,100 articles covering publications from 1988 to April 2016, where 423 genes were reported to be associated with RC. We then performed a gene set enrichment analysis (GSEA) and a sub-network enrichment analysis (SNEA) to study the functional profile and pathogenic significance of these genes with RC. Lastly, we performed a network connectivity analysis (NCA) to study the associations between the reported genes. Literature and enrichment metrics analyses were used to discover genes with specific significance to the disease. Results: 329/423 genes enriched 100 pathways (ptextless1.2e-10), demonstrating multiple associations with RC. Ten genes (IL6, VEGFA, HIF1A, EGFR, PTEN, TP53, FGF2, CTNNB1, HMOX1, and BRCA1) were identified as the top genes associated with leukemia in terms of both functional diversity and replication frequency. Additionally, three novel genes, CD274, NOTCH1, and CREB1, were found to play roles within many significant RC related pathways, suggesting that they were worthy of further study. Moreover, SNEA and NCA results indicated that many of these genes work as a functional network that plays roles in the pathogenesis of other RC related disorders. Conclusion: Our results suggest that the genetic causes of RC were linked to a genetic network composed of a large group of genes. The gene lists, together with the literature and enrichment metrics provided in this study, can serve as a groundwork for further biological/genetic studies in the field.
BibTeX:
@article{Zhou2016,
  author = {Zhou, Peng and Wang, Yuping and Cao, Hongbao and Manor, Lydia C},
  title = {Literature Data Mining and Enrichment Analysis Reveal Med One Literature Data Mining and Enrichment Analysis Reveal A Genetic Network of 423 Genes for Renal Cancer},
  year = {2016},
  volume = {1111},
  number = {3310},
  doi = {http://doi.org/10.20900/mo.20160010}
}
Zhou, Y., Xu, J.C. and Xu, C.S. Co-expression network analysis prioritizes signaling pathways regulating liver regeneration after partial hepatectomy in rats 2016 funpecrp.com.br Genetics and Molecular Research Genet. Mol. Res
Vol. 15(152) 
article DOI URL 
Abstract: The liver has extraordinary powers of regeneration following partial hepatectomy (PH). Changes in gene expression levels play a key role in cell proliferation and differentiation during liver regeneration (LR). To understand the molecular mechanisms underlying LR, this study was designed to assess the time-dependent changes in rat hepatic gene expression. We obtained a gene expression profile of rat LR with high temporal resolution. We then constructed gene co-expression networks of regenerating liver tissue and identified 13 LR-specific modules from 1772 differentially expressed genes, and prioritized signaling pathways that regulated LR after PH. The results indicated that adipocytokine signaling, histone acetylation, and IL-6-related pathways play an important role in LR. Co-expression network analysis provides novel insight into understanding the molecular mechanisms behind LR.
BibTeX:
@article{Zhou2016a,
  author = {Zhou, Y and Xu, J C and Xu, C S},
  title = {Co-expression network analysis prioritizes signaling pathways regulating liver regeneration after partial hepatectomy in rats},
  journal = {funpecrp.com.br Genetics and Molecular Research Genet. Mol. Res},
  year = {2016},
  volume = {15},
  number = {152},
  url = {http://www.geneticsmr.com/sites/default/files/articles/year2016/vol15-2/pdf/gmr75961.pdf},
  doi = {http://doi.org/10.4238/gmr.15027596}
}
Zhu, R., Yang, T., Kobeissy, F., Mouhieddine, T.H., Raad, M., Nokkari, A., Gold, M.S., Wang, K.K. and Mechref, Y. The Effect of Chronic Methamphetamine Exposure on the Hippocampal and Olfactory Bulb Neuroproteomes of Rats. 2016 PloS one
Vol. 11(4), pp. e0151034 
article URL 
Abstract: Nowadays, drug abuse and addiction are serious public health problems in the USA. Methamphetamine (METH) is one of the most abused drugs and is known to cause brain damage after repeated exposure. In this paper, we conducted a neuroproteomic study to evaluate METH-induced brain protein dynamics, following a two-week chronic regimen of an escalating dose of METH exposure. Proteins were extracted from rat brain hippocampal and olfactory bulb tissues and subjected to liquid chromatography-mass spectrometry (LC-MS/MS) analysis. Both shotgun and targeted proteomic analysis were performed. Protein quantification was initially based on comparing the spectral counts between METH exposed animals and their control counterparts. Quantitative differences were further confirmed through multiple reaction monitoring (MRM) LC-MS/MS experiments. According to the quantitative results, the expression of 18 proteins (11 in the hippocampus and 7 in the olfactory bulb) underwent a significant alteration as a result of exposing rats to METH. 13 of these proteins were up-regulated after METH exposure while 5 were down-regulated. The altered proteins belonging to different structural and functional families were involved in processes such as cell death, inflammation, oxidation, and apoptosis.
BibTeX:
@article{Zhu2016,
  author = {Zhu, Rui and Yang, Tianjiao and Kobeissy, Firas and Mouhieddine, Tarek H and Raad, Mohamad and Nokkari, Amaly and Gold, Mark S and Wang, Kevin K and Mechref, Yehia},
  title = {The Effect of Chronic Methamphetamine Exposure on the Hippocampal and Olfactory Bulb Neuroproteomes of Rats.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2016},
  volume = {11},
  number = {4},
  pages = {e0151034},
  url = {http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0151034}
}
Data dissection | Scientific Computing World 2016   misc URL 
BibTeX:
@misc{,,
  title = {Data dissection | Scientific Computing World},
  year = {2016},
  url = {https://www.scientific-computing.com/feature/data-dissection-0}
}
Reduced bone marrow adrenergic receptor signaling modulates PVN inflammatory factors 2016 The FASEB Journal
Vol. 30(1 Supplement) 
article URL 
Abstract: INTRODUCTION Neurogenic hypertension is characterized by neuroinflammation and increased sympathetic nerve activity (SNA) to the periphery, including the bone marrow (BM). The BM SNA governs diurnal regulation of the BM hematopoietic cell turnover, with inflammatory cells typically released during the active period. We have previously shown that chronic increase in the BM SNA leads to elevation of inflammatory factors and release of inflammatory cells in angiotensin II (Ang II) hypertension (HTN). Moreover, extravasation of the BM-derived inflammatory cells to the brain cardioregulatory regions, including the paraventricular nucleus (PVN), contributes to neuroinflammation and thus the pathophysiology of HTN. Therefore, we hypothesize that reduction in the effects of SNA on BM inflammatory cells will result in suppression of the inflammatory profiles in BM and PVN.
BibTeX:
@article{,,
  title = {Reduced bone marrow adrenergic receptor signaling modulates PVN inflammatory factors},
  journal = {The FASEB Journal},
  year = {2016},
  volume = {30},
  number = {1 Supplement},
  url = {http://www.fasebj.org/content/30/1Supplement/1237.6.abstract}
}
In Pulmonary Artery Smooth Muscle Cells, HIF-1α Downregulates Endothelin Expression Via microRNA-543 (ATS Journals) 2016 American Thoracic Society International Conference Meetings Abstracts  article URL 
BibTeX:
@article{,,
  title = {In Pulmonary Artery Smooth Muscle Cells, HIF-1α Downregulates Endothelin Expression Via microRNA-543 (ATS Journals)},
  journal = {American Thoracic Society International Conference Meetings Abstracts},
  year = {2016},
  url = {http://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2016.193.1MeetingAbstracts.A7915}
}
Qingres-Functional network composed of 1,219 genes for Schizophrenia-- a literature data mining and enrichment analysis 2016   misc URL 
BibTeX:
@misc{,,
  title = {Qingres-Functional network composed of 1,219 genes for Schizophrenia-- a literature data mining and enrichment analysis},
  year = {2016},
  url = {http://jpbs.qingres.com/periodical/750}
}
Major histocompatibility complex expression in a rotenone model of Parkinson's disease in rats 2016   misc URL 
BibTeX:
@misc{,,
  title = {Major histocompatibility complex expression in a rotenone model of Parkinson's disease in rats},
  year = {2016},
  url = {http://www2.e-kenkyu.com/ftsjournal/uploads/manuscript/file/90/3101.pdf}
}
Altered Salivary Protein Profiles among Individuals Diagnosed with Cervical Dysplasia and Cervical Carcinoma in Situ 2016   misc URL 
BibTeX:
@misc{,,
  title = {Altered Salivary Protein Profiles among Individuals Diagnosed with Cervical Dysplasia and Cervical Carcinoma in Situ},
  year = {2016},
  url = {http://www.ccsenet.org/journal/index.php/cco/article/viewFile/57583/31188}
}
SoftGenetics, Elsevier Sign Software Integration Deal | GenomeWeb 2016   misc URL 
BibTeX:
@misc{,,
  title = {SoftGenetics, Elsevier Sign Software Integration Deal | GenomeWeb},
  year = {2016},
  url = {https://www.genomeweb.com/informatics/softgenetics-elsevier-sign-software-integration-deal}
}
Elsevier Continues Focus on Pharmacovigilance, Updates Sequence Analysis Software | GenomeWeb 2016   misc URL 
BibTeX:
@misc{,,
  title = {Elsevier Continues Focus on Pharmacovigilance, Updates Sequence Analysis Software | GenomeWeb},
  year = {2016},
  url = {https://www.genomeweb.com/informatics/elsevier-continues-focus-pharmacovigilance-updates-sequence-analysis-software}
}
Agarwal, P., Pathak, S., Lakhwani, D., Gupta, P., Asif, M.H. and Trivedi, P.K. Comparative analysis of transcription factor gene families from Papaver somniferum: identification of regulatory factors involved in benzylisoquinoline alkaloid biosynthesis 2015 Protoplasma, pp. 1-15  article DOI URL 
Abstract: Opium poppy (Papaver somniferum L.), known for biosynthesis of several therapeutically important benzylisoquinoline alkaloids (BIAs), has emerged as the premier organism to study plant alkaloid metabolism. The most prominent molecules produced in opium poppy include narcotic analgesic morphine, the cough suppressant codeine, the muscle relaxant papaverine and the anti-microbial agent sanguinarine and berberine. Despite several health benefits, biosynthesis of some of these molecules is very low due to tight temporal and spatial regulation of the genes committed to their biosynthesis. Transcription factors, one of the prime regulators of secondary plant product biosynthesis, might be involved in controlled biosynthesis of BIAs in P. somniferum. In this study, identification of members of different transcription factor gene families using transcriptome datasets of 10 cultivars of P. somniferum with distinct chemoprofile has been carried out. Analysis suggests that most represented transcription factor gene family in all the poppy cultivars is WRKY. Comparative transcriptome analysis revealed differential expression pattern of the members of a set of transcription factor gene families among 10 cultivars. Through analysis, two members of WRKY and one member of C3H gene family were identified as potential candidates which might regulate thebaine and papaverine biosynthesis, respectively, in poppy.
BibTeX:
@article{Agarwal2015,
  author = {Agarwal, Parul and Pathak, Sumya and Lakhwani, Deepika and Gupta, Parul and Asif, Mehar Hasan and Trivedi, Prabodh Kumar},
  title = {Comparative analysis of transcription factor gene families from Papaver somniferum: identification of regulatory factors involved in benzylisoquinoline alkaloid biosynthesis},
  journal = {Protoplasma},
  year = {2015},
  pages = {1--15},
  url = {http://link.springer.com/article/10.1007/s00709-015-0848-8},
  doi = {http://doi.org/10.1007/s00709-015-0848-8}
}
Alayev, A., Salamon, R.S., Berger, S.M., Schwartz, N.S., Cuesta, R., Snyder, R.B. and Holz, M.K. mTORC1 directly phosphorylates and activates ERα upon estrogen stimulation. 2015 Oncogene  article DOI URL 
Abstract: Breast cancer is the leading cause of cancer-related deaths among women. Approximately 75% of breast cancers are estrogen receptor-α (ERα) positive, underscoring the dependence of cancer cells on estrogen for growth and survival. Patients treated with endocrine therapy often develop resistance, either de novo or acquired, which in some cases is caused by aberrations within the growth factor signaling pathways. The mechanistic target of rapamycin complex 1 (mTORC1) has emerged as a critical node in estrogenic signaling. We have previously shown that mTORC1 can phosphorylate and activate ERα on S167 via its effector-the 40S ribosomal S6 kinase 1 (S6K1). Presently, we have uncovered a direct link between mTORC1 and ERα. We found that ERα binds to regulatory-associated protein of mTOR (Raptor) and causes it to translocate to the nucleus upon estrogen stimulation. In addition, we identified mTOR as the kinase that phosphorylates ERα on S104/106 and activates transcription of ER target genes. Our findings show a direct link between mTORC1 and ERα, which further implicates mTORC1 signaling in the pathogenesis of ER-positive breast cancer and provides rationale for FDA-approved use of mTORC1 inhibitors in combination with endocrine agents for treatment of this disease.Oncogene advance online publication, 2 November 2015; doi:10.1038/onc.2015.414.
BibTeX:
@article{Alayev2015,
  author = {Alayev, A and Salamon, R S and Berger, S M and Schwartz, N S and Cuesta, R and Snyder, R B and Holz, M K},
  title = {mTORC1 directly phosphorylates and activates ERα upon estrogen stimulation.},
  journal = {Oncogene},
  publisher = {Macmillan Publishers Limited},
  year = {2015},
  url = {http://dx.doi.org/10.1038/onc.2015.414},
  doi = {http://doi.org/10.1038/onc.2015.414}
}
Alisoltani, A., Shiran, B., Fallahi, H. and Ebrahimie, E. Gene regulatory network in almond (Prunus dulcis Mill.) in response to frost stress 2015 Tree Genetics & Genomes
Vol. 11(5), pp. 1-15 
article DOI URL 
BibTeX:
@article{Alisoltani2015,
  author = {Alisoltani, Arghavan and Shiran, Behrouz and Fallahi, Hossein and Ebrahimie, Esmaeil},
  title = {Gene regulatory network in almond (Prunus dulcis Mill.) in response to frost stress},
  journal = {Tree Genetics & Genomes},
  year = {2015},
  volume = {11},
  number = {5},
  pages = {1--15},
  url = {http://link.springer.com/article/10.1007/s11295-015-0929-z},
  doi = {http://doi.org/10.1007/s11295-015-0929-z}
}
Baldacci-Cresp, F., Moussawi, J., Leplé, J.-C., Van Acker, R., Kohler, A., Candiracci, J., Twyffels, L., Spokevicius, A.V., Bossinger, G., Laurans, F., Brunel, N., Vermeersch, M., Boerjan, W., El Jaziri, M. and Baucher, M. PtaRHE1, a Populus tremula x P. alba RING-H2 protein of the ATL family, has a regulatory role in secondary phloem fiber development 2015 The Plant Journal, pp. n/a-n/a  article DOI URL 
Abstract: REALLY INTERESTING NEW GENE (RING) proteins play important roles in the regulation of many processes by recognizing target proteins for ubiquitination. Previously, we have shown that the expression of PtaRHE1, encoding a Populus tremula x P. alba RING-H2 protein with E3 ubiquitin ligase activity, is associated with tissues undergoing secondary growth. To further elucidate the role of PtaRHE1 in vascular tissues, we have undertaken a reverse genetic analysis in poplar. Within stem secondary vascular tissues, PtaRHE1 and its corresponding protein are expressed predominantly in the phloem. Down-regulation of PtaRHE1 in poplar by artificial miRNA triggers alterations in phloem fiber patterning characterized by an increased portion of secondary phloem fibers that have a reduced cell wall thickness and a change in lignin composition with lower amounts of syringyl units as compared to wild type plants. Following a RNA-seq analysis, a biological network involving hormone, stress signalling as well as developmental processes could be delineated. Several candidate genes possibly associated with the altered phloem fiber phenotype observed in amiRPtaRHE1 poplar were identified. Altogether, our data suggest a regulatory role for PtaRHE1 in secondary phloem fiber development. This article is protected by copyright. All rights reserved.
BibTeX:
@article{Baldacci-Cresp2015,
  author = {Baldacci-Cresp, Fabien and Moussawi, Jihad and Leplé, Jean-Charles and Van Acker, Rebecca and Kohler, Annegret and Candiracci, Julie and Twyffels, Laure and Spokevicius, Antanas V and Bossinger, Gerd and Laurans, Françoise and Brunel, Nicole and Vermeersch, Marjorie and Boerjan, Wout and El Jaziri, Mondher and Baucher, Marie},
  title = {PtaRHE1, a Populus tremula x P. alba RING-H2 protein of the ATL family, has a regulatory role in secondary phloem fiber development},
  journal = {The Plant Journal},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1111/tpj.12867/abstract http://onlinelibrary.wiley.com/doi/10.1111/tpj.12867/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false},
  doi = {http://doi.org/10.1111/tpj.12867}
}
Bidabadi, M.S., Shiran, B., Fallahi, H., Rafiei, F., Esmaeili, F. and Ebrahimie, E. Identification of differential expressed transcripts of almond (Prunus dulcis ‘Sefied') in response to water-deficit stress by cDNA-AFLP 2015 Journal of Forest Research, pp. 1-8  article DOI URL 
Abstract: Drought is the major abiotic stress with adverse effects on growth and productivity of plants. It induces the expression of various genes that are involved in stress response and tolerant/sensitive phenotypes. In this study, the expression of several genes were analyzed in response to dehydration in almond (Prunus dulcis ‘Sefied') to shed light on the underlying genetic basis of water-deficit tolerance in almond. The advantages of using almond as a model system for studying dehydration tolerance in woody species are its small diploid genome and its adaptation to drought. Differential expression technique, cDNA-AFLP (amplified fragment length polymorphism), was used to find transcripts accumulated in young trees subjected to water-deficit treatment. Twenty transcript-derived fragments (TDFs) with differential expression between control and stress conditions were generated, amplified, and sequenced. The TDFs showing high homology with genes having known functions were validated by quantitative real-time PCR and their possible function(s) were discussed. These genes include: 2-deoxyglucose-6-phosphate phosphatase, protein kinase MK5 (AFC2) and urease, which up-regulated by 1.61, 2.39 and 4.87 fold under the water-deficit stress condition, respectively. In addition, network analysis unraveled a drought response mechanism displaying activation of the ABA signaling pathway via phosphorylation by 2-deoxyglucose-6-phosphate phosphatase and protein kinase MK5. Protein kinase MK5 was found to be a central element in the drought response network, displaying numerous interactions with RNA-splicing proteins, the sugar-mediated signaling pathway and an epigenetics response (histone phosphorylation).
BibTeX:
@article{Bidabadi2015,
  author = {Bidabadi, Maryam Shirani and Shiran, Behrouz and Fallahi, Hossein and Rafiei, Fariba and Esmaeili, Fazileh and Ebrahimie, Esmaeil},
  title = {Identification of differential expressed transcripts of almond (Prunus dulcis ‘Sefied') in response to water-deficit stress by cDNA-AFLP},
  journal = {Journal of Forest Research},
  year = {2015},
  pages = {1--8},
  url = {http://link.springer.com/article/10.1007/s10310-015-0494-1},
  doi = {http://doi.org/10.1007/s10310-015-0494-1}
}
Bohler, A., Eijssen, L.M.T., van Iersel, M.P., Leemans, C., Willighagen, E.L., Kutmon, M., Jaillard, M. and Evelo, C.T. Automatically visualise and analyse data on pathways using PathVisioRPC from any programming environment 2015 BMC Bioinformatics
Vol. 16(1), pp. 267 
article DOI URL 
Abstract: PMID: 26298294
BibTeX:
@article{Bohler2015,
  author = {Bohler, Anwesha and Eijssen, Lars M T and van Iersel, Martijn P and Leemans, Christ and Willighagen, Egon L and Kutmon, Martina and Jaillard, Magali and Evelo, Chris T},
  title = {Automatically visualise and analyse data on pathways using PathVisioRPC from any programming environment},
  journal = {BMC Bioinformatics},
  year = {2015},
  volume = {16},
  number = {1},
  pages = {267},
  url = {http://www.biomedcentral.com/1471-2105/16/267/abstract http://www.biomedcentral.com/1471-2105/16/267/},
  doi = {http://doi.org/10.1186/s12859-015-0708-8}
}
Chang, C., Yang, J., Li, X., Zhao, W., Li, Y., Guo, P., Wang, G. and Xu, C. Thrombopoietin Signaling Pathway Regulates Hepatocyte Activation in Rat Liver Regeneration 2015 Biochemical Genetics, pp. 1-16  article DOI URL 
Abstract: Thrombopoietin (THPO) signaling pathway regulates cell activation and many other physiological activities. To study its role in liver regeneration (LR), hepatocytes were isolated from rat regenerating livers and gene expression profile was detected using the Rat Genome 230 2.0 Array. Spectral function (E t ) and information correlation coefficient (ICC) were used to analyze gene synergy based on gene expression changes. The results showed that 35 genes related to THPO signaling pathway were significantly changed during rat LR. Functional analysis with ICC showed that five genes, STAT3, PLSCR1, CTGF, PRLR, and LCP1, played a key role in hepatocyte activation. Fourteen channels of THPO signaling pathway participated in regulating hepatocyte activation during rat LR.
BibTeX:
@article{Chang2015,
  author = {Chang, Cuifang and Yang, Jing and Li, Xiaofang and Zhao, Weiming and Li, Yu and Guo, Pengjuan and Wang, Gaiping and Xu, Cunshuan},
  title = {Thrombopoietin Signaling Pathway Regulates Hepatocyte Activation in Rat Liver Regeneration},
  journal = {Biochemical Genetics},
  year = {2015},
  pages = {1--16},
  url = {http://link.springer.com/article/10.1007/s10528-015-9685-x},
  doi = {http://doi.org/10.1007/s10528-015-9685-x}
}
Chepelev, N.L., Moffat, I.D., Labib, S., Bourdon-Lacombe, J., Kuo, B., Buick, J.K., Lemieux, F., Malik, A.I., Halappanavar, S., Williams, A. and Yauk, C.L. Integrating toxicogenomics into human health risk assessment: Lessons learned from the benzo[a]pyrene case study 2015 Critical Reviews in Toxicology
Vol. 45(1), pp. 44-52 
article DOI URL 
Abstract: Abstract The use of short-term toxicogenomic tests to predict cancer (or other health effects) offers considerable advantages relative to traditional toxicity testing methods. The advantages include increased throughput, increased mechanistic data, and significantly reduced costs. However, precisely how toxicogenomics data can be used to support human health risk assessment (RA) is unclear. In a companion paper ( Moffat et al. 2014 ), we present a case study evaluating the utility of toxicogenomics in the RA of benzo[a]pyrene (BaP), a known human carcinogen. The case study is meant as a proof-of-principle exercise using a well-established mode of action (MOA) that impacts multiple tissues, which should provide a best case example. We found that toxicogenomics provided rich mechanistic data applicable to hazard identification, dose-response analysis, and quantitative RA of BaP. Based on this work, here we share some useful lessons for both research and RA, and outline our perspective on how toxicogenomics can benefit RA in the short- and long-term. Specifically, we focus on (1) obtaining biologically relevant data that are readily suitable for establishing an MOA for toxicants, (2) examining the human relevance of an MOA from animal testing, and (3) proposing appropriate quantitative values for RA. We describe our envisioned strategy on how toxicogenomics can become a tool in RA, especially when anchored to other short-term toxicity tests (apical endpoints) to increase confidence in the proposed MOA, and emphasize the need for additional studies on other MOAs to define the best practices in the application of toxicogenomics in RA.
BibTeX:
@article{Chepelev2015,
  author = {Chepelev, Nikolai L and Moffat, Ivy D and Labib, Sarah and Bourdon-Lacombe, Julie and Kuo, Byron and Buick, Julie K and Lemieux, France and Malik, Amal I and Halappanavar, Sabina and Williams, Andrew and Yauk, Carole L},
  title = {Integrating toxicogenomics into human health risk assessment: Lessons learned from the benzo[a]pyrene case study},
  journal = {Critical Reviews in Toxicology},
  year = {2015},
  volume = {45},
  number = {1},
  pages = {44--52},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/25605027},
  doi = {http://doi.org/10.3109/10408444.2014.973935}
}
Chien, C.-H., Chow, C.-N., Wu, N.-Y., Chiang-Hsieh, Y.-F., Hou, P.-F. and Chang, W.-C. EXPath: a database of comparative expression analysis inferring metabolic pathways for plants 2015 BMC Genomics
Vol. 16(Suppl 2), pp. S6 
article DOI URL 
Abstract: In general, the expression of gene alters conditionally to catalyze a specific metabolic pathway. Microarray-based datasets have been massively produced to monitor gene expression levels in parallel with numerous experimental treatments. Although several studies facilitated the linkage of gene expression data and metabolic pathways, none of them are amassed for plants. Moreover, advanced analysis such as pathways enrichment or how genes express under different conditions is not rendered.
BibTeX:
@article{Chien2015,
  author = {Chien, Chia-Hung and Chow, Chi-Nga and Wu, Nai-Yun and Chiang-Hsieh, Yi-Fan and Hou, Ping-Fu and Chang, Wen-Chi},
  title = {EXPath: a database of comparative expression analysis inferring metabolic pathways for plants},
  journal = {BMC Genomics},
  year = {2015},
  volume = {16},
  number = {Suppl 2},
  pages = {S6},
  url = {http://www.biomedcentral.com/qc/1471-2164/16/S2/S6/abstract},
  doi = {http://doi.org/10.1186/1471-2164-16-S2-S6}
}
Claire E, P. Using Cancer Gene Profiling to Distinguish Benign from Malignant Follicular Thyroid Lesions 2015 International Journal of Endocrinology and Metabolic Disorders
Vol. 1(2) 
article DOI URL 
BibTeX:
@article{ClaireE2015,
  author = {Claire E, Peeples},
  title = {Using Cancer Gene Profiling to Distinguish Benign from Malignant Follicular Thyroid Lesions},
  journal = {International Journal of Endocrinology and Metabolic Disorders},
  year = {2015},
  volume = {1},
  number = {2},
  url = {https://www.sciforschenonline.org/journals/endocrinology/IJEMD-1-105.php},
  doi = {http://doi.org/10.16966/2380-548X.105}
}
Colla, S., Ong, D., Ogoti, Y., Marchesini, M., Mistry, N., Clise-Dwyer, K., Ang, S., Storti, P., Viale, A., Giuliani, N., Ruisaard, K., Ganan Gomez, I., Bristow, C., Estecio, M., Weksberg, D., Ho, Y., Hu, B., Genovese, G., Pettazzoni, P., Multani, A., Jiang, S., Hua, S., Ryan, M., Carugo, A., Nezi, L., Wei, Y., Yang, H., D'Anca, M., Zhang, L., Gaddis, S., Gong, T., Horner, J., Heffernan, T., Jones, P., Cooper, L.N., Liang, H., Kantarjian, H., Wang, Y.A., Chin, L., Bueso-Ramos, C., Garcia-Manero, G. and DePinho, R. Telomere Dysfunction Drives Aberrant Hematopoietic Differentiation and Myelodysplastic Syndrome 2015 Cancer Cell
Vol. 27(5), pp. 644-657 
article DOI URL 
Abstract: Summary Myelodysplastic syndrome (MDS) risk correlates with advancing age, therapy-induced DNA damage, and/or shorter telomeres, but whether telomere erosion directly induces MDS is unknown. Here, we provide the genetic evidence that telomere dysfunction-induced DNA damage drives classical MDS phenotypes and alters common myeloid progenitor (CMP) differentiation by repressing the expression of mRNA splicing/processing genes, including SRSF2. RNA-seq analyses of telomere dysfunctional CMP identified aberrantly spliced transcripts linked to pathways relevant to MDS pathogenesis such as genome stability, DNA repair, chromatin remodeling, and histone modification, which are also enriched in mouse CMP haploinsufficient for SRSF2 and in CD34+ CMML patient cells harboring SRSF2 mutation. Together, our studies establish an intimate link across telomere biology, aberrant RNA splicing, and myeloid progenitor differentiation.
BibTeX:
@article{Colla2015,
  author = {Colla, Simona and Ong, Derrick Sek Tong and Ogoti, Yamini and Marchesini, Matteo and Mistry, Nipun A. and Clise-Dwyer, Karen and Ang, Sonny A. and Storti, Paola and Viale, Andrea and Giuliani, Nicola and Ruisaard, Kathryn and Ganan Gomez, Irene and Bristow, Christopher A. and Estecio, Marcos and Weksberg, David C. and Ho, Yan Wing and Hu, Baoli and Genovese, Giannicola and Pettazzoni, Piergiorgio and Multani, Asha S. and Jiang, Shan and Hua, Sujun and Ryan, Michael C. and Carugo, Alessandro and Nezi, Luigi and Wei, Yue and Yang, Hui and D'Anca, Marianna and Zhang, Li and Gaddis, Sarah and Gong, Ting and Horner, James W. and Heffernan, Timothy P. and Jones, Philip and Cooper, Laurence J. N and Liang, Han and Kantarjian, Hagop and Wang, Y Alan and Chin, Lynda and Bueso-Ramos, Carlos and Garcia-Manero, Guillermo and DePinho, Ronald A.},
  title = {Telomere Dysfunction Drives Aberrant Hematopoietic Differentiation and Myelodysplastic Syndrome},
  journal = {Cancer Cell},
  year = {2015},
  volume = {27},
  number = {5},
  pages = {644--657},
  url = {http://www.sciencedirect.com/science/article/pii/S1535610815001403},
  doi = {http://doi.org/10.1016/j.ccell.2015.04.007}
}
Collard, J.F. and Hinsenkamp, M. Cellular processes involved in human epidermal cells exposed to extremely low frequency electric fields 2015 Cellular Signalling
Vol. 27(5), pp. 889-898 
article DOI URL 
Abstract: We observed on different tissues and organisms a biological response after exposure to pulsed low frequency and low amplitude electric or electromagnetic fields but the precise mechanism of cell response remains unknown. The aim of this publication is to understand, using bioinformatics, the biological relevance of processes involved in the modification of gene expression. The list of genes analyzed was obtained after microarray protocol realized on cultures of human epidermal explants growing on deepidermized human skin exposed to a pulsed low frequency electric field. The directed acyclic graph on a WebGestalt Gene Ontology module shows six categories under the biological process root: “biological regulation”, “cellular process”, “cell proliferation”, “death”, “metabolic process” and “response to stimulus”. Enriched derived categories are coherent with the type of in vitro culture, the stimulation protocol or with the previous results showing a decrease of cell proliferation and an increase of differentiation. The Kegg module on WebGestalt has highlighted “cell cycle” and “p53 signaling pathway” as significantly involved. The Kegg website brings out interactions between FoxO, MAPK, JNK, p53, p38, PI3K/Akt, Wnt, mTor or NF-KappaB. Some genes expressed by the stimulation are known to have an exclusive function on these pathways. Analyses performed with Pathway Studio linked cell proliferation, cell differentiation, apoptosis, cell cycle, mitosis, cell death etc. with our microarrays results. Medline citation generated by the software and the fold change variation confirms a diminution of the proliferation, activation of the differentiation and a less well-defined role of apoptosis or wound healing. Wnt and DKK functional classes, DKK1, MACF1, ATF3, MME, TXNRD1, and BMP-2 genes proposed in previous publications after a manual analysis are also highlighted with other genes after Pathway Studio automatic procedure. Finally, an analysis conducted on a list of genes characterized by an accelerated regulation after extremely low frequency pulsed stimulation also confirms their role in the processes of cell proliferation and differentiation. Bioinformatics approach allows in-depth research, without the bias of pre-selection, on cellular processes involved in a huge gene list.
BibTeX:
@article{Collard2015,
  author = {Collard, J -F. and Hinsenkamp, M},
  title = {Cellular processes involved in human epidermal cells exposed to extremely low frequency electric fields},
  journal = {Cellular Signalling},
  year = {2015},
  volume = {27},
  number = {5},
  pages = {889--898},
  url = {http://www.sciencedirect.com/science/article/pii/S0898656815000418},
  doi = {http://doi.org/10.1016/j.cellsig.2015.02.007}
}
Cotter, F., Deguara, C. and Davis, C. Biomarkers For Endometriosis 2015   misc URL 
BibTeX:
@misc{Cotter2015,
  author = {Cotter, Finbar and Deguara, Christine and Davis, Colin},
  title = {Biomarkers For Endometriosis},
  year = {2015},
  url = {http://www.freepatentsonline.com/y2017/0016067.html}
}
Cui, R., Zhang, H., Guo, X., Cui, Q., Wang, J. and Dai, J. Proteomic analysis of cell proliferation in a human hepatic cell line (HL-7702) induced by perfluorooctane sulfonate using iTRAQ 2015 Journal of Hazardous Materials  article DOI URL 
Abstract: Perfluorooctane sulfonate (PFOS) is a commonly used and widely distributed perfluorinated compound proven to cause adverse health outcomes. However, how PFOS affects liver cell proliferation is not well understood. In this experiment, we exposed a human liver cell line (HL-7702) to 50 μM PFOS for 48 h and 96 h. We identified 52 differentially expressed proteins using a quantitative proteomic approach. Among them, 27 were associated with cell proliferation, including hepatoma-derived growth factor (Hdgf) and proliferation biomarkers Mk167 (Ki67) and Top2α. Results from MTT, cell counting, and cell cycle analysis showed low-dose PFOS (textless200 μM) stimulated HL-7702 cell viability at 48 h and 96 h, reduced the G0/G1 percentage, and increased the S + G2/M percentage. Moreover, levels of Cyclin D1, Cyclin E2, Cyclin A2, Cyclin B1 and their partner Cdks were elevated, and the expression of regulating proteins like c-Myc, p53, p21 waf/cip1 and Myt1, as well as the phosphorylation levels of p-Wee1(S642), p-Chk1(S345) and p-Chk2(T68), were disturbed. We hypothesized that low-dose PFOS stimulated HL-7702 proliferation by driving cells into G1 through elevating cyclins/cdks expression, and by promoting cell cycle progression through altering other regulating proteins. This research will shed light on the mechanisms behind PFOS-mediated human hepatotoxicity.
BibTeX:
@article{Cui2015,
  author = {Cui, Ruina and Zhang, Hongxia and Guo, Xuejiang and Cui, Qianqian and Wang, Jianshe and Dai, Jiayin},
  title = {Proteomic analysis of cell proliferation in a human hepatic cell line (HL-7702) induced by perfluorooctane sulfonate using iTRAQ},
  journal = {Journal of Hazardous Materials},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S0304389415004872},
  doi = {http://doi.org/10.1016/j.jhazmat.2015.06.031}
}
Davis, M., Li, J., Knight, E., Daniels, K.K. and Bushel, P.R. Toxicogenomics profiling of bone marrow from rats treated with topotecan in combination with oxaliplatin: a mechanistic strategy to inform combination toxicity 2015 Toxicogenomics
Vol. 6, pp. 14 
article DOI URL 
BibTeX:
@article{Davis2015,
  author = {Davis, Myrtle and Li, Jianying and Knight, Elaine and Daniels, Kellye K and Bushel, Pierre R},
  title = {Toxicogenomics profiling of bone marrow from rats treated with topotecan in combination with oxaliplatin: a mechanistic strategy to inform combination toxicity},
  journal = {Toxicogenomics},
  year = {2015},
  volume = {6},
  pages = {14},
  url = {http://journal.frontiersin.org/Journal/10.3389/fgene.2015.00014/abstract},
  doi = {http://doi.org/10.3389/fgene.2015.00014}
}
Deyati, A., Bagewadi, S., Senger, P., Hofmann-Apitius, M. and Novac, N. Systems approach for the selection of micro-RNAs as therapeutic biomarkers of anti-EGFR monoclonal antibody treatment in colorectal cancer 2015 Scientific Reports
Vol. 5 
article DOI URL 
Abstract: miRNA plays an important role in tumourgenesis by regulating expression of oncogenes and tumour suppressors. Thus affects cell proliferation and differentiation, apoptosis, invasion and angiogenesis. miRNAs are potential biomarkers for diagnosis, prognosis and therapies of different forms of cancer. However, relationship between response of cancer patients towards targeted therapy and the resulting modifications of the miRNA transcriptome in the context of pathway regulation is poorly understood. With ever-increasing pathways and miRNA-mRNA interaction databases, freely available mRNA and miRNA expression data in multiple cancer therapy have produced an unprecedented opportunity to decipher the role of miRNAs in early prediction of therapeutic efficacy in diseases. Efficient translation of -omics data and accumulated knowledge to clinical decision-making are of paramount scientific and public health interest. Well-structured translational algorithms are needed to bridge the gap from databases to decisions. Herein, we present a novel SMARTmiR algorithm to prospectively predict the role of miRNA as therapeutic biomarker for an anti-EGFR monoclonal antibody i.e. cetuximab treatment in colorectal cancer.
BibTeX:
@article{Deyati2015,
  author = {Deyati, Avisek and Bagewadi, Shweta and Senger, Philipp and Hofmann-Apitius, Martin and Novac, Natalia},
  title = {Systems approach for the selection of micro-RNAs as therapeutic biomarkers of anti-EGFR monoclonal antibody treatment in colorectal cancer},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  url = {http://www.nature.com/srep/2015/150126/srep08013/full/srep08013.html},
  doi = {http://doi.org/10.1038/srep08013}
}
Doğramacı, M., Foley, M.E., Horvath, D.P., Hernandez, A.G., Khetani, R.S., Fields, C.J., Keating, K.M., Mikel, M.A. and Anderson, J.V. Glyphosate's impact on vegetative growth in leafy spurge identifies molecular processes and hormone cross-talk associated with increased branching 2015 BMC Genomics
Vol. 16(1), pp. 1-22 
article DOI URL 
Abstract: Background Leafy spurge (Euphorbia esula) is a perennial weed that is considered glyphosate tolerant, which is partially attributed to escape through establishment of new vegetative shoots from an abundance of underground adventitious buds. Leafy spurge plants treated with sub-lethal concentrations of foliar-applied glyphosate produce new vegetative shoots with reduced main stem elongation and increased branching. Processes associated with the glyphosate-induced phenotype were determined by RNAseq using aerial shoots derived from crown buds of glyphosate-treated and -untreated plants. Comparison between transcript abundance and accumulation of shikimate or phytohormones (abscisic acid, auxin, cytokinins, and gibberellins) from these same samples was also done to reveal correlations. Results Transcriptome assembly and analyses confirmed differential abundance among 12,918 transcripts (FDR ≤ 0.05) and highlighted numerous processes associated with shoot apical meristem maintenance and stem growth, which is consistent with the increased number of actively growing meristems in response to glyphosate. Foliar applied glyphosate increased shikimate abundance in crown buds prior to decapitation of aboveground shoots, which induces growth from these buds, indicating that 5-enolpyruvylshikimate 3-phosphate (EPSPS) the target site of glyphosate was inhibited. However, abundance of shikimate was similar in a subsequent generation of aerial shoots derived from crown buds of treated and untreated plants, suggesting EPSPS is no longer inhibited or abundance of shikimate initially observed in crown buds dissipated over time. Overall, auxins, gibberellins (precursors and catabolites of bioactive gibberellins), and cytokinins (precursors and bioactive cytokinins) were more abundant in the aboveground shoots derived from glyphosate-treated plants. Conclusion Based on the overall data, we propose that the glyphosate-induced phenotype resulted from complex interactions involving shoot apical meristem maintenance, hormone biosynthesis and signaling (auxin, cytokinins, gibberellins, and strigolactones), cellular transport, and detoxification mechanisms.
BibTeX:
@article{Dogramac2015,
  author = {Doğramacı, Münevver and Foley, Michael E and Horvath, David P and Hernandez, Alvaro G and Khetani, Radhika S and Fields, Christopher J and Keating, Kathleen M and Mikel, Mark A and Anderson, James V},
  title = {Glyphosate's impact on vegetative growth in leafy spurge identifies molecular processes and hormone cross-talk associated with increased branching},
  journal = {BMC Genomics},
  year = {2015},
  volume = {16},
  number = {1},
  pages = {1--22},
  url = {http://link.springer.com/article/10.1186/s12864-015-1627-9 http://link.springer.com/content/pdf/10.1186%2Fs12864-015-1627-9.pdf http://www.biomedcentral.com/content/pdf/s12864-015-1627-9.pdf http://www.biomedcentral.com/1471-2164/16/395},
  doi = {http://doi.org/10.1186/s12864-015-1627-9}
}
Duhamel, M., Rodet, F., Delhem, N., Abeele, F.V., Kobeissy, F., Nataf, S., Pays, L., Desjardins, R., Gagnon, H., Wisztorski, M., Fournier, I., Day, R. and Salzet, M. Molecular consequences of proprotein convertase 1/3 inhibition in macrophages for application to cancer immunotherapy: a proteomic study 2015 Molecular & Cellular Proteomics, pp. mcp.M115.052480  article DOI URL 
Abstract: Macrophages provide the first line of host immune defense. Their activation triggers the secretion of pro-inflammatory cytokines and chemokines recruiting other immune cells. In cancer, macrophages present an M2 anti-inflammatory phenotype promoting tumor growth. In this way, strategies need to be develop to reactivate macrophages. Previously thought to be expressed only in cells with a neural/neuroendocrine phenotype, the proprotein convertase 1/3 has been shown to also be expressed in macrophages and regulated as a function of the Toll-like receptor immune response. Here, we investigated the intracellular impact of the down-regulation of the proprotein convertase 1/3 in NR8383 macrophages. A complete proteomic study of secretomes and intracellular proteins was undertaken and revealed that inhibition of proprotein convertase 1/3 orient macrophages toward an M1 activated phenotype. This phenotype is characterized by filopodial extensions, Toll-like receptor 4 MyD88-dependent signaling, calcium entry augmentation and the secretion of pro-inflammatory factors. In response to endotoxin/lipopolysaccharide, these intracellular modifications increased, and the secreted factors attracted naive T helper lymphocytes to promote the cytotoxic response. Importantly, the application of these factors onto breast and ovarian cancer cells resulted in a decrease viability or resistance. Under inhibitory conditions using interleukin 10, PC1/3-knockdown macrophages continued to secrete inflammatory factors. These data indicate that targeted inhibition of proprotein convertase 1/3 could represent a novel type of immune therapy to reactivate intra-tumoral macrophages.
BibTeX:
@article{Duhamel2015,
  author = {Duhamel, Marie and Rodet, Franck and Delhem, Nadira and Abeele, Fabien Vanden and Kobeissy, Firas and Nataf, Serge and Pays, Laurent and Desjardins, Roxanne and Gagnon, Hugo and Wisztorski, Maxence and Fournier, Isabelle and Day, Robert and Salzet, Michel},
  title = {Molecular consequences of proprotein convertase 1/3 inhibition in macrophages for application to cancer immunotherapy: a proteomic study},
  journal = {Molecular & Cellular Proteomics},
  year = {2015},
  pages = {mcp.M115.052480},
  url = {http://www.mcponline.org/content/early/2015/09/01/mcp.M115.052480 http://www.ncbi.nlm.nih.gov/pubmed/26330543 http://www.mcponline.org/content/early/2015/09/01/mcp.M115.052480.abstract},
  doi = {http://doi.org/10.1074/mcp.M115.052480}
}
Dumpala, P.R., Peterson, B.C., Lawrence, M.L. and Karsi, A. Identification of Differentially Abundant Proteins of Edwardsiella ictaluri during Iron Restriction 2015 PLoS ONE
Vol. 10(7), pp. e0132504 
article DOI URL 
Abstract: Edwardsiella ictaluri is a Gram-negative facultative anaerobe intracellular bacterium that causes enteric septicemia in channel catfish. Iron is an essential inorganic nutrient of bacteria and is crucial for bacterial invasion. Reduced availability of iron by the host may cause significant stress for bacterial pathogens and is considered a signal that leads to significant alteration in virulence gene expression. However, the precise effect of iron-restriction on E. ictaluri protein abundance is unknown. The purpose of this study was to identify differentially abundant proteins of E. ictaluri during in vitro iron-restricted conditions. We applied two-dimensional difference in gel electrophoresis (2D-DIGE) for determining differentially abundant proteins and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI TOF/TOF MS) for protein identification. Gene ontology and pathway-based functional modeling of differentially abundant proteins was also conducted. A total of 50 unique differentially abundant proteins at a minimum of 2-fold (p ≤ 0.05) difference in abundance due to iron-restriction were detected. The numbers of up- and down-regulated proteins were 37 and 13, respectively. We noted several proteins, including EsrB, LamB, MalM, MalE, FdaA, and TonB-dependent heme/hemoglobin receptor family proteins responded to iron restriction in E. ictaluri.
BibTeX:
@article{Dumpala2015,
  author = {Dumpala, Pradeep R and Peterson, Brian C and Lawrence, Mark L and Karsi, Attila},
  title = {Identification of Differentially Abundant Proteins of Edwardsiella ictaluri during Iron Restriction},
  journal = {PLoS ONE},
  year = {2015},
  volume = {10},
  number = {7},
  pages = {e0132504},
  url = {http://dx.doi.org/10.1371/journal.pone.0132504},
  doi = {http://doi.org/10.1371/journal.pone.0132504}
}
Ebrahimie, E., Nurollah, Z., Ebrahimi, M., Hemmatzadeh, F. and Ignjatovic, J. Unique ability of pandemic influenza to downregulate the genes involved in neuronal disorders 2015 Molecular Biology Reports, pp. 1-14  article DOI URL 
Abstract: Pandemic influenza remains as a substantial threat to humans with a widespread panic worldwide. In contrast, seasonal (non-pandemic) has a mild non-lethal infection each year. The underlying mechanisms governing the detrimental effects of pandemic influenza are yet to be known. Transcriptomic-based network discovery and gene ontology (GO) analysis of host response to pandemic influenza, compared to seasonal influenza, can shed light on the differential mechanisms which pandemic influenza is employed during evolution. Here, using microarray data of infected ferrets with pandemic and seasonal influenza (as a model), we evaluated the possible link between altered genes after pandemic infection with activation of neuronal disorders. To this end, we utilized novel computational biology techniques including differential transcriptome analysis, network construction, GO enrichment, and GO network to investigate the underlying mechanisms of pandemic influenza infection and host interaction. In comparison to seasonal influenza, pandemic influenza differentially altered the expression of 31 genes with direct involvement in activity of central nervous system (CNS). Network topology highlighted the high interactions of IRF1, NKX2-1 and NR5A1 as well as MIR27A, MIR19A, and MIR17. TGFB2, NCOA3 and SP1 were the central transcription factors in the networks. Pandemic influenza remarkably downregulated GPM6A and GTPase. GO network demonstrated the key roles of GPM6A and GTPase in regulation of important functions such as synapse assembly and neuron projection. For the first time, we showed that besides interference with cytokine/chemokine storm and neuraminidase enzyme, H1N1 pandemic influenza is able to directly affect neuronal gene networks. The possibility of application of some key regulators such as GPM6A protein, MIR128, and MIR367 as candidate therapeutic agents is discussed. The presented approach established a new way to unravel unknown pathways in virus-associated CNS dysfunction by utilizing global transcriptomic data, network and GO analysis.
BibTeX:
@article{Ebrahimie2015,
  author = {Ebrahimie, Esmaeil and Nurollah, Zahra and Ebrahimi, Mansour and Hemmatzadeh, Farhid and Ignjatovic, Jagoda},
  title = {Unique ability of pandemic influenza to downregulate the genes involved in neuronal disorders},
  journal = {Molecular Biology Reports},
  year = {2015},
  pages = {1--14},
  url = {http://link.springer.com/article/10.1007/s11033-015-3916-4},
  doi = {http://doi.org/10.1007/s11033-015-3916-4}
}
Ee, J.-H., Seol, Y.-J., Hahn, J.-H., Won, S.-Y., Won, Y.-J., Kim, Y.-K., Kim, Y.-H., Kim, B.-K. and Kim, C.-K. Transcriptomics analyses of genes regulating anthocyanin production in black rice 2015 BioChip Journal  article DOI URL 
BibTeX:
@article{Ee2015,
  author = {Ee, Jae-Hee and Seol, Young-Joo and Hahn, Jang-Ho and Won, So-Youn and Won, Yong-Jae and Kim, Yong-Kab and Kim, Yong-Hwan and Kim, Byung-Ki and Kim, Chang-Kug},
  title = {Transcriptomics analyses of genes regulating anthocyanin production in black rice},
  journal = {BioChip Journal},
  year = {2015},
  url = {http://link.springer.com/10.1007/s13206-014-9108-9 http://link.springer.com/article/10.1007/s13206-014-9108-9page-1},
  doi = {http://doi.org/10.1007/s13206-014-9108-9}
}
Esakova, N.V., Saakyan, E.K., Kondratieva, N.S., Kokaeva, Z.G., Nesterova, A.P., Golovatenko-Abramov, P.K., Klimov, E.A., Treneva, M.S. and Pampura, A.N. Platelet-Activating Factor-Acetylhydrolase Gene (PLA2G7) Expression in Children with a History of Food Anaphylaxis 2015 J Allergy Ther
Vol. 6(211), pp. 2 
article  
BibTeX:
@article{Esakova2015,
  author = {Esakova, N V and Saakyan, E K and Kondratieva, N S and Kokaeva, Z G and Nesterova, A P and Golovatenko-Abramov, P K and Klimov, E A and Treneva, M S and Pampura, A N},
  title = {Platelet-Activating Factor-Acetylhydrolase Gene (PLA2G7) Expression in Children with a History of Food Anaphylaxis},
  journal = {J Allergy Ther},
  year = {2015},
  volume = {6},
  number = {211},
  pages = {2}
}
Franco, S.S., Raveh-Amit, H., Kobolák, J., Alqahtani, M.H., Mobasheri, A., Dinnyes, A., Raveh-Amit, H., Kobolák, J., Alqahtani, M., Mobasheri, A., Dinnyes, A., Hayflick, L., Shay, J., Wright, W., Salama, R., Sadaie, M., Hoare, M., Narita, M., Toussaint, O., Royer, V., Salmon, M., Remacle, J., Campisi, J., Campisi, J., Pazolli, E., Luo, X., Brehm, S., Carbery, K., Wettenhall, J., Smyth, G., Krull, M., Pistor, S., Voss, N., Kel, A., Reuter, I., Kronenberg, D., Michael, H., Schwarzer, K., Potapov, A., Choi, C., Kel-Margoulis, O., Wingender, E., Matys, V., Kel-Margoulis, O., Fricke, E., Liebich, I., Land, S., Barre-Dirrie, A., Reuter, I., Chekmenev, D., Krull, M., Hornischer, K., Voss, N., Stegmaier, P., Lewicki-Potapov, B., Saxel, H., Kel, A., Wingender, E., Kel, A., Voss, N., Jauregui, R., Kel-Margoulis, O., Wingender, E., Kel, A., Gössling, E., Reuter, I., Cheremushkin, E., Kel-Margoulis, O., Wingender, E., Stepanova, M., Tiazhelova, T., Skoblov, M., Baranova, A., Cahan, P., Rovegno, F., Mooney, D., Newman, J., Laurent, G.S., McCaffrey, T., Yang, I., Kim, S., Piwowar, H., Day, R., Fridsma, D., Yilmaz, Y., Shagisultanova, E., Dunbrack, R., Golemis, E., Geigl, J., Langer, S., Barwisch, S., Pfleghaar, K., Lederer, G., Speicher, M., Dekker, P., Gunn, D., McBryan, T., Dirks, R., Heemst, D., Lim, F., Jochemsen, A., Vries, M.V.-d., Nagel, J., Adams, P., Tanke, H., Westendorp, R., Maier, A., Begley, L., Monteleon, C., Shah, R., Macdonald, J., Macoska, J., Hoffmeyer, K., Raggioli, A., Rudloff, S., Anton, R., Hierholzer, A., Valle, I., Hein, K., Vogt, R., Kemler, R., Harten, I., Zahr, R., Lemire, J., Machan, J., Moses, M., Doiron, R., Curatolo, A., Rothman, F., Wight, T., Toole, B., Gordon, L., Vierkötter, A., Schikowski, T., Sugiri, D., Matsui, M., Krämer, U., Krutmann, J., Stallings-Mann, M., Waldmann, J., Zhang, Y., Miller, E., Gauthier, M., Visscher, D., Downey, G., Radisky, E., Fields, A., Radisky, D., Mehner, C., Miller, E., Khauv, D., Nassar, A., Oberg, A., Bamlet, W., Zhang, L., Waldmann, J., Radisky, E., Crawford, H., Radisky, D., Ding, N., Nie, H., Sun, X., Sun, W., Qu, Y., Liu, X., Yao, Y., Liang, X., Chen, C., Li, Y., Vanhooren, V., Dewaele, S., Libert, C., Engelborghs, S., Deyn, P., Toussaint, O., Debacq-Chainiaux, F., Poulain, M., Glupczynski, Y., Franceschi, C., Jaspers, K., Pluijm, I., Hoeijmakers, J., Chen, C., Semren, N., Welk, V., Korfei, M., Keller, I., Fernandez, I., Adler, H., Günther, A., Eickelberg, O., Meiners, S., Venkataraman, K., Futerman, A., Tacutu, R., Craig, T., Budovsky, A., Wuttke, D., Lehmann, G., Taranukha, D., Costa, J., Fraifeld, V., Magalhães, J., Sfikas, A., Batsi, C., Tselikou, E., Vartholomatos, G., Monokrousos, N., Pappas, P., Christoforidis, S., Tzavaras, T., Kanavaros, P., Gorgoulis, V., Marcu, K., Kolettas, E., Liu, C., Rosa, S., Hagos, E., Zhang, W., Ji, W., Yang, L., Yao, L., Wang, G., Xuan, A., Zhuang, Z., Sadaie, M., Dillon, C., Narita, M., Young, A., Cairney, C., Godwin, L., Torrance, C., Bennett, D., Keith, W., Narita, M., McEvilly, R., Erkman, L., Luo, L., Sawchenko, P., Ryan, A., Rosenfeld, M., Hohenauer, T., Berking, C., Schmidt, A., Haferkamp, S., Senft, D., Kammerbauer, C., Fraschka, S., Graf, S., Irmler, M., Beckers, J., Flaig, M., Aigner, A., Höbel, S., Hoffmann, F., Hermeking, H., Rothenfusser, S., Endres, S., Ruzicka, T., Besch, R., Liu, T., Zhou, W., Cai, B., Chu, J., Shi, G., Teng, H., Xu, J., Xiao, J., Wang, Y., Liu, T., Zhou, W., Zhang, F., Shi, G., Teng, H., Xiao, J., Wang, Y., Kowalik, L., Hudspeth, A., Faryna, M., Konermann, C., Aulmann, S., Bermejo, J., Brugger, M., Diederichs, S., Rom, J., Weichenhan, D., Claus, R., Rehli, M., Schirmacher, P., Sinn, H., Plass, C., Gerhauser, C., Kitchen, M., Bryan, R., Emes, R., Glossop, J., Luscombe, C., Cheng, K., Zeegers, M., James, N., Devall, A., Mein, C., Gommersall, L., Fryer, A., Farrell, W., Delgado-Calle, J., Fernández, A., Sainz, J., Zarrabeitia, M., Sañudo, C., García-Renedo, R., Pérez-Núñez, M., García-Ibarbia, C., Fraga, M., Riancho, J., Gravallese, E., Jiang, S., Chen, C., Tseng, K., Tsai, F., Wang, M., Chang, I., Lin, J., Lin, S., Hsu, Y., Zillikens, M., Wilson, S., Farber, C., Demissie, S., Soranzo, N., Bianchi, E., Grundberg, E., Liang, L., Richards, J., Estrada, K., Zhou, Y., Nas, A., Moffatt, M., Zhai, G., Hofman, A., Meurs, J., Pols, H., Price, R., Nilsson, O., Pastinen, T., Cupples, L., Lusis, A., Schadt, E., Ferrari, S., Uitterlinden, A., Rivadeneira, F., Spector, T., Karasik, D., Kiel, D., Pazolli, E., Alspach, E., Milczarek, A., Prior, J., Piwnica-Worms, D. and Stewart, S. The crossroads between cancer stem cells and aging 2015 BMC Cancer
Vol. 15(S1), pp. S1 
article DOI URL 
Abstract: In culturing normal diploid cells, senescence may either happen naturally, in the form of replicative senescence, or it may be a consequence of external challenges such as oxidative stress. Here we present a comparative analysis aimed at reconstruction of molecular cascades specific for replicative (RS) and stressinduced senescence (SIPS) in human fibroblasts. An involvement of caspase-3/keratin-18 pathway and serine/threonine kinase Aurora A/ MDM2 pathway was shared between RS and SIPS. Moreover, stromelysin/MMP3 and N-acetylglucosaminyltransferase enzyme MGAT1, which initiates the synthesis of hybrid and complex Nglycans, were identified as key orchestrating components in RS and SIPS, respectively. In RS only, Aurora-B driven cell cycle signaling was deregulated in concert with the suppression of anabolic branches of the fatty acids and estrogen metabolism. In SIPS, Aurora-B signaling is deprioritized, and the synthetic branches of cholesterol metabolism are upregulated, rather than downregulated. Moreover, in SIPS, proteasome/ubiquitin ligase pathways of protein degradation dominate the regulatory landscape. This picture indicates that SIPS proceeds in cells that are actively fighting stress which facilitates premature senescence while failing to completely activate the orderly program of RS. The promoters of genes differentially expressed in either RS or SIPS are unusually enriched by the binding sites for homeobox family proteins, with particular emphasis on HMX1, IRX2, HDX and HOXC13. Additionally, we identified Iroquois Homeobox 2 (IRX2) as a master regulator for the secretion of SPP1-encoded osteopontin, a stromal driver for tumor growth that is overexpressed by both RS and SIPS fibroblasts. The latter supports the hypothesis that senescence-specific de-repression of SPP1 aids in SIPS-dependent stromal activation. Reanalysis of previously published experimental data is cost-effective approach for extraction of additional insignts into the functioning of biological systems.
BibTeX:
@article{Franco2015,
  author = {Franco, Sara Santos and Raveh-Amit, Hadas and Kobolák, Julianna and Alqahtani, Mohammed H and Mobasheri, Ali and Dinnyes, András and Raveh-Amit, H and Kobolák, J and Alqahtani, MH and Mobasheri, A and Dinnyes, A and Hayflick, L and Shay, JW and Wright, WE and Salama, R and Sadaie, M and Hoare, M and Narita, M and Toussaint, O and Royer, V and Salmon, M and Remacle, J and Campisi, J and Campisi, J and Pazolli, E and Luo, X and Brehm, S and Carbery, K and Wettenhall, JM and Smyth, GK and Krull, M and Pistor, S and Voss, N and Kel, A and Reuter, I and Kronenberg, D and Michael, H and Schwarzer, K and Potapov, A and Choi, C and Kel-Margoulis, O and Wingender, E and Matys, V and Kel-Margoulis, OV and Fricke, E and Liebich, I and Land, S and Barre-Dirrie, A and Reuter, I and Chekmenev, D and Krull, M and Hornischer, K and Voss, N and Stegmaier, P and Lewicki-Potapov, B and Saxel, H and Kel, AE and Wingender, E and Kel, A and Voss, N and Jauregui, R and Kel-Margoulis, O and Wingender, E and Kel, AE and Gössling, E and Reuter, I and Cheremushkin, E and Kel-Margoulis, OV and Wingender, E and Stepanova, M and Tiazhelova, T and Skoblov, M and Baranova, A and Cahan, P and Rovegno, F and Mooney, D and Newman, JC and Laurent, G St and McCaffrey, TA and Yang, IS and Kim, S and Piwowar, HA and Day, RS and Fridsma, DB and Yilmaz, Y and Shagisultanova, E and Dunbrack, RL and Golemis, EA and Geigl, JB and Langer, S and Barwisch, S and Pfleghaar, K and Lederer, G and Speicher, MR and Dekker, P and Gunn, D and McBryan, T and Dirks, RW and Heemst, D and Lim, FL and Jochemsen, AG and Vries, M Verlaan-de and Nagel, J and Adams, PD and Tanke, HJ and Westendorp, RG and Maier, AB and Begley, L and Monteleon, C and Shah, RB and Macdonald, JW and Macoska, JA and Hoffmeyer, K and Raggioli, A and Rudloff, S and Anton, R and Hierholzer, A and Valle, I and Hein, K and Vogt, R and Kemler, R and Harten, IA and Zahr, RS and Lemire, JM and Machan, JT and Moses, MA and Doiron, RJ and Curatolo, AS and Rothman, FG and Wight, TN and Toole, BP and Gordon, LB and Vierkötter, A and Schikowski, T and Sugiri, D and Matsui, MS and Krämer, U and Krutmann, J and Stallings-Mann, ML and Waldmann, J and Zhang, Y and Miller, E and Gauthier, ML and Visscher, DW and Downey, GP and Radisky, ES and Fields, AP and Radisky, DC and Mehner, C and Miller, E and Khauv, D and Nassar, A and Oberg, AL and Bamlet, WR and Zhang, L and Waldmann, J and Radisky, ES and Crawford, HC and Radisky, DC and Ding, N and Nie, H and Sun, X and Sun, W and Qu, Y and Liu, X and Yao, Y and Liang, X and Chen, CC and Li, Y and Vanhooren, V and Dewaele, S and Libert, C and Engelborghs, S and Deyn, PP and Toussaint, O and Debacq-Chainiaux, F and Poulain, M and Glupczynski, Y and Franceschi, C and Jaspers, K and Pluijm, I and Hoeijmakers, J and Chen, CC and Semren, N and Welk, V and Korfei, M and Keller, IE and Fernandez, IE and Adler, H and Günther, A and Eickelberg, O and Meiners, S and Venkataraman, K and Futerman, AH and Tacutu, R and Craig, T and Budovsky, A and Wuttke, D and Lehmann, G and Taranukha, D and Costa, J and Fraifeld, VE and Magalhães, JP and Sfikas, A and Batsi, C and Tselikou, E and Vartholomatos, G and Monokrousos, N and Pappas, P and Christoforidis, S and Tzavaras, T and Kanavaros, P and Gorgoulis, VG and Marcu, KB and Kolettas, E and Liu, C and Rosa, S and Hagos, EG and Zhang, W and Ji, W and Yang, L and Yao, L and Wang, G and Xuan, A and Zhuang, Z and Sadaie, M and Dillon, C and Narita, M and Young, AR and Cairney, CJ and Godwin, LS and Torrance, CJ and Bennett, DC and Keith, WN and Narita, M and McEvilly, RJ and Erkman, L and Luo, L and Sawchenko, PE and Ryan, AF and Rosenfeld, MG and Hohenauer, T and Berking, C and Schmidt, A and Haferkamp, S and Senft, D and Kammerbauer, C and Fraschka, S and Graf, SA and Irmler, M and Beckers, J and Flaig, M and Aigner, A and Höbel, S and Hoffmann, F and Hermeking, H and Rothenfusser, S and Endres, S and Ruzicka, T and Besch, R and Liu, T and Zhou, W and Cai, B and Chu, J and Shi, G and Teng, H and Xu, J and Xiao, J and Wang, Y and Liu, T and Zhou, W and Zhang, F and Shi, G and Teng, H and Xiao, J and Wang, Y and Kowalik, L and Hudspeth, AJ and Faryna, M and Konermann, C and Aulmann, S and Bermejo, JL and Brugger, M and Diederichs, S and Rom, J and Weichenhan, D and Claus, R and Rehli, M and Schirmacher, P and Sinn, HP and Plass, C and Gerhauser, C and Kitchen, MO and Bryan, RT and Emes, RD and Glossop, JR and Luscombe, C and Cheng, KK and Zeegers, MP and James, ND and Devall, AJ and Mein, CA and Gommersall, L and Fryer, AA and Farrell, WE and Delgado-Calle, J and Fernández, AF and Sainz, J and Zarrabeitia, MT and Sañudo, C and García-Renedo, R and Pérez-Núñez, MI and García-Ibarbia, C and Fraga, MF and Riancho, JA and Gravallese, EM and Jiang, SS and Chen, CH and Tseng, KY and Tsai, FY and Wang, MJ and Chang, IS and Lin, JL and Lin, S and Hsu, YH and Zillikens, MC and Wilson, SG and Farber, CR and Demissie, S and Soranzo, N and Bianchi, EN and Grundberg, E and Liang, L and Richards, JB and Estrada, K and Zhou, Y and Nas, A and Moffatt, MF and Zhai, G and Hofman, A and Meurs, JB and Pols, HA and Price, RI and Nilsson, O and Pastinen, T and Cupples, LA and Lusis, AJ and Schadt, EE and Ferrari, S and Uitterlinden, AG and Rivadeneira, F and Spector, TD and Karasik, D and Kiel, DP and Pazolli, E and Alspach, E and Milczarek, A and Prior, J and Piwnica-Worms, D and Stewart, SA},
  title = {The crossroads between cancer stem cells and aging},
  journal = {BMC Cancer},
  publisher = {BioMed Central},
  year = {2015},
  volume = {15},
  number = {S1},
  pages = {S1},
  url = {http://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-15-S1-S1},
  doi = {http://doi.org/10.1186/1471-2407-15-S1-S1}
}
Glaab, E. and Schneider, R. Comparative pathway and network analysis of brain transcriptome changes during adult aging and in Parkinson's disease 2015 Neurobiology of Disease
Vol. 74, pp. 1-13 
article DOI URL 
Abstract: Aging is considered as one of the main factors promoting the risk for Parkinson's disease (PD), and common mechanisms of dopamine neuron degeneration in aging and PD have been proposed in recent years. Here, we use a statistical meta-analysis of human brain transcriptomics data to investigate potential mechanistic relationships between adult brain aging and PD pathogenesis at the pathway and network level. The analyses identify statistically significant shared pathway and network alterations in aging and PD and an enrichment in PD-associated sequence variants from genome-wide association studies among the jointly deregulated genes. We find robust discriminative patterns for groups of functionally related genes with potential applications as combined risk biomarkers to detect aging- and PD-linked oxidative stress, e.g., a consistent over-expression of metallothioneins matching with findings in previous independent studies. Interestingly, analyzing the regulatory network and mouse knockout expression data for NR4A2, a transcription factor previously associated with rare mutations in PD and here found as the most significantly under-expressed gene in PD among the jointly altered genes, suggests that aging-related NR4A2 expression changes may increase PD risk via downstream effects similar to disease-linked mutations and to expression changes in sporadic PD. Overall, the analyses suggest mechanistic explanations for the age-dependence of PD risk and reveal significant and robust shared process alterations with potential applications in biomarker development for pre-symptomatic risk assessment or early stage diagnosis.
BibTeX:
@article{Glaab2015,
  author = {Glaab, Enrico and Schneider, Reinhard},
  title = {Comparative pathway and network analysis of brain transcriptome changes during adult aging and in Parkinson's disease},
  journal = {Neurobiology of Disease},
  year = {2015},
  volume = {74},
  pages = {1--13},
  url = {http://www.sciencedirect.com/science/article/pii/S0969996114003404},
  doi = {http://doi.org/10.1016/j.nbd.2014.11.002}
}
Glotov, A.S., Tiys, E.S., Vashukova, E.S., Pakin, V.S., Demenkov, P.S., Saik, O.V., Ivanisenko, T.V., Arzhanova, O.N., Mozgovaya, E.V., Zainulina, M.S., Kolchanov, N.A., Baranov, V.S. and Ivanisenko, V.A. Molecular association of pathogenetic contributors to pre-eclampsia (pre-eclampsia associome) 2015 BMC Systems Biology
Vol. 9(Suppl 2), pp. S4 
article DOI URL 
Abstract: PMID: 25879409
BibTeX:
@article{Glotov2015,
  author = {Glotov, Andrey S and Tiys, Evgeny S and Vashukova, Elena S and Pakin, Vladimir S and Demenkov, Pavel S and Saik, Olga V and Ivanisenko, Timofey V and Arzhanova, Olga N and Mozgovaya, Elena V and Zainulina, Marina S and Kolchanov, Nikolay A and Baranov, Vladislav S and Ivanisenko, Vladimir A},
  title = {Molecular association of pathogenetic contributors to pre-eclampsia (pre-eclampsia associome)},
  journal = {BMC Systems Biology},
  year = {2015},
  volume = {9},
  number = {Suppl 2},
  pages = {S4},
  url = {http://www.biomedcentral.com/1752-0509/9/S2/S4/abstract http://www.biomedcentral.com/content/pdf/1752-0509-9-S2-S4.pdf http://www.biomedcentral.com/1752-0509/9/S2/S4},
  doi = {http://doi.org/10.1186/1752-0509-9-S2-S4}
}
Godbersen, C., Paiva, C., Danilova, O.V., Berger, A., Brown, J.R. and Danilov, A.V. Targeting neddylation effectively antagonizes nuclear factor-kB in chronic lymphocytic leukemia B-cells 2015 Leukemia & Lymphoma
Vol. 56(5), pp. 1566-1569 
article  
BibTeX:
@article{Godbersen2015,
  author = {Godbersen, Claire and Paiva, Cody and Danilova, Olga V and Berger, Allison and Brown, Jennifer R and Danilov, Alexey V},
  title = {Targeting neddylation effectively antagonizes nuclear factor-kB in chronic lymphocytic leukemia B-cells},
  journal = {Leukemia & Lymphoma},
  year = {2015},
  volume = {56},
  number = {5},
  pages = {1566--1569}
}
Hart, A.B. and Kranzler, H.R. Alcohol Dependence Genetics: Lessons Learned From Genome-Wide Association Studies (GWAS) and Post-GWAS Analyses 2015 Alcoholism: Clinical and Experimental Research, pp. n/a-n/a  article DOI URL 
Abstract: Background Alcohol dependence (AD) is a complex psychiatric disorder and a significant public health problem. Twin and family-based studies have consistently estimated its heritability to be approximately 50%, and many studies have sought to identify specific genetic variants associated with susceptibility to AD. These studies have been primarily linkage or candidate gene based and have been mostly unsuccessful in identifying replicable risk loci. Genome-wide association studies (GWAS) have improved the detection of specific loci associated with complex traits, including AD. However, findings from GWAS explain only a small proportion of phenotypic variance, and alternative methods have been proposed to investigate the associations that do not meet strict genome-wide significance criteria. Methods This review summarizes all published AD GWAS and post-GWAS analyses that have sought to exploit GWAS data to identify AD-associated loci. Results Findings from AD GWAS have been largely inconsistent, with the exception of variants encoding the alcohol-metabolizing enzymes. Analyses of GWAS data that go beyond standard association testing have demonstrated the polygenic nature of AD and the large contribution of common variants to risk, nominating novel genes and pathways for AD susceptibility. Conclusions Findings from AD GWAS and post-GWAS analyses have greatly increased our understanding of the genetic etiology of AD. However, it is clear that larger samples will be necessary to detect loci in addition to those that encode alcohol-metabolizing enzymes, which may only be possible through consortium-based efforts. Post-GWAS approaches to studying the genetic influences on AD are increasingly common and could greatly increase our knowledge of both the genetic architecture of AD and the specific genes and pathways that influence risk.
BibTeX:
@article{Hart2015,
  author = {Hart, Amy B and Kranzler, Henry R},
  title = {Alcohol Dependence Genetics: Lessons Learned From Genome-Wide Association Studies (GWAS) and Post-GWAS Analyses},
  journal = {Alcoholism: Clinical and Experimental Research},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1111/acer.12792/abstract jsessionid=A701279E8368AE037D1E9EFE01971F91.f01t01?deniedAccessCustomisedMessage=&userIsAuthenticated=false},
  doi = {http://doi.org/10.1111/acer.12792}
}
Hinkelbein, J., Böhm, L., Hm, L., Spelten, O., Sander, D., Soltész, S. and Braunecker, S. Hyperoxia-Induced Protein Alterations in Renal Rat Tissue: A Quantitative Proteomic Approach to Identify Hyperoxia-Induced Effects in Cellular Signaling Pathways 2015 Disease Markers
Vol. 2015, pp. e964263 
article DOI URL 
Abstract: Introduction. In renal tissue as well as in other organs, supranormal oxygen pressure may lead to deleterious consequences on a cellular level. Additionally, hyperoxia-induced effect in cells and related free radicals may potentially contribute to renal failure. The aim of this study was to analyze time-dependent alterations of rat kidney protein expression after short-term normobaric hyperoxia using proteomics and bioinformatic approaches. Material and Methods. Wistar rats were randomized into six different groups: three groups with normobaric hyperoxia (exposure to 100&x25; oxygen for 3&x2009;h) and three groups with normobaric normoxia (NN; room air). After hyperoxia exposure, kidneys were removed immediately, after 3 days and after 7 days. Kidney lysates were analyzed by two-dimensional gel electrophoresis followed by peptide mass fingerprinting using tandem mass spectrometry. Statistical analysis was performed with DeCyder 2D software (). Biological functions of differential regulated proteins were studied using functional network analysis (Ingenuity Pathways Analysis and PathwayStudio). Results. Expression of 14 proteins was significantly altered : eight proteins (MEP1A&x5f;RAT, RSSA&x5f;RAT, F16P1&x5f;RAT, STML2&x5f;RAT, BPNT1&x5f;RAT, LGMN&x5f;RAT, ATPA&x5f;RAT, and VDAC1&x5f;RAT) were downregulated and six proteins (MTUS1&x5f;RAT, F16P1&x5f;RAT, ACTG&x5f;RAT, ACTB&x5f;RAT, 2ABA&x5f;RAT, and RAB1A&x5f;RAT) were upregulated. Bioinformatic analyses revealed an association of regulated proteins with inflammation. Conclusions. Significant alterations in renal protein expression could be demonstrated for up to 7 days even after short-term hyperoxia. The identified proteins indicate an association with inflammation signaling cascades. MEP1A and VDAC1 could be promising candidates to identify hyperoxic injury in kidney cells.
BibTeX:
@article{Hinkelbein2015,
  author = {Hinkelbein, Jochen and Böhm, Lennert and Hm, Lennert and Spelten, Oliver and Sander, David and Soltész, Stefan and Braunecker, Stefan},
  title = {Hyperoxia-Induced Protein Alterations in Renal Rat Tissue: A Quantitative Proteomic Approach to Identify Hyperoxia-Induced Effects in Cellular Signaling Pathways},
  journal = {Disease Markers},
  year = {2015},
  volume = {2015},
  pages = {e964263},
  url = {http://www.hindawi.com/journals/dm/2015/964263/abs/ http://downloads.hindawi.com/journals/dm/2015/964263.pdf},
  doi = {http://doi.org/10.1155/2015/964263}
}
Horvath, D.P., Hansen, S.A., Moriles-Miller, J.P., Pierik, R., Yan, C., Clay, D.E., Scheffler, B. and Clay, S.A. RNAseq reveals weed-induced PIF3-like as a candidate target to manipulate weed stress response in soybean 2015 New Phytologist, pp. n/a-n/a  article DOI URL 
Abstract: * Weeds reduce yield in soybeans (Glycine max) through incompletely defined mechanisms. The effects of weeds on the soybean transcriptome were evaluated in field conditions during four separate growing seasons. * RNASeq data were collected from six biological samples of soybeans growing with or without weeds. Weed species and the methods to maintain weed-free controls varied between years to mitigate treatment effects, and to allow detection of general soybean weed responses. * Soybean plants were not visibly nutrient- or water-stressed. We identified 55 consistently downregulated genes in weedy plots. Many of the downregulated genes were heat shock genes. Fourteen genes were consistently upregulated. Several transcription factors including a PHYTOCHROME INTERACTING FACTOR 3-like gene (PIF3) were included among the upregulated genes. Gene set enrichment analysis indicated roles for increased oxidative stress and jasmonic acid signaling responses during weed stress. * The relationship of this weed-induced PIF3 gene to genes involved in shade avoidance responses in Arabidopsis provide evidence that this gene may be important in the response of soybean to weeds. These results suggest that the weed-induced PIF3 gene will be a target for manipulating weed tolerance in soybean.
BibTeX:
@article{Horvath2015,
  author = {Horvath, David P and Hansen, Stephanie A and Moriles-Miller, Janet P and Pierik, Ronald and Yan, Changhui and Clay, David E and Scheffler, Brian and Clay, Sharon A},
  title = {RNAseq reveals weed-induced PIF3-like as a candidate target to manipulate weed stress response in soybean},
  journal = {New Phytologist},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1111/nph.13351/abstract http://onlinelibrary.wiley.com/doi/10.1111/nph.13351/abstract?systemMessage=Wiley+Online+Library+will+be+disrupted+on+7th+March+from+10%3A00-13%3A00+GMT+%2805%3A00-08%3A00+EST%29+for+essential+},
  doi = {http://doi.org/10.1111/nph.13351}
}
Huang, S., Cui, Y., Guo, X., Wang, L., Li, S., Lu, Y., Bi, Y., Huang, X., Lin, M., Xia, Y., Wang, S., Wang, X., Zhou, Z. and Sha, J. 2,2′,4,4′-Tetrabromodiphenyl ether disrupts spermatogenesis, impairs mitochondrial function and induces apoptosis of early leptotene spermatocytes in rats 2015 Reproductive Toxicology  article DOI URL 
Abstract: Our objective was to explore molecular markers and mechanism of BDE47 on spermatogenesis in mammals. Adult male SD rats were gavaged daily with corn oil containing 0, 0.001, 0.03, 1 or 20 mg BDE47/kg bw for eight weeks. Testes morphology was analyzed using electron microscopy, TUNEL, immunohistochemistry and morphometry. Differential proteome profile and western blotting were applied to determine molecular markers and protein expression. GC1-spg cells (mouse spermatogonial cells) were used to verify mechanism of BDE47. Data showed BDE47 reduced tubular epithelial thickness, impaired mitochondrial function and induced apoptosis in early leptotene spermatocytes. Proteomic study identified 70 differential spots corresponding to 64 proteins. 20 proteins related to apoptosis, 15 located in mitochondria. Exposure of GC1-spg cells showed BDE47 induced apoptosis, impaired mitochondria and decreased Bcl-2 in cells. Data indicate that BDE47 disrupts spermatogenesis, impairs mitochondrial function and induces apoptosis of early leptotene spermatocytes in rats probably via mitochondrial pathway.
BibTeX:
@article{Huang2015,
  author = {Huang, Shaoping and Cui, Yiqiang and Guo, Xuejiang and Wang, Lei and Li, Suying and Lu, Ying and Bi, Ye and Huang, Xiaoyan and Lin, Min and Xia, Yankai and Wang, Shoulin and Wang, Xinru and Zhou, Zuomin and Sha, Jiahao},
  title = {2,2′,4,4′-Tetrabromodiphenyl ether disrupts spermatogenesis, impairs mitochondrial function and induces apoptosis of early leptotene spermatocytes in rats},
  journal = {Reproductive Toxicology},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S0890623815000106 http://www.sciencedirect.com/science/article/pii/S0890623815000106/pdfft?md5=9a0df4b3673168e41623003bf1ae2309&pid=1-s2.0-S0890623815000106-main.pdf},
  doi = {http://doi.org/10.1016/j.reprotox.2015.01.009}
}
Ishola, P., Greene, E., Nguyen, P., Bottje, W., Cline, M., Anthony, N. and Dridi, S. Leptin and Autophagy: When the Two Masters Meet 2015 Anatomy & Physiology
Vol. 5(173), pp. 73 
article  
Abstract: Autophagy or cellular self-digestion, a lysosomal degradation pathway that is conserved from yeast to human, plays a key role in recycling cellular constituents, including damaged organelles. It also plays a pivotal role in the adaptation of cells to a plethora of distinct stressors including starvation. Leptin is an adipocytokine that is mostly produced by white adipose cells in mammals and functions as a hormonal sensing mechanism to inhibit feed intake and increase energy expenditure. In this review, we will describe the autophagy and leptin systems and summarized recent advances regarding their interactions in the regulation of energy homeostasis.
BibTeX:
@article{Ishola2015,
  author = {Ishola, Peter and Greene, Elizabeth and Nguyen, Phuong and Bottje, Walter and Cline, Mark and Anthony, Nicholas and Dridi, Sami},
  title = {Leptin and Autophagy: When the Two Masters Meet},
  journal = {Anatomy & Physiology},
  year = {2015},
  volume = {5},
  number = {173},
  pages = {73}
}
Ivanisenko, V.A., Saik, O.V., Ivanisenko, N.V., Tiys, E.S., Ivanisenko, T.V., Demenkov, P.S. and Kolchanov, N.A. ANDSystem: an Associative Network Discovery System for automated literature mining in the field of biology 2015 BMC Systems Biology
Vol. 9(Suppl 2), pp. S2 
article DOI URL 
Abstract: PMID: 25881313
BibTeX:
@article{Ivanisenko2015,
  author = {Ivanisenko, Vladimir A and Saik, Olga V and Ivanisenko, Nikita V and Tiys, Evgeny S and Ivanisenko, Timofey V and Demenkov, Pavel S and Kolchanov, Nikolay A},
  title = {ANDSystem: an Associative Network Discovery System for automated literature mining in the field of biology},
  journal = {BMC Systems Biology},
  year = {2015},
  volume = {9},
  number = {Suppl 2},
  pages = {S2},
  url = {http://www.biomedcentral.com/1752-0509/9/S2/S2/abstract http://www.biomedcentral.com/content/pdf/1752-0509-9-S2-S2.pdf http://www.biomedcentral.com/1752-0509/9/S2/S2/},
  doi = {http://doi.org/10.1186/1752-0509-9-S2-S2}
}
Jang, H.-J., Lee, H.-J., Kang, K.S., Song, K.-D., Kim, T.-H., Song, C.-S. and Park, M.N. Molecular responses to the influenza A virus in chicken trachea-derived cells 2015 Poultry Science, pp. pev033  article DOI URL 
Abstract: The influenza A virus infects a broad range of species and spreads easily through the respiratory tract. Because of these characteristics, the influenza A virus has caused pandemic disease in humans and livestock. To investigate the early molecular responses after influenza A virus infection in chickens, we infected tracheal epithelial cells derived from 20-day-old chick embryos with influenza A virus (H1N1). The gene expression patterns of the infected tracheal epithelial cells were analyzed via DNA microarray at different time points (0, 6, 12, 24, and 36 hr) after viral infection. Differentially expressed genes were identified in 6, 12, 24, and 36 hours post infection. A total of 1,936, 2,168, 3,670 and 2,894 genes were upregulated (≥2-fold, P textless 0.05), whereas 884, 592, 1,503 and 1,925 genes were downregulated at the respective time points (≤0.5-fold, P textless 0.05). When the differentially expressed genes were functionally categorized, immune-related and defense response gene ontology terms were detected in 12, 24, or 36 hours post infection. Interestingly, in the defense response, most of the gallinacin (GAL) genes were rapidly induced within 24 hr post infection. Subsequently, we predicted transcription factor binding sites within promoters of the GAL gene family, and analyzed the gene expression pattern for the common GAL gene regulatory factors to identify the viral infection-induced immune mechanism. Our results might contribute to an understanding of early host responses and regulatory mechanisms for host defense peptide induction against viral infections in chicken.
BibTeX:
@article{Jang2015,
  author = {Jang, Hyun-Jun and Lee, Hyun-Jeong and Kang, Kyung Soo and Song, Ki-Duk and Kim, Tae-Hun and Song, Chang-Seon and Park, Mi Na},
  title = {Molecular responses to the influenza A virus in chicken trachea-derived cells},
  journal = {Poultry Science},
  year = {2015},
  pages = {pev033},
  url = {http://ps.oxfordjournals.org/content/early/2015/04/15/ps.pev033 http://ps.oxfordjournals.org/content/early/2015/04/15/ps.pev033.full.pdf http://www.ncbi.nlm.nih.gov/pubmed/25877411 http://ps.oxfordjournals.org/content/early/2015/04/15/ps.pev033.abstract},
  doi = {http://doi.org/10.3382/ps/pev033}
}
Jena, M.K., Janjanam, J., Naru, J., Kumar, S., Kumar, S., Singh, S., Mohapatra, S.K., Kola, S., Anand, V., Jaswal, S., Verma, A.K., Malakar, D., Dang, A.K., Kaushik, J.K., Reddy, V.S. and Mohanty, A.K. DIGE based proteome analysis of mammary gland tissue in water buffalo (Bubalus bubalis): Lactating vis-a-vis heifer 2015 Journal of Proteomics  article DOI URL 
Abstract: Mammary gland is an exocrine and sebaceous gland made up of branching network of ducts that end in alveoli. Milk is synthesized in the alveoli and secreted into alveolar lumen. Mammary gland represents an ideal system for the study of organogenesis that undergoes successive cycles of pregnancy, lactation and involution. To gain insights on the molecular events that take place in pubertal and lactating mammary gland, we have identified 43 differentially expressed proteins in mammary tissue of heifer (non-lactating representing a virgin mammary gland), and lactating buffaloes (Bubalus bubalis) by 2D-difference gel electrophoresis (2D-DIGE) and mass spectrometry. 21 proteins were upregulated during lactation whereas 8 proteins were upregulated in heifer mammary gland. Bioinformatics analyses of the identified proteins showed that a majority of the proteins are involved in metabolic processes. The differentially expressed proteins were validated by real-time PCR and Western blotting. We observed differential expressions of certain new proteins including EEF1D, HSPA5, HSPD1 and PRDX6 during lactation which have not been reported before. The differentially expressed proteins were mapped to available biological pathways and networks involved in lactation. This study signifies the importance of some proteins which are preferentially expressed during lactation and in heifer mammary gland. Biological significance This work is important because we have generated information in water buffalo (B. bubalis) for the first time which is the major milk producing animal in Indian Subcontinent. Out of a present production of 133 million tons of milk produced in India, contribution of buffalo milk is around 54%. Its physiology is somewhat different from the lactating cows. Buffalo milk composition varies from cow milk in terms of higher fat and total solid content, which confers an advantage in preparation of specialized cheese, curd and other dairy products. Being a major milk producing animal in India it is highly essential to understand the lactation associated proteins in the mammary gland of a buffalo. In the present investigation our attempt has been to identify new protein evidences which are expressed in lactating buffalo mammary gland and have not been reported before. The findings reported in the present study will help in the understanding of the lactation biology in the buffalo mammary gland in particular and the mammary gland biology in general.
BibTeX:
@article{Jena2015,
  author = {Jena, Manoj K and Janjanam, Jagadeesh and Naru, Jasmine and Kumar, Saravanan and Kumar, Sudarshan and Singh, Surender and Mohapatra, Sushil K and Kola, Srujana and Anand, Vijay and Jaswal, Shalini and Verma, Arvind K and Malakar, Dhruba and Dang, Ajay K and Kaushik, Jai K and Reddy, Vanga S and Mohanty, Ashok K},
  title = {DIGE based proteome analysis of mammary gland tissue in water buffalo (Bubalus bubalis): Lactating vis-a-vis heifer},
  journal = {Journal of Proteomics},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S1874391915000275},
  doi = {http://doi.org/10.1016/j.jprot.2015.01.018}
}
Julia Azimova1, 2., Natalia Kondratieva3, A.S., Kirill Skorobogatykh2, T.K., Zarema Kokaeva2, A.R., Gyusal Tabeeva2, 2 and Euge, 4 The Role of Polymorphism of Regulatory Region of MTDH Gene (Rs1835740) in Migraine and Other Forms of Primary Headaches 2015 Journal of Neurology & Stroke
Vol. 3(5), pp. 1-5 
article DOI URL 
BibTeX:
@article{JuliaAzimova12015,
  author = {Julia Azimova1, 2 and Natalia Kondratieva3, Alexey Sergeev2 and Kirill Skorobogatykh2, Taisiya Kochetkova3 and Zarema Kokaeva2, Andrey Rachin1 and 2, Gyusal Tabeeva2 and 4, Euge},
  title = {The Role of Polymorphism of Regulatory Region of MTDH Gene (Rs1835740) in Migraine and Other Forms of Primary Headaches},
  journal = {Journal of Neurology & Stroke},
  publisher = {MedCrave Online},
  year = {2015},
  volume = {3},
  number = {5},
  pages = {1--5},
  url = {http://medcraveonline.com/JNSK/JNSK-03-00101.php},
  doi = {http://doi.org/10.15406/jnsk.2015.3.00101}
}
Kaspric, N., Reichstadt, M., Picard, B., Tournayre, J. and Bonnet, M. Protein Function Easily Investigated by Genomics Data Mining Using the ProteINSIDE Online Tool 2015 Genomics and Computational Biology
Vol. 1(1), pp. 16 
article URL 
Abstract: Nowadays, genomic and proteomic studies produce vast amounts of data. To get the biological meaning of these data and to generate testable new hypothesis, scientists must use several tools often not designed for ruminant studies. Here we present ProteINSIDE: an online tool to analyse lists of protein or gene identifiers from well-annotated species (human, rat, and mouse) and ruminants (cow, sheep, and goat). The aims of ProteINSIDE modules are to gather biological information stores in well-updated public databases, to proceed to annotations according to the Gene Ontology consortium, to predict potentially secreted proteins, and to search for proteins interactions. ProteINSIDE provides results from several software and databases in a single query. From a list of identifiers, ProteINSIDE uses orthologs or homologs to extend analyses and biological information retrieval. As a tutorial, we presented how to launch, to recover, to view, and to interpret the results provided by the two types of analysis available with ProteINSIDE (basic and custom analyses). ProteINSIDE is freely available using a simple internet browser at www.proteinside.org. The results of this article are provided on the home page of ProteINSIDE website as the example of an analysis results.
BibTeX:
@article{Kaspric2015,
  author = {Kaspric, Nicolas and Reichstadt, Matthieu and Picard, Brigitte and Tournayre, Jérémy and Bonnet, Muriel},
  title = {Protein Function Easily Investigated by Genomics Data Mining Using the ProteINSIDE Online Tool},
  journal = {Genomics and Computational Biology},
  year = {2015},
  volume = {1},
  number = {1},
  pages = {16},
  url = {https://genomicscomputbiol.org/ojs/index.php/GCB/article/view/16}
}
Kettenbach, A.N., Sano, H., Keller, S.R., Lienhard, G.E. and Gerber, S.A. SPECHT – Single-stage phosphopeptide enrichment and stable-isotope chemical tagging: Quantitative phosphoproteomics of insulin action in muscle 2015 Journal of Proteomics
Vol. 114, pp. 48-60 
article DOI URL 
Abstract: The study of cellular signaling remains a significant challenge for translational and clinical research. In particular, robust and accurate methods for quantitative phosphoproteomics in tissues and tumors represent significant hurdles for such efforts. In the present work, we design, implement and validate a method for single-stage phosphopeptide enrichment and stable isotope chemical tagging, or SPECHT, that enables the use of iTRAQ, TMT and/or reductive dimethyl-labeling strategies to be applied to phosphoproteomics experiments performed on primary tissue. We develop and validate our approach using reductive dimethyl-labeling and HeLa cells in culture, and find these results indistinguishable from data generated from more traditional SILAC-labeled HeLa cells mixed at the cell level. We apply the SPECHT approach to the quantitative analysis of insulin signaling in a murine myotube cell line and muscle tissue, identify known as well as new phosphorylation events, and validate these phosphorylation sites using phospho-specific antibodies. Taken together, our work validates chemical tagging post-single-stage phosphoenrichment as a general strategy for studying cellular signaling in primary tissues. Biological significance Through the use of a quantitatively reproducible, proteome-wide phosphopeptide enrichment strategy, we demonstrated the feasibility of post-phosphopeptide purification chemical labeling and tagging as an enabling approach for quantitative phosphoproteomics of primary tissues. Using reductive dimethyl labeling as a generalized chemical tagging strategy, we compared the performance of post-phosphopeptide purification chemical tagging to the well established community standard, SILAC, in insulin-stimulated tissue culture cells. We then extended our method to the analysis of low-dose insulin signaling in murine muscle tissue, and report on the analytical and biological significance of our results.
BibTeX:
@article{Kettenbach2015,
  author = {Kettenbach, Arminja N and Sano, Hiroyuki and Keller, Susanna R and Lienhard, Gustav E and Gerber, Scott A},
  title = {SPECHT – Single-stage phosphopeptide enrichment and stable-isotope chemical tagging: Quantitative phosphoproteomics of insulin action in muscle},
  journal = {Journal of Proteomics},
  year = {2015},
  volume = {114},
  pages = {48--60},
  url = {http://www.sciencedirect.com/science/article/pii/S1874391914005065},
  doi = {http://doi.org/10.1016/j.jprot.2014.11.001}
}
Kim, C.-K., Seol, Y.-J., Shin, Y., Lim, H.-M., Lee, G.-S., Kim, A.-R., Lee, T.-H., Lee, J.-H., Park, D.-S., Yoo, S., Kim, Y.-H. and Kim, Y.-K. Whole-Genome Resequencing and Transcriptomic Analysis to Identify Genes Involved in Leaf-Color Diversity in Ornamental Rice Plants 2015 PLOS ONE
Vol. 10(4), pp. e0124071 
article DOI URL 
BibTeX:
@article{Kim2015,
  author = {Kim, Chang-Kug and Seol, Young-Joo and Shin, Younhee and Lim, Hye-Min and Lee, Gang-Seob and Kim, A-Ram and Lee, Tae-Ho and Lee, Jae-Hee and Park, Dong-Suk and Yoo, Seungil and Kim, Yong-Hwan and Kim, Yong-Kab},
  title = {Whole-Genome Resequencing and Transcriptomic Analysis to Identify Genes Involved in Leaf-Color Diversity in Ornamental Rice Plants},
  journal = {PLOS ONE},
  year = {2015},
  volume = {10},
  number = {4},
  pages = {e0124071},
  url = {http://dx.plos.org/10.1371/journal.pone.0124071},
  doi = {http://doi.org/10.1371/journal.pone.0124071}
}
Koltes, J.E., Kumar, D., Kataria, R.S., Cooper, V. and Reecy, J.M. Transcriptional profiling of PRKG2-null growth plate identifies putative down-stream targets of PRKG2. 2015 BMC research notes
Vol. 8(1), pp. 177 
article URL 
Abstract: BACKGROUND: Kinase activity of cGMP-dependent, type II, protein kinase (PRKG2) is required for the proliferative to hypertrophic transition of growth plate chondrocytes during endochondral ossification. Loss of PRKG2 function in rodent and bovine models results in dwarfism. The objective of this study was to identify pathways regulated or impacted by PRKG2 loss of function that may be responsible for disproportionate dwarfism at the molecular level.

METHODS: Microarray technology was used to compare growth plate cartilage gene expression in dwarf versus unaffected Angus cattle to identify putative downstream targets of PRGK2.

RESULTS: Pathway enrichment of 1284 transcripts (nominal p textless 0.05) was used to identify candidate pathways consistent with the molecular phenotype of disproportionate dwarfism. Analysis with the DAVID pathway suite identified differentially expressed genes that clustered in the MHC, cytochrome B, WNT, and Muc1 pathways. A second analysis with pathway studio software identified differentially expressed genes in a host of pathways (e.g. CREB1, P21, CTNNB1, EGFR, EP300, JUN, P53, RHOA, and SRC). As a proof of concept, we validated the differential expression of five genes regulated by P53, including CEBPA, BRCA1, BUB1, CD58, and VDR by real-time PCR (p textless 0.05).

CONCLUSIONS: Known and novel targets of PRKG2 were identified as enriched pathways in this study. This study indicates that loss of PRKG2 function results in differential expression of P53 regulated genes as well as additional pathways consistent with increased proliferation and apoptosis in the growth plate due to achondroplastic dwarfism.
BibTeX:
@article{Koltes2015,
  author = {Koltes, James E and Kumar, Dinesh and Kataria, Ranjit S and Cooper, Vickie and Reecy, James M},
  title = {Transcriptional profiling of PRKG2-null growth plate identifies putative down-stream targets of PRKG2.},
  journal = {BMC research notes},
  publisher = {BioMed Central},
  year = {2015},
  volume = {8},
  number = {1},
  pages = {177},
  url = {http://bmcresnotes.biomedcentral.com/articles/10.1186/s13104-015-1136-6}
}
Krzyzanowska, A., García-Consuegra, I., Pascual, C., Antequera, D., Ferrer, I. and Carro, E. Expression of Regulatory Proteins in Choroid Plexus Changes in Early Stages of Alzheimer Disease 2015 Journal of Neuropathology and Experimental Neurology  article DOI URL 
Abstract: Recent studies indicate that the choroid plexus has important physiologic and pathologic roles in Alzheimer disease (AD). To obtain additional insight on choroid plexus function, we performed a proteomic analysis of choroid plexus samples from patients with AD stages I to II (n = 16), III to IV (n = 16), and V to VI (n = 11) and 7 age-matched control subjects. We used 2-dimensional differential gel electrophoresis coupled with mass spectrometry to generate a complete picture of changes in choroid plexus protein expression occurring in AD patients. We identified 6 proteins: 14-3-3 β/α, 14-3-3 ε, moesin, proteasome activator complex subunit 1, annexin V, and aldehyde dehydrogenase, which were significantly regulated in AD patient samples (p textless 0.05, textgreater1.5-fold variation in expression vs control samples). These proteins are implicated in major physiologic functions including mitochondrial dysfunction and apoptosis regulation. These findings contribute additional significance to the emerging importance of molecular and functional changes of choroid plexus function in the pathophysiology of AD.
BibTeX:
@article{Krzyzanowska2015,
  author = {Krzyzanowska, Agnieszka and García-Consuegra, Inés and Pascual, Consuelo and Antequera, Desiree and Ferrer, Isidro and Carro, Eva},
  title = {Expression of Regulatory Proteins in Choroid Plexus Changes in Early Stages of Alzheimer Disease},
  journal = {Journal of Neuropathology and Experimental Neurology},
  year = {2015},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/25756589},
  doi = {http://doi.org/10.1097/NEN.0000000000000181}
}
Kwon, W.-S., Rahman, M.S., Lee, J.-S., Yoon, S.-J., Park, Y.-J. and Pang, M.-G. Discovery of predictive biomarkers for litter size in boar spermatozoa 2015 Molecular & Cellular Proteomics, pp. mcp.M114.045369  article DOI URL 
Abstract: Conventional semen analysis has been utilized to prognose and diagnose male fertility. While this tool is essential for providing initial quantitative information about semen, it remains a subject of debate. Therefore, development of new methods for the prognosis and diagnosis of male fertility should be seriously considered for animal species of economic importance as well as for humans. In the present study, we applied a comprehensive proteomic approach to identify global protein biomarkers in boar spermatozoa in order to increase the precision of male fertility prognoses and diagnoses. We determined that L-amino-acid oxidase, mitochondrial malate dehydrogenase 2, NAD (MDH2), cytosolic 5'-nucleotidase 1B, lysozyme-like protein 4, and calmodulin (CALM) were significantly and abundantly expressed in high-litter size spermatozoa. We also found that equatorin, spermadhesin AWN, triosephosphate isomerase (TPI), Ras-related protein Rab-2A (RAB2A), spermadhesin AQN-3, and NADH dehydrogenase [ubiquinone] iron-sulfur protein 2 (NDUFS2) were significantly and abundantly expressed in low-litter size spermatozoa (textgreater3-fold). Moreover, RAB2A, TPI, and NDUFS2 were negatively correlated with litter size, while CALM and MDH2 were positively correlated. This study provides novel biomarkers for the prediction of male fertility. To the best of our knowledge, this is the first work that shows significantly increased litter size using male fertility biomarkers in a field trial. Moreover, these protein markers may provide new developmental tools for the selection of superior sires as well as for the prognosis and diagnosis of male fertility.
BibTeX:
@article{Kwon2015,
  author = {Kwon, Woo-Sung and Rahman, Md Saidur and Lee, June-Sub and Yoon, Sung-Jae and Park, Yoo-Jin and Pang, Myung-Geol},
  title = {Discovery of predictive biomarkers for litter size in boar spermatozoa},
  journal = {Molecular & Cellular Proteomics},
  year = {2015},
  pages = {mcp.M114.045369},
  url = {http://www.mcponline.org/content/early/2015/02/18/mcp.M114.045369 http://www.ncbi.nlm.nih.gov/pubmed/25693803},
  doi = {http://doi.org/10.1074/mcp.M114.045369}
}
Kwon, W.-S., Oh, S.-A., Kim, Y.-J., Rahman, M.S., Park, Y.-J. and Pang, M.-G. Proteomic approaches for profiling negative fertility markers in inferior boar spermatozoa 2015 Scientific Reports
Vol. 5, pp. 13821 
article DOI URL 
BibTeX:
@article{Kwon2015a,
  author = {Kwon, Woo-Sung and Oh, Shin-Ae and Kim, Ye-Ji and Rahman, Md Saidur and Park, Yoo-Jin and Pang, Myung-Geol},
  title = {Proteomic approaches for profiling negative fertility markers in inferior boar spermatozoa},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  pages = {13821},
  url = {http://www.nature.com/doifinder/10.1038/srep13821},
  doi = {http://doi.org/10.1038/srep13821}
}
Larrainzar, E., Riely, B., Kim, S.C., Carrasquilla-Garcia, N., Yu, H.-J., Hwang, H.-J., Oh, M., Kim, G.B., Surendrarao, A., Chasman, D., Siahpirani, A.F., Penmetsa, R.V., Lee, G.-S., Kim, N., Roy, S., Mun, J.-H. and Cook, D.R. Deep sequencing of the Medicago truncatula root transcriptome reveals a massive and early interaction between Nod factor and ethylene signals 2015 Plant Physiology, pp. pp.00350.2015  article DOI URL 
Abstract: The legume-rhizobium symbiosis is initiated through activation of the Nod factor-signaling cascade, leading to a rapid reprogramming of host cell developmental pathways. In this work we combine transcriptome sequencing (RNA-seq) with molecular genetics and network analysis to quantify and categorize the transcriptional changes occurring in roots of barrel medic (Medicago truncatula) from minutes to days after inoculation with Sinorhizobium medicae. To identify the nature of the inductive and regulatory cues, we employed mutants with absent or decreased Nod factor sensitivities (nfp and lyk3, respectively) and an ethylene (ET)-insensitive, Nod factor hypersensitive mutant (skl). This unique dataset encompasses nine time points allowing observation of the symbiotic regulation of diverse biological processes with high temporal resolution. Among the many outputs of the study is the early Nod factor-induced, ET-regulated expression of ET signaling and biosynthesis genes. These results suggest that Nod factor signaling activates ET production to attenuate its own signal. Promoter:GUS fusions report ET biosynthesis both in root hairs responding to rhizobium as well as in meristematic tissue during nodule organogenesis and growth, indicating that ET signaling functions at multiple developmental stages during symbiosis. In addition, we identified thousands of novel candidate genes undergoing a Nod-factor dependent, ET-regulated expression. We leveraged the power of this large dataset to model Nod factor and ET-regulated signaling networks using MERLIN, a regulator network inference algorithm. These analyses predict key nodes regulating the biological process impacted by Nod factor perception. We have made these results available to the research community through a searchable online resource.
BibTeX:
@article{Larrainzar2015,
  author = {Larrainzar, Estibaliz and Riely, Brendan and Kim, Sang Cheol and Carrasquilla-Garcia, Noelia and Yu, Hee-Ju and Hwang, Hyun-Ju and Oh, Mijin and Kim, Goon Bo and Surendrarao, Anandkumar and Chasman, Deborah and Siahpirani, Alireza F and Penmetsa, R Varma and Lee, Gang-Seob and Kim, Namshin and Roy, Sushmita and Mun, Jeong-Hwan and Cook, Douglas R},
  title = {Deep sequencing of the Medicago truncatula root transcriptome reveals a massive and early interaction between Nod factor and ethylene signals},
  journal = {Plant Physiology},
  year = {2015},
  pages = {pp.00350.2015},
  url = {http://www.plantphysiol.org/content/early/2015/07/14/pp.15.00350 http://www.ncbi.nlm.nih.gov/pubmed/26175514 http://www.plantphysiol.org/content/early/2015/07/14/pp.15.00350.abstract},
  doi = {http://doi.org/10.1104/pp.15.00350}
}
Lee, J.H., Yoo, J.Y., You, Y.-A., Kwon, W.S., mi Lee, S., Pang, M.G. and Kim, Y.J. Proteomic analysis of fetal programming-related obesity markers 2015 PROTEOMICS, pp. n/a-n/a  article DOI URL 
Abstract: The objectives of this study were to analyze fetal programming in rat brain using proteomic analysis and to identify fetal programming-related obesity markers. Sprague Dawley rats were divided into four feeding groups: (1) the Ad Libitum (AdLib)/AdLib group was given a normal diet during pregnancy and the lactation period; (2) the AdLib/maternal food restriction group (FR) was subjected to 50% FR during the lactation period; (3) the FR/Ad Lib group was subjected to 50% FR during pregnancy; and (4) the FR/FR group was subjected to 50% FR during pregnancy and the lactation period. Offspring from each group were sacrificed at 3 weeks of age and whole brains were dissected. To obtain a maximum number of protein markers related to obesity, two-dimensional (2D) gel electrophoresis and Pathway Studio bioinformatics analysis were performed. The identities of the markers among the selected and candidate proteins were confirmed by Western blotting and immunohistochemistry. Proteomic and bioinformatics analyses revealed that expression of ubiquitin carboxy-terminal hydrolase L1 (UCHL1) and Secernin 1 (SCRN1) were significantly different in the FR/AdLib group compared with the AdLib/AdLib group for both male and female offspring. These findings suggest that UCHL1 and SCRN1 may be used as fetal programming-related obesity markers. This article is protected by copyright. All rights reserved
BibTeX:
@article{Lee2015,
  author = {Lee, Ji Hye and Yoo, Jae Young and You, Young-Ah and Kwon, Woo Sung and mi Lee, Sang and Pang, Myung Geol and Kim, Young Ju},
  title = {Proteomic analysis of fetal programming-related obesity markers},
  journal = {PROTEOMICS},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1002/pmic.201400359/abstract},
  doi = {http://doi.org/10.1002/pmic.201400359}
}
Leslie, K., Whitley, G.S., Herse, F., Dechend, R., Ashton, S.V., Laing, K., Thilaganathan, B. and Cartwright, J.E. Increased Apoptosis, Altered Oxygen Signaling, and Antioxidant Defenses in First-Trimester Pregnancies with High-Resistance Uterine Artery Blood Flow 2015 The American Journal of Pathology  article DOI URL 
Abstract: The mechanisms of deficient placentation in the first trimester remain poorly understood, although apoptosis, hypoxia, and oxidative stress have been implicated. High uterine artery Doppler resistance indexes (RIs) are predictive of placental complications of pregnancy, such as preeclampsia, fetal growth restriction, and stillbirth. We provide evidence that even in the first trimester, pregnancies with high uterine artery Doppler RI demonstrate alterations in placental gene and protein expression. Apoptosis was significantly higher in high RI placental tissue, as determined by Western blot analysis of cleaved poly (ADP-ribose) polymerase and caspase 3. Protein expression of the trophoblast survival factor insulin-like growth factor-2 was significantly lower. Both high and normal RI placentas showed evidence of hypoxia and oxidative stress with expression of hypoxia-inducible factors 1α and 2α, heat shock protein 70, presence of nitrotyrosine residues, and lipid peroxidation. We observed no exaggerated placental hypoxia or oxidative stress associated with high RI pregnancies. High RI placental tissue demonstrated an altered balance of antioxidant enzyme activity. Hypoxia and oxidative stress appear to be a physiological state in early pregnancy; our data did not support the hypothesis that they are associated with deficient placentation in the first trimester. Higher levels of apoptosis, reduced insulin-like growth factor-2 expression, and altered antioxidant defenses may contribute to abnormal placentation and the later development of pregnancy complications, such as preeclampsia, fetal growth restriction, and stillbirth.
BibTeX:
@article{Leslie2015,
  author = {Leslie, Karin and Whitley, Guy StJ. and Herse, Florian and Dechend, Ralf and Ashton, Sandra V and Laing, Ken and Thilaganathan, Baskaran and Cartwright, Judith E},
  title = {Increased Apoptosis, Altered Oxygen Signaling, and Antioxidant Defenses in First-Trimester Pregnancies with High-Resistance Uterine Artery Blood Flow},
  journal = {The American Journal of Pathology},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S0002944015004253},
  doi = {http://doi.org/10.1016/j.ajpath.2015.06.020}
}
Lesur, I., Bechade, A., Lalanne, C., Klopp, C., Noirot, C., Leplé, J.-C., Kremer, A., Plomion, C. and Le Provost, G. A unigene set for European beech (Fagus sylvatica L.) and its use to decipher the molecular mechanisms involved in dormancy regulation 2015 Molecular Ecology Resources, pp. n/a-n/a  article DOI URL 
Abstract: Systematic sequencing is the method of choice for generating genomic resources for molecular marker development and candidate gene identification in non-model species. We generated 47,357 Sanger ESTs and 2.2M Roche-454 reads from five cDNA libraries for European beech (Fagus sylvatica L.). This tree species of high ecological and economic value in Europe is among the most representative trees of deciduous broadleaf forests. The sequences generated were assembled into 21,057 contigs with MIRA software. Functional annotations were obtained for 85% of these contigs, from the proteomes of four plant species, Swissprot accessions and the Gene Ontology database. We were able to identify 28,079 in silico SNPs for future marker development. Moreover, RNAseq and qPCR approaches identified genes and gene networks regulated differentially between two critical phenological stages preceding vegetative bud burst (the quiescent and swelling buds stages). According to climatic model based projection, some European beech populations may be endangered, particularly at the southern and eastern edges of the European distribution range, which are strongly affected by current climate change. This first genomic resource for the genus Fagus should facilitate the identification of key genes for beech adaptation and management strategies for preserving beech adaptability. This article is protected by copyright. All rights reserved.
BibTeX:
@article{Lesur2015,
  author = {Lesur, Isabelle and Bechade, Alison and Lalanne, Céline and Klopp, Christophe and Noirot, Céline and Leplé, Jean-Charles and Kremer, Antoine and Plomion, Christophe and Le Provost, Grégoire},
  title = {A unigene set for European beech (Fagus sylvatica L.) and its use to decipher the molecular mechanisms involved in dormancy regulation},
  journal = {Molecular Ecology Resources},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1111/1755-0998.12373/abstract},
  doi = {http://doi.org/10.1111/1755-0998.12373}
}
Lesur, I., Provost, G.L., Bento, P., Silva, C.D., Leplé, J.-C., Murat, F., Ueno, S., Bartholomé, J., Lalanne, C., Ehrenmann, F., Noirot, C., Burban, C., Léger, V., Amselem, J., Belser, C., Quesneville, H., Stierschneider, M., Fluch, S., Feldhahn, L., Tarkka, M., Herrmann, S., Buscot, F., Klopp, C., Kremer, A., Salse, J., Aury, J.-M. and Plomion, C. The oak gene expression atlas: insights into Fagaceae genome evolution and the discovery of genes regulated during bud dormancy release 2015 BMC Genomics
Vol. 16(1), pp. 112 
article DOI URL 
BibTeX:
@article{Lesur2015a,
  author = {Lesur, Isabelle and Provost, Grégoire Le and Bento, Pascal and Silva, Corinne Da and Leplé, Jean-Charles and Murat, Florent and Ueno, Saneyoshi and Bartholomé, Jerôme and Lalanne, Céline and Ehrenmann, François and Noirot, Céline and Burban, Christian and Léger, Valérie and Amselem, Joelle and Belser, Caroline and Quesneville, Hadi and Stierschneider, Michael and Fluch, Silvia and Feldhahn, Lasse and Tarkka, Mika and Herrmann, Sylvie and Buscot, François and Klopp, Christophe and Kremer, Antoine and Salse, Jérôme and Aury, Jean-Marc and Plomion, Christophe},
  title = {The oak gene expression atlas: insights into Fagaceae genome evolution and the discovery of genes regulated during bud dormancy release},
  journal = {BMC Genomics},
  year = {2015},
  volume = {16},
  number = {1},
  pages = {112},
  url = {http://www.biomedcentral.com/1471-2164/16/112/abstract http://www.biomedcentral.com/content/pdf/s12864-015-1331-9.pdf},
  doi = {http://doi.org/10.1186/s12864-015-1331-9}
}
Ligaba, S.B., Khurana, A., Graham, G., Krawczyk, E., Jablonski, S., Petricoin, E.F., Glazer, R.I. and Upadhyay, G. Multifactorial Analysis of Conditional Reprogramming of Human Keratinocytes 2015 PLoS ONE
Vol. 10(2), pp. e0116755 
article DOI URL 
Abstract: Co-culture of human primary epithelial cells with irradiated 3T3 fibroblast feeder cells (J2 cells) and the Rho kinase inhibitor Y-27632 (Y) allows for the unrestricted growth of cells of epithelial origin by the process termed conditional reprogramming. To better understand the nature of the signaling processes associated with conditionally reprogrammed cells, the effect of the two critical components of the co-culture conditions, J2 cells and Y, on the growth of human foreskin keratinocytes (HFKs) was evaluated by gene expression profiling, reverse-phase protein arrays and siRNA screening. J2 cells and Y acted cooperatively to down-regulate differentiation, and upregulate proliferation and cell adhesion, including increased pT308Akt and pERK, and reduced TGF-β pathway signaling. These findings establish a mechanistic basis for the unlimited growth potential of human epithelial cells that will be invaluable to assess the effect of genetic changes in pathologic tissues and their response to therapeutic agents.
BibTeX:
@article{Ligaba2015,
  author = {Ligaba, Segni B and Khurana, Anikita and Graham, Garrett and Krawczyk, Ewa and Jablonski, Sandra and Petricoin, Emanuel F and Glazer, Robert I and Upadhyay, Geeta},
  title = {Multifactorial Analysis of Conditional Reprogramming of Human Keratinocytes},
  journal = {PLoS ONE},
  year = {2015},
  volume = {10},
  number = {2},
  pages = {e0116755},
  url = {http://dx.doi.org/10.1371/journal.pone.0116755 http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0116755&representation=PDF},
  doi = {http://doi.org/10.1371/journal.pone.0116755}
}
Lim, D., Chai, H.-H., Lee, S.-H., Cho, Y.-M., Choi, J.-W. and Kim, N.-K. Gene Expression Patterns Associated with Peroxisome Proliferator-activated Receptor (PPAR) Signaling in the textlessitextgreaterLongissimus dorsitextless/itextgreater of Hanwoo (Korean Cattle) 2015 Asian-Australasian Journal of Animal Sciences  article DOI URL 
BibTeX:
@article{Lim2015,
  author = {Lim, Dajeong and Chai, Han-Ha and Lee, Seung-Hwan and Cho, Yong-Min and Choi, Jung-Woo and Kim, Nam-Kuk},
  title = {Gene Expression Patterns Associated with Peroxisome Proliferator-activated Receptor (PPAR) Signaling in the textlessitextgreaterLongissimus dorsitextless/itextgreater of Hanwoo (Korean Cattle)},
  journal = {Asian-Australasian Journal of Animal Sciences},
  year = {2015},
  url = {http://www.ajas.info/journal/view.php?doi=10.5713/ajas.14.0811},
  doi = {http://doi.org/10.5713/ajas.14.0811}
}
Linde, J., Schulze, S., Henkel, S.G. and Guthke, R. Data- and knowledge-based modeling of gene regulatory networks: an update 2015 EXCLI Journal  article DOI URL 
BibTeX:
@article{Linde2015,
  author = {Linde, Jörg and Schulze, Sylvie and Henkel, Sebastian G and Guthke, Reinhard},
  title = {Data- and knowledge-based modeling of gene regulatory networks: an update},
  journal = {EXCLI Journal},
  year = {2015},
  url = {http://dx.doi.org/10.17179/excli2015-168},
  doi = {http://doi.org/10.17179/excli2015-168}
}
Liu, H., Zhang, H., Cui, R., Guo, X., Wang, D. and Dai, J. Activation of peroxisome proliferator-activated receptor α ameliorates perfluorododecanoic acid-induced production of reactive oxygen species in rat liver 2015 Archives of Toxicology, pp. 1-15  article DOI URL 
Abstract: Perfluorododecanoic acid (PFDoA) is a ubiquitous environmental pollutant known to cause hepatocellular hypertrophy; however, the mechanisms of hepatotoxicity remain poorly understood. In this study, male rats were exposed to 0, 0.05, 0.2 and 0.5 mg/kg/day of PFDoA for 110 days. After two-dimensional differential gel electrophoresis and MALDI-TOF/TOF analysis, 73 differentially expressed proteins involved in lipid metabolism, inflammation, stress response and other functions were successfully identified. Among them, six significantly changed proteins (CTE1, MTE1, HADHA, ECH1, ALDH2 and CPS1) were found to be regulated by peroxisome proliferator-activated receptor alpha (PPARα). The anti-oxidant enzyme activity assays of superoxide dismutase and glutathione peroxidase and the content of thiobarbituric acid-reactive substances in the liver implied that PFDoA caused oxidative stress. The mRNA levels of PPARα in rat primary hepatocytes were knocked down by lentivirus-mediated RNAi. Furthermore, targeted protein levels of CTE1 and MTE1 were down-regulated, while those of HADHA, ALDH2 and CPS1 were up-regulated. After PFDoA exposure, however, the targeted protein levels of CTE1 and ALDH2 increased compared with those of the knockdown untreated group. The reactive oxygen species (ROS) content in rat hepatocytes assayed by flow cytometry significantly increased in the PPARα knockdown groups, consistent with the PPARα antagonist GW6471- and agonist WY14643-treated groups. These results strongly suggested that PPARα played an important role in suppressing ROS content in hepatocytes following PFDoA exposure.
BibTeX:
@article{Liu2015,
  author = {Liu, Hui and Zhang, Hongxia and Cui, Ruina and Guo, Xuejiang and Wang, Dazhi and Dai, Jiayin},
  title = {Activation of peroxisome proliferator-activated receptor α ameliorates perfluorododecanoic acid-induced production of reactive oxygen species in rat liver},
  journal = {Archives of Toxicology},
  year = {2015},
  pages = {1--15},
  url = {http://link.springer.com/article/10.1007/s00204-015-1559-9},
  doi = {http://doi.org/10.1007/s00204-015-1559-9}
}
Lv, J., Fan, N., Wang, Y., Wang, X. and Gao, C. Identification of Differentially Expressed Proteins of Normal and Cancerous Human Colorectal Tissues by Liquid Chromatograph-Mass Spectrometer Based on iTRAQ Approach 2015 Cancer Investigation  article DOI URL 
Abstract: Liquid chromatograph-mass spectrometer (LC/MS) based labeled with isobaric mass tags for relative and absolute quantitation (iTRAQ) analyses were performed to identify differentially expressed proteins from normal and cancerous human colorectal tissues. Around 802 proteins were identified, 68 proteins of which were defined as differentially expressed proteins. Bioinformatics analysis indicated that these differentially expressed proteins correlated with several specific cellular processes and pathways which have relationships with pathological changes of colorectal cancer (CRC). EHD2 were selected to verify its expression patterns and localization using western blotting and immunohistochemistry respectively. LC/MS-based iTRAQ proteomic approach would provide new information about the character of CRC.
BibTeX:
@article{Lv2015,
  author = {Lv, Jingjing and Fan, Naijun and Wang, Yangkun and Wang, Xiuli and Gao, Chunfang},
  title = {Identification of Differentially Expressed Proteins of Normal and Cancerous Human Colorectal Tissues by Liquid Chromatograph-Mass Spectrometer Based on iTRAQ Approach},
  journal = {Cancer Investigation},
  year = {2015},
  url = {http://informahealthcare.com/doi/abs/10.3109/07357907.2015.1055757},
  doi = {http://doi.org/10.3109/07357907.2015.1055757}
}
Madhavan, S., Gusev, Y., Singh, S. and Riggins, R.B. ERRγ target genes are poor prognostic factors in Tamoxifen-treated breast cancer 2015 Journal of experimental & clinical cancer research: CR
Vol. 34(1), pp. 45 
article DOI URL 
Abstract: BACKGROUND: One-third of estrogen (ER+) and/or progesterone receptor-positive (PGR+) breast tumors treated with Tamoxifen (TAM) do not respond to initial treatment, and the remaining 70% are at risk to relapse in the future. Estrogen-related receptor gamma (ESRRG, ERRγ) is an orphan nuclear receptor with broad, structural similarities to classical ER that is widely implicated in the transcriptional regulation of energy homeostasis. We have previously demonstrated that ERRγ induces resistance to TAM in ER+ breast cancer models, and that the receptor's transcriptional activity is modified by activation of the ERK/MAPK pathway. We hypothesize that hyper-activation or over-expression of ERRγ induces a pro-survival transcriptional program that impairs the ability of TAM to inhibit the growth of ER+ breast cancer. The goal of the present study is to determine whether ERRγ target genes are associated with reduced distant metastasis-free survival (DMFS) in ER+ breast cancer treated with TAM. METHODS: Raw gene expression data was obtained from 3 publicly available breast cancer clinical studies of women with ER+ breast cancer who received TAM as their sole endocrine therapy. ERRγ target genes were selected from 2 studies that published validated chromatin immunoprecipitation (ChIP) analyses of ERRγ promoter occupancy. Kaplan-Meier estimation was used to determine the association of ERRγ target genes with DMFS, and selected genes were validated in ER+, MCF7 breast cancer cells that express exogenous ERRγ. RESULTS: Thirty-seven validated receptor target genes were statistically significantly altered in women who experienced a DM within 5 years, and could classify several independent studies into poor vs. good DMFS. Two genes (EEF1A2 and PPIF) could similarly separate ER+, TAM-treated breast tumors by DMFS, and their protein levels were measured in an ER+ breast cancer cell line model with exogenous ERRγ. Finally, expression of ERRγ and these two target genes are elevated in models of ER+ breast cancer with hyperactivation of ERK/MAPK. CONCLUSIONS: ERRγ signaling is associated with poor DMFS in ER+, TAM-treated breast cancer, and ESRRG, EEF1A2, and PPIF comprise a 3-gene signaling node that may contribute to TAM resistance in the context of an active ERK/MAPK pathway.
BibTeX:
@article{Madhavan2015,
  author = {Madhavan, Subha and Gusev, Yuriy and Singh, Salendra and Riggins, Rebecca B},
  title = {ERRγ target genes are poor prognostic factors in Tamoxifen-treated breast cancer},
  journal = {Journal of experimental & clinical cancer research: CR},
  year = {2015},
  volume = {34},
  number = {1},
  pages = {45},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/25971350},
  doi = {http://doi.org/10.1186/s13046-015-0150-9}
}
Makoukji, J., Raad, M., Genadry, K., El-Sitt, S., Makhoul, N.J., Saad Aldin, E., Nohra, E., Jabbour, M., Sangaralingam, A., Chelala, C., Habib, R.H., Boulos, F., Tfayli, A. and Boustany, R.-M. Association between CLN3 (Neuronal Ceroid Lipofuscinosis, CLN3 Type) Gene Expression and Clinical Characteristics of Breast Cancer Patients 2015 Frontiers in Oncology
Vol. 5 
article DOI URL 
Abstract: Breast cancer is the most common cancer in women worldwide. Elucidation of underlying biology and molecular pathways is necessary for improving therapeutic options and clinical outcomes. CLN3 protein (CLN3p), deficient in neurodegenerative CLN3 disease is anti-apoptotic, and defects in the CLN3 gene cause accelerated apoptosis of neurons in CLN3 disease and up-regulation of ceramide. Dysregulated apoptotic pathways are often implicated in the development of the oncogenic phenotype. Predictably, CLN3 mRNA expression and CLN3 protein were up-regulated in a number of human and murine breast cancer-cell lines. Here, we determine CLN3 expression in non-tumor vs. tumor samples from fresh and formalin-fixed/paraffin-embedded (FFPE) breast tissue and analyze the association between CLN3 overexpression and different clinicopathological characteristics of breast cancer patients. Additionally, gene expression of 28 enzymes involved in sphingolipid metabolism was determined. CLN3 mRNA is overexpressed in tumor vs. non-tumor breast tissue from FFPE and fresh samples, as well as in mouse MCF7 breast cancer compared to MCF10A normal cells. Of the clinicopathological characteristics of tumor grade, age, menopause status, estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2), only absence of HER2 expression correlated with CLN3 overexpression. Sphingolipid genes for ceramide synthases 2 and 6 (CerS2; CerS6), delta(4)-desaturase sphingolipid 2 (DEGS2), and acidic sphingomyelinase (SMPD1) displayed higher expression levels in breast cancer vs. control tissue, whereas ceramide galactosyltransferase (UGT8) was underexpressed in breast cancer samples. CLN3 may be a novel molecular target for cancer drug discovery with the goal of modulation of ceramide pathways.
BibTeX:
@article{Makoukji2015,
  author = {Makoukji, Joelle and Raad, Mohamad and Genadry, Katia and El-Sitt, Sally and Makhoul, Nadine J and Saad Aldin, Ehab and Nohra, Eden and Jabbour, Mark and Sangaralingam, Ajanthah and Chelala, Claude and Habib, Robert H and Boulos, Fouad and Tfayli, Arafat and Boustany, Rose-Mary},
  title = {Association between CLN3 (Neuronal Ceroid Lipofuscinosis, CLN3 Type) Gene Expression and Clinical Characteristics of Breast Cancer Patients},
  journal = {Frontiers in Oncology},
  year = {2015},
  volume = {5},
  url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4601263/ files/3999/Makoukji et al. - 2015 - Association between CLN3 (Neuronal Ceroid Lipofusc.pdf},
  doi = {http://doi.org/10.3389/fonc.2015.00215}
}
Mandloi, S. and Chakrabarti, S. PALM-IST: Pathway Assembly from Literature Mining - an Information Search Tool 2015 Scientific Reports
Vol. 5 
article DOI URL 
Abstract: Manual curation of biomedical literature has become extremely tedious process due to its exponential growth in recent years. To extract meaningful information from such large and unstructured text, newer and more efficient mining tool is required. Here, we introduce PALM-IST, a computational platform that not only allows users to explore biomedical abstracts using keyword based text mining but also extracts biological entity (e.g., gene/protein, drug, disease, biological processes, cellular component, etc.) information from the extracted text and subsequently mines various databases to provide their comprehensive inter-relation (e.g., interaction, expression, etc.). PALM-IST constructs protein interaction network and pathway information data relevant to the text search using multiple data mining tools and assembles them to create a meta-interaction network. It also analyzes scientific collaboration by extraction and creation of “co-authorship network,” for a given search context. Hence, this useful combination of literature and data mining provided in PALM-IST can be used to extract novel protein-protein interaction (PPI), to generate meta-pathways and further to identify key crosstalk and bottleneck proteins. PALM-IST is available at www.hpppi.iicb.res.in/ctm.
BibTeX:
@article{Mandloi2015,
  author = {Mandloi, Sapan and Chakrabarti, Saikat},
  title = {PALM-IST: Pathway Assembly from Literature Mining - an Information Search Tool},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  url = {http://www.nature.com/srep/2015/150519/srep10021/full/srep10021.html http://www.nature.com/srep/2015/150519/srep10021/pdf/srep10021.pdf},
  doi = {http://doi.org/10.1038/srep10021}
}
Martins-de-Souza, D., Cassoli, J.S., Nascimento, J.M., Hensley, K., Guest, P.C., Velasco, A.P. and Turck, C.W. The protein interactome of collapsing response mediator protein-2 (CRMP2/DPYSL2) reveals novel partner proteins in brain tissue 2015 PROTEOMICS – Clinical Applications, pp. n/a-n/a  article DOI URL 
Abstract: Purpose : Collapsin response mediator protein-2 (CRMP2) is a central nervous system protein involved in neuronal development, axonal and neuronal growth, cell migration, and protein trafficking. Recent studies have linked perturbations in CRMP2 function to neurodegenerative disorders such as Alzheimer's disease, neuropathic pain and Batten disease, and to psychiatric disorders such as schizophrenia. Like most proteins, CRMP2 functions though interactions with a molecular network of proteins and other molecules. Experimental design : Here, we have attempted to identify additional proteins of the CRMP2 interactome to provide further leads about its roles in neurological functions. We used a combined co-immunoprecipitation and shotgun proteomic approach in order to identify CRMP2 protein partners. Results : We identified 78 CRMP2 protein partners not previously reported in public protein interaction databases. These were involved in 7 biological processes, which included cell signaling, growth, metabolism, trafficking and immune function, according to Gene Ontology classifications. Furthermore, 32 different molecular functions were found to be associated with these proteins, such as RNA binding, ribosomal functions, transporter activity, receptor activity, serine/threonine phosphatase activity, cell adhesion, cytoskeletal protein binding and catalytic activity. In silico pathway interactome construction revealed a highly connected network with the most overrepresented functions corresponding to semaphorin interactions, along with axon guidance and WNT5A-signalling. Conclusions and clinical relevance : Taken together, these findings suggest that the CRMP2 pathway is critical for regulating neuronal and synaptic architecture. Further studies along these lines might uncover novel biomarkers and drug targets for use in drug discovery. This article is protected by copyright. All rights reserved
BibTeX:
@article{Martins-de-Souza2015,
  author = {Martins-de-Souza, Daniel and Cassoli, Juliana S and Nascimento, Juliana M and Hensley, Kenneth and Guest, Paul C and Velasco, Andrés P and Turck, Christoph W},
  title = {The protein interactome of collapsing response mediator protein-2 (CRMP2/DPYSL2) reveals novel partner proteins in brain tissue},
  journal = {PROTEOMICS – Clinical Applications},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1002/prca.201500004/abstract},
  doi = {http://doi.org/10.1002/prca.201500004}
}
Mauriat, M., LEPLE, J.-C., Claverol, S., Bartholome, J., Negroni, L., Richet, N., Lalanne, C., Bonneu, M., Coutand, C. and Plomion, C. Quantitative proteomic and phosphoproteomic approaches for deciphering the signaling pathway for tension wood formation in poplar 2015 Journal of Proteome Research  article DOI URL 
Abstract: Trees adjust their growth following forced changes in orientation, to re-establish a vertical position. In angiosperms this adjustment involves the differential regulation of vascular cambial activity between the lower (opposite wood) and upper (tension wood) sides of the leaning stem. We investigated the molecular mechanisms leading to the formation of differential wood types, through a quantitative proteomic and phosphoproteomic analysis on poplar subjected to a gravitropic stimulus. We identified and quantified 675 phosphopeptides, corresponding to 468 phosphoproteins, and 3,763 non-phosphorylated peptides, corresponding to 1,155 proteins, in the differentiating xylem of straight-growing trees (control) and trees subjected to a gravitational stimulus during 8 weeks. About 1% of the peptides was specific to a wood type (straight, opposite or tension wood). Proteins quantified in more than one type of wood were more numerous: a mixed linear model showed 389 phosphopeptides and 556 proteins to differ in abundance between tension wood and opposite wood. 21% of the phosphoproteins identified here were described in their phosphorylated form for the first time. Our analyses revealed remarkable developmental molecular plasticity, with wood type-specific phosphorylation events, and highlighted the involvement of different proteins in the biosynthesis of cell wall components during the formation of the three types of wood.
BibTeX:
@article{Mauriat2015,
  author = {Mauriat, Mélanie and LEPLE, Jean-Charles and Claverol, Stéphane and Bartholome, Jérôme and Negroni, Luc and Richet, Nicolas and Lalanne, Céline and Bonneu, Marc and Coutand, Catherine and Plomion, Christophe},
  title = {Quantitative proteomic and phosphoproteomic approaches for deciphering the signaling pathway for tension wood formation in poplar},
  journal = {Journal of Proteome Research},
  year = {2015},
  url = {http://dx.doi.org/10.1021/acs.jproteome.5b00140 http://pubs.acs.org/doi/abs/10.1021/acs.jproteome.5b00140},
  doi = {http://doi.org/10.1021/acs.jproteome.5b00140}
}
McLennan, R., Schumacher, L.J., Morrison, J.A., Teddy, J.M., Ridenour, D.A., Box, A.C., Semerad, C.L., Li, H., McDowell, W., Kay, D., Maini, P.K., Baker, R.E. and Kulesa, P.M. Neural crest migration is driven by a few trailblazer cells with a unique molecular signature narrowly confined to the invasive front 2015 Development, pp. dev.117507  article DOI URL 
Abstract: Neural crest (NC) cell migration is crucial to the formation of peripheral tissues during vertebrate development. However, how NC cells respond to different microenvironments to maintain persistence of direction and cohesion in multicellular streams remains unclear. To address this, we profiled eight subregions of a typical cranial NC cell migratory stream. Hierarchical clustering showed significant differences in the expression profiles of the lead three subregions compared with newly emerged cells. Multiplexed imaging of mRNA expression using fluorescent hybridization chain reaction (HCR) quantitatively confirmed the expression profiles of lead cells. Computational modeling predicted that a small fraction of lead cells that detect directional information is optimal for successful stream migration. Single-cell profiling then revealed a unique molecular signature that is consistent and stable over time in a subset of lead cells within the most advanced portion of the migratory front, which we term trailblazers. Model simulations that forced a lead cell behavior in the trailing subpopulation predicted cell bunching near the migratory domain entrance. Misexpression of the trailblazer molecular signature by perturbation of two upstream transcription factors agreed with the in silico prediction and showed alterations to NC cell migration distance and stream shape. These data are the first to characterize the molecular diversity within an NC cell migratory stream and offer insights into how molecular patterns are transduced into cell behaviors.
BibTeX:
@article{McLennan2015,
  author = {McLennan, Rebecca and Schumacher, Linus J and Morrison, Jason A and Teddy, Jessica M and Ridenour, Dennis A and Box, Andrew C and Semerad, Craig L and Li, Hua and McDowell, William and Kay, David and Maini, Philip K and Baker, Ruth E and Kulesa, Paul M},
  title = {Neural crest migration is driven by a few trailblazer cells with a unique molecular signature narrowly confined to the invasive front},
  journal = {Development},
  year = {2015},
  pages = {dev.117507},
  url = {http://dev.biologists.org/content/early/2015/05/14/dev.117507 http://www.ncbi.nlm.nih.gov/pubmed/25977364 http://dev.biologists.org/content/early/2015/05/14/dev.117507.abstract},
  doi = {http://doi.org/10.1242/dev.117507}
}
Moyon, S., Dubessy, A.L., Aigrot, M.S., Trotter, M., Huang, J.K., Dauphinot, L., Potier, M.C., Kerninon, C., Parsadaniantz, S.M., Franklin, R.J.M. and Lubetzki, C. Demyelination Causes Adult CNS Progenitors to Revert to an Immature State and Express Immune Cues That Support Their Migration 2015 The Journal of Neuroscience
Vol. 35(1), pp. 4-20 
article DOI URL 
Abstract: The declining efficiency of myelin regeneration in individuals with multiple sclerosis has stimulated a search for ways by which it might be therapeutically enhanced. Here we have used gene expression profiling on purified murine oligodendrocyte progenitor cells (OPCs), the remyelinating cells of the adult CNS, to obtain a comprehensive picture of how they become activated after demyelination and how this enables them to contribute to remyelination. We find that adult OPCs have a transcriptome more similar to that of oligodendrocytes than to neonatal OPCs, but revert to a neonatal-like transcriptome when activated. Part of the activation response involves increased expression of two genes of the innate immune system, IL1β and CCL2, which enhance the mobilization of OPCs. Our results add a new dimension to the role of the innate immune system in CNS regeneration, revealing how OPCs themselves contribute to the postinjury inflammatory milieu by producing cytokines that directly enhance their repopulation of areas of demyelination and hence their ability to contribute to remyelination.
BibTeX:
@article{Moyon2015,
  author = {Moyon, Sarah and Dubessy, Anne Laure and Aigrot, Marie Stephane and Trotter, Matthew and Huang, Jeffrey K and Dauphinot, Luce and Potier, Marie Claude and Kerninon, Christophe and Parsadaniantz, Stephane Melik and Franklin, Robin J M and Lubetzki, Catherine},
  title = {Demyelination Causes Adult CNS Progenitors to Revert to an Immature State and Express Immune Cues That Support Their Migration},
  journal = {The Journal of Neuroscience},
  year = {2015},
  volume = {35},
  number = {1},
  pages = {4--20},
  url = {http://www.jneurosci.org/content/35/1/4 http://www.ncbi.nlm.nih.gov/pubmed/25568099},
  doi = {http://doi.org/10.1523/JNEUROSCI.0849-14.2015}
}
Nalluri, J.J., Kamapantula, B.K., Barh, D., Jain, N., Bhattacharya, A., de Almeida, S.S., Ramos, R.T.J., Silva, A., Azevedo, V. and Ghosh, P. DISMIRA: Prioritization of disease candidates in miRNA-disease associations based on maximum weighted matching inference model and motif-based analysis 2015 BMC Genomics
Vol. 16(Suppl 5), pp. S12 
article DOI URL 
BibTeX:
@article{Nalluri2015,
  author = {Nalluri, Joseph J and Kamapantula, Bhanu K and Barh, Debmalya and Jain, Neha and Bhattacharya, Antaripa and de Almeida, Sintia S and Ramos, Rommel T Juca and Silva, Artur and Azevedo, Vasco and Ghosh, Preetam},
  title = {DISMIRA: Prioritization of disease candidates in miRNA-disease associations based on maximum weighted matching inference model and motif-based analysis},
  journal = {BMC Genomics},
  year = {2015},
  volume = {16},
  number = {Suppl 5},
  pages = {S12},
  url = {http://www.biomedcentral.com/1471-2164/16/S5/S12/abstract http://www.biomedcentral.com/content/pdf/1471-2164-16-S5-S12.pdf http://www.biomedcentral.com/1471-2164/16/S5/S12/},
  doi = {http://doi.org/10.1186/1471-2164-16-S5-S12}
}
Naville, M., Ishibashi, M., Ferg, M., Bengani, H., Rinkwitz, S., Krecsmarik, M., Hawkins, T.A., Wilson, S.W., Manning, E., Chilamakuri, C.S.R., Wilson, D.I., Louis, A., Lucy Raymond, F., Rastegar, S., Strähle, U., Lenhard, B., Bally-Cuif, L., van Heyningen, V., FitzPatrick, D.R., Becker, T.S. and Roest Crollius, H. Long-range evolutionary constraints reveal cis-regulatory interactions on the human X chromosome 2015 Nature Communications
Vol. 6 
article DOI URL 
Abstract: Enhancers can regulate the transcription of genes over long genomic distances. This is thought to lead to selection against genomic rearrangements within such regions that may disrupt this functional linkage. Here we test this concept experimentally using the human X chromosome. We describe a scoring method to identify evolutionary maintenance of linkage between conserved noncoding elements and neighbouring genes. Chromatin marks associated with enhancer function are strongly correlated with this linkage score. We test textgreater1,000 putative enhancers by transgenesis assays in zebrafish to ascertain the identity of the target gene. The majority of active enhancers drive a transgenic expression in a pattern consistent with the known expression of a linked gene. These results show that evolutionary maintenance of linkage is a reliable predictor of an enhancer's function, and provide new information to discover the genetic basis of diseases caused by the mis-regulation of gene expression.
BibTeX:
@article{Naville2015,
  author = {Naville, Magali and Ishibashi, Minaka and Ferg, Marco and Bengani, Hemant and Rinkwitz, Silke and Krecsmarik, Monika and Hawkins, Thomas A and Wilson, Stephen W and Manning, Elizabeth and Chilamakuri, Chandra S R and Wilson, David I and Louis, Alexandra and Lucy Raymond, F and Rastegar, Sepand and Strähle, Uwe and Lenhard, Boris and Bally-Cuif, Laure and van Heyningen, Veronica and FitzPatrick, David R and Becker, Thomas S and Roest Crollius, Hugues},
  title = {Long-range evolutionary constraints reveal cis-regulatory interactions on the human X chromosome},
  journal = {Nature Communications},
  year = {2015},
  volume = {6},
  url = {http://www.nature.com/ncomms/2015/150424/ncomms7904/full/ncomms7904.htmlaffil-auth http://www.nature.com/ncomms/2015/150424/ncomms7904/pdf/ncomms7904.pdf http://www.nature.com/ncomms/2015/150424/ncomms7904/full/ncomms7904.html?WT.ecid=NCOMMS-20150429},
  doi = {http://doi.org/10.1038/ncomms7904}
}
Nguyen, N.T.H., Miwa, M., Tsuruoka, Y., Chikayama, T. and Tojo, S. Wide-coverage relation extraction from MEDLINE using deep syntax 2015 BMC Bioinformatics
Vol. 16(1), pp. 107 
article DOI URL 
Abstract: PMID: 25887686
BibTeX:
@article{Nguyen2015,
  author = {Nguyen, Nhung T H and Miwa, Makoto and Tsuruoka, Yoshimasa and Chikayama, Takashi and Tojo, Satoshi},
  title = {Wide-coverage relation extraction from MEDLINE using deep syntax},
  journal = {BMC Bioinformatics},
  year = {2015},
  volume = {16},
  number = {1},
  pages = {107},
  url = {http://www.biomedcentral.com/1471-2105/16/107/abstract http://www.biomedcentral.com/content/pdf/s12859-015-0538-8.pdf http://www.biomedcentral.com/1471-2105/16/107},
  doi = {http://doi.org/10.1186/s12859-015-0538-8}
}
Nokkari, A., Mouhieddine, T.H., Itani, M.M., Abou-Kheir, W., Daoud, G., Zhu, R., Meshref, Y., Soueid, J., Al Hariri, M., Mondello, S., Jaffa, A.A. and Kobeissy, F. Characterization of the Kallikrein-Kinin System Post Chemical Neuronal Injury: An In Vitro Biochemical and Neuroproteomics Assessment 2015 PLoS ONE
Vol. 10(6), pp. e0128601 
article DOI URL 
Abstract: Traumatic Brain Injury (TBI) is the result of a mechanical impact on the brain provoking mild, moderate or severe symptoms. It is acknowledged that TBI leads to apoptotic and necrotic cell death; however, the exact mechanism by which brain trauma leads to neural injury is not fully elucidated. Some studies have highlighted the pivotal role of the Kallikrein-Kinin System (KKS) in brain trauma but the results are still controversial and inconclusive. In this study, we investigated both the expression and the role of Bradykinin 1 and 2 receptors (B1R and B2R), in mediating neuronal injury under chemical neurotoxicity paradigm in PC12 cell lines. The neuronal cell line PC12 was treated with the apoptotic drug Staurosporine (STS) to induce cell death. Intracellular calcium release was evaluated by Fluo 4-AM staining and showed that inhibition of the B2R prevented calcium release following STS treatment. Differential analyses utilizing immunofluorescence, Western blot and Real-time Polymerase Chain Reaction revealed an upregulation of both bradykinin receptors occurring at 3h and 12h post-STS treatment, but with a higher induction of B2R compared to B1R. This implies that STS-mediated apoptosis in PC12 cells is mainly conducted through B2R and partly via B1R. Finally, a neuroproteomics approach was conducted to find relevant proteins associated to STS and KKS in PC12 cells. Neuroproteomics results confirmed the presence of an inflammatory response leading to cell death during apoptosis-mediated STS treatment; however, a “survival” capacity was shown following inhibition of B2R coupled with STS treatment. Our data suggest that B2R is a key player in the inflammatory pathway following STS-mediated apoptosis in PC12 cells and its inhibition may represent a potential therapeutic tool in TBI.
BibTeX:
@article{Nokkari2015,
  author = {Nokkari, Amaly and Mouhieddine, Tarek H and Itani, Muhieddine M and Abou-Kheir, Wassim and Daoud, Georges and Zhu, Rui and Meshref, Yehia and Soueid, Jihane and Al Hariri, Moustafa and Mondello, Stefania and Jaffa, Ayad A and Kobeissy, Firas},
  title = {Characterization of the Kallikrein-Kinin System Post Chemical Neuronal Injury: An In Vitro Biochemical and Neuroproteomics Assessment},
  journal = {PLoS ONE},
  year = {2015},
  volume = {10},
  number = {6},
  pages = {e0128601},
  url = {http://dx.doi.org/10.1371/journal.pone.0128601 http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0128601&representation=PDF},
  doi = {http://doi.org/10.1371/journal.pone.0128601}
}
Ornostay, A., Marr, J., Loughery, J.R. and Martyniuk, C.J. Transcriptional networks associated with 5-alpha-dihydrotestosterone in the fathead minnow (Pimephales promelas) ovary 2015 General and Comparative Endocrinology  article DOI URL 
Abstract: Androgens play a significant role in regulating oogenesis in teleost fishes. The androgen dihydrotestosterone (DHT) is a potent non-aromatizable androgen involved in sexual differentiation in mammals; however, its actions are not well understood in teleost fish. To better characterize the physiological role of DHT in the fathead minnow (FHM) ovary on a temporal scale, in vitro assays for 17β-estradiol (E2) production were conducted in parallel with microarray analysis. Ovarian explants were incubated at different concentrations of DHT (10-6, 10-7, and 10-8M DHT) in three separate experiments conducted at 6, 9, and 12 h. DHT treatment resulted in a rapid and consistent increase in E2 production from the ovary at all three time points. Therefore, DHT may act to shift the balance of metabolites in the steroidogenic pathway within the ovary. Major biological themes affected by DHT in the ovary in one or more of the time points included those related to blood (e.g. vasodilation, blood vessel contraction, clotting), lipids (e.g. lipid storage, cholesterol metabolism, lipid degradation) and reproduction (e.g. hormone and steroid metabolism). Gene networks related to immune responses and calcium signaling were also affected by DHT, suggesting that this androgen may play a role in regulating these processes in the ovary. This study detected no change in mRNA levels of steroidogenic enzymes (cyp19a1, star, 11βhsd, 17βhsd, srd5a isoforms), suggesting that the observed increase in E2 production is likely more dependent on the pre-existing gene or protein complement in the ovary rather than the de novo expression of transcripts. This study increases knowledge regarding the roles of DHT and androgens in general in the teleost ovary and identifies molecular signaling pathways that may be associated with increased E2 production.
BibTeX:
@article{Ornostay2015,
  author = {Ornostay, Anna and Marr, Joshua and Loughery, Jennifer R and Martyniuk, Christopher J},
  title = {Transcriptional networks associated with 5-alpha-dihydrotestosterone in the fathead minnow (Pimephales promelas) ovary},
  journal = {General and Comparative Endocrinology},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S0016648015002464},
  doi = {http://doi.org/10.1016/j.ygcen.2015.09.005}
}
Pai, V.P., Martyniuk, C.J., Echeverri, K., Sundelacruz, S., Kaplan, D.L. and Levin, M. Genome-wide analysis reveals conserved transcriptional responses downstream of resting potential change in Xenopus embryos, axolotl regeneration, and human mesenchymal cell differentiation 2015 Regeneration, pp. n/a-n/a  article DOI URL 
Abstract: Endogenous bioelectric signaling via changes in cellular resting potential (Vmem) is a key regulator of patterning during regeneration and embryogenesis in numerous model systems. Depolarization of Vmem has been functionally implicated in de-differentiation, tumorigenesis, anatomical re-specification, and appendage regeneration. However, no unbiased analyses have been performed to understand genome-wide transcriptional responses to Vmem change in vivo. Moreover, it is unknown which genes or gene networks represent conserved targets of bioelectrical signaling across different patterning contexts and species. Here, we use microarray analysis to comparatively analyze transcriptional responses to Vmem depolarization. We compare the response of the transcriptome during embryogenesis (Xenopus development), regeneration (axolotl regeneration), and stem cell differentiation (human mesenchymal stem cells in culture) to identify common networks across model species that are associated with depolarization. Both sub-network enrichment and PANTHER analyses identified a number of key genetic modules as targets of Vmem change, and also revealed important (well-conserved) commonalities in bioelectric signal transduction, despite highly diverse experimental contexts and species. Depolarization regulates specific transcriptional networks across all three germ layers (ectoderm, mesoderm and endoderm) such as cell differentiation and apoptosis, and this information will be used for developing mechanistic models of bioelectric regulation of patterning. Moreover, our analysis reveals that Vmem change regulates transcripts related to important disease pathways such as cancer and neurodegeneration, which may represent novel targets for emerging electroceutical therapies. This article is protected by copyright. All rights reserved
BibTeX:
@article{Pai2015,
  author = {Pai, Vaibhav P and Martyniuk, Christopher J and Echeverri, Karen and Sundelacruz, Sarah and Kaplan, David L and Levin, Michael},
  title = {Genome-wide analysis reveals conserved transcriptional responses downstream of resting potential change in Xenopus embryos, axolotl regeneration, and human mesenchymal cell differentiation},
  journal = {Regeneration},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1002/reg2.48/abstract},
  doi = {http://doi.org/10.1002/reg2.48}
}
Panahi, B., Mohammadi, S.A., Khaksefidi, R.E., Fallah, J. and Ebrahimie, E. Genome-wide analysis of alternative splicing events in Hordeum vulgare: Highlighting retention of intron-based splicing and its possible function through network analysis 2015 FEBS Letters
Vol. 0(0) 
article DOI URL 
Abstract: In this study, using homology mapping of assembled expressed sequence tags against the genomic data, we identified alternative splicing events in barley. Results demonstrated that intron retention is frequently associated with specific abiotic stresses. Network analysis resulted in discovery of some specific sub networks between miRNAs and transcription factors in genes with high number of alternative splicing, such as cross talk between SPL2, SPL10 and SPL11 regulated by miR156 and miR157 families. To confirm the alternative splicing events, elongation factor protein (MLOC3412) was selected followed by experimental verification of the predicted splice variants by quantitative Reverse Transcription PCR (qRT-PCR). Our novel integrative approach opens a new avenue for functional annotation of alternative splicing through regulatory-based network discovery.
BibTeX:
@article{Panahi2015,
  author = {Panahi, Bahman and Mohammadi, Seyed Abolghasem and Khaksefidi, Reyhaneh Ebrahimi and Fallah, Jalil and Ebrahimie, Esmaeil},
  title = {Genome-wide analysis of alternative splicing events in Hordeum vulgare: Highlighting retention of intron-based splicing and its possible function through network analysis},
  journal = {FEBS Letters},
  year = {2015},
  volume = {0},
  number = {0},
  url = {http://www.febsletters.org/article/S0014579315008728/abstract http://www.febsletters.org/article/S0014-5793(15)00872-8/abstract},
  doi = {http://doi.org/10.1016/j.febslet.2015.09.023}
}
Pandey, A., Misra, P., Choudhary, D., Yadav, R., Goel, R., Bhambhani, S., Sanyal, I., Trivedi, R. and Kumar Trivedi, P. AtMYB12 expression in tomato leads to large scale differential modulation in transcriptome and flavonoid content in leaf and fruit tissues 2015 Scientific Reports
Vol. 5 
article DOI URL 
Abstract: Plants synthesize secondary metabolites, including flavonoids, which play important role during various stresses for their survival. These metabolites are also considered as health-protective components in functional foods. Flavonols, one of the important groups of flavonoids, apart from performing several roles in plants have been recognized as potent phytoceuticals for human health. Tomato fruits are deficient in this group of flavonoids and have been an important target for enhancing the accumulation of flavonols through genetic manipulations. In the present study, AtMYB12 transcription factor of the Arabidopsis has been expressed under constitutive promoter in tomato. Transgenic tomato lines exhibited enhanced accumulation of flavonols and chlorogenic acid (CGA) in leaf and fruit accompanied with elevated expression of phenylpropanoid pathway genes involved in flavonol biosynthesis. In addition, global gene expression analysis in leaf and fruit suggested that AtMYB12 modulates number of molecular processes including aromatic amino acid biosynthesis, phytohormone signaling and stress responses. Besides this, a differential modulation of the genes in fruits and leaves is reported in this study. Taken together, results demonstrate that modulation of primary carbon metabolism and other pathways by AtMYB12 in tomato may lead to sufficient substrate supply for enhanced content of phenolics in general and flavonols in particular.
BibTeX:
@article{Pandey2015,
  author = {Pandey, Ashutosh and Misra, Prashant and Choudhary, Dharmendra and Yadav, Reena and Goel, Ridhi and Bhambhani, Sweta and Sanyal, Indraneel and Trivedi, Ritu and Kumar Trivedi, Prabodh},
  title = {AtMYB12 expression in tomato leads to large scale differential modulation in transcriptome and flavonoid content in leaf and fruit tissues},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  url = {http://www.nature.com/srep/2015/150724/srep12412/full/srep12412.html},
  doi = {http://doi.org/10.1038/srep12412}
}
Panepistēmio tēs Krētēs., S., Pellat, L., Ahmetaga, A., Bano, G., Mason, H.D. and Whitehead, S.A. International journal of molecular medicine. 2015
Vol. 35(4)International Journal of Molecular Medicine, pp. 1088-1094 
book DOI URL 
Abstract: A short chain di-urea cross-linked poly(oxyethylene) (POE)/siloxane hybrid host (di-ureasil), designated as d-U(600), was doped with the Na3[Eu(dipic)s]textperiodcenteredxH2O (where dipic2- is the dipicolinate ion) complex. The resulting material is non-porous, semi-crystalline and thermally stable up to 145 °C. Because of the presence of the bulky dipic2- ligands, the addition of the complex to d-U(600) leads to the partial destruction of the hydrogen-bonded POE/urea aggregates of the hybrid matrix and to the formation of extra urea/urea aggregates. The incorporation of the complex into d-U(600) accounts for an increase of both the 5D0 lifetime and quantum efficiency values (1.950 ± 0.007 ms and 0.50, respectively) with respect to those of the isolated complex (1.7 ms and 0.46, respectively). The addition of the complex also contributes to an enhancement of the absolute emission quantum yield value, whose maximum value (0.66 excited at 280 nm) is the highest value reported for organic-inorganic hybrids modified by lanthanide complexes. textcopyright 2009 Elsevier B.V. All rights reserved.
BibTeX:
@book{PanepistemiotesKretes.2015,
  author = {Panepistēmio tēs Krētēs., S. and Pellat, L. and Ahmetaga, A. and Bano, G. and Mason, H. D. and Whitehead, S. A.},
  title = {International journal of molecular medicine.},
  booktitle = {International Journal of Molecular Medicine},
  publisher = {University of Crete, Faculty of Medicine},
  year = {2015},
  volume = {35},
  number = {4},
  pages = {1088--1094},
  url = {https://www.spandidos-publications.com/10.3892/ijmm.2015.2108},
  doi = {http://doi.org/10.1016/j.jphotochem.2009.04.022}
}
Pavlopoulos, G.A., Malliarakis, D., Papanikolaou, N., Theodosiou, T., Enright, A.J. and Iliopoulos, I. Visualizing genome and systems biology: technologies, tools, implementation techniques and trends, past, present and future 2015 GigaScience
Vol. 4 
article DOI URL 
Abstract: “Α picture is worth a thousand words.” This widely used adage sums up in a few words the notion that a successful visual representation of a concept should enable easy and rapid absorption of large amounts of information. Although, in general, the notion of capturing complex ideas using images is very appealing, would 1000 words be enough to describe the unknown in a research field such as the life sciences? Life sciences is one of the biggest generators of enormous datasets, mainly as a result of recent and rapid technological advances; their complexity can make these datasets incomprehensible without effective visualization methods. Here we discuss the past, present and future of genomic and systems biology visualization. We briefly comment on many visualization and analysis tools and the purposes that they serve. We focus on the latest libraries and programming languages that enable more effective, efficient and faster approaches for visualizing biological concepts, and also comment on the future human-computer interaction trends that would enable for enhancing visualization further.
BibTeX:
@article{Pavlopoulos2015,
  author = {Pavlopoulos, Georgios A and Malliarakis, Dimitris and Papanikolaou, Nikolas and Theodosiou, Theodosis and Enright, Anton J and Iliopoulos, Ioannis},
  title = {Visualizing genome and systems biology: technologies, tools, implementation techniques and trends, past, present and future},
  journal = {GigaScience},
  year = {2015},
  volume = {4},
  url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548842/},
  doi = {http://doi.org/10.1186/s13742-015-0077-2}
}
Peng, B., Lei, N., Chai, Y., Chan, E. and Zhang, J. CIP2A regulates cancer metabolism and CREB phosphorylation in non-small cell lung cancer 2015 Molecular BioSystems
Vol. 11, pp. 105-114 
article DOI URL 
Abstract: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently characterized endogenous inhibitor of the phosphatase activity of protein phosphatase 2A (PP2A), which extends the half-life of oncogenic protein c-myc and promotes in vivo tumor growth. The function of CIP2A in cancer progression is still poorly understood. To uncover the underlying mechanism of CIP2A-mediated cell proliferation, we implemented two-dimensional electrophoresis (2DE)-based proteomic approach to examine lung cancer cell H1299 with and without CIP2A. We found 47 proteins differentially expressed where 19 proteins were upregulated and 28 proteins were downregulated. These were categorized into functional groups as metabolism (25%), transcriptional and translational control (23%), and signaling pathway and protein degradation (20%). On one hand, we validate our proteomic work by measuring the metabolic change. The knockdown of CIP2A decreased the expression of LDH-A as well as the enzymatic activity, accompanying with decreased lactate production, increased NADH/NAD+ ratio and ROS production. On the other hand, we found CIP2A may regulate CREB activity through bioinformatics analysis. Our following experiments showed that, CIP2A positively regulated the phosphorylation of CREB in response to the serum treatment. Therefore, our proteomic study suggested CIP2A mediate cancer progression through metabolic pathway and intracellular signaling cascade.
BibTeX:
@article{Peng2015,
  author = {Peng, Bo and Lei, Ningjing and Chai, Yurong and Chan, Edward and Zhang, Jianying},
  title = {CIP2A regulates cancer metabolism and CREB phosphorylation in non-small cell lung cancer},
  journal = {Molecular BioSystems},
  year = {2015},
  volume = {11},
  pages = {105--114},
  url = {http://pubs.rsc.org/en/content/articlelanding/2014/mb/c4mb00513a},
  doi = {http://doi.org/10.1039/C4MB00513A}
}
Pibiri, M., Sulas, P., Leoni, V.P., Perra, A., Kowalik, M.A., Cordella, A., Saggese, P., Nassa, G. and Ravo, M. Global gene expression profile of normal and regenerating liver in young and old mice 2015 AGE
Vol. 37(3), pp. 1-14 
article DOI URL 
Abstract: The ability of the liver to regenerate and adjust its size after two/third partial hepatectomy (PH) is impaired in old rodents and humans. Here, we investigated by microarray analysis the expression pattern of hepatic genes in young and old untreated mice and the differences in gene expression profile following PH. Of the 10,237 messenger RNAs that had detectable expression, only 108 displayed a greater than 2-fold modification in gene expression levels between the two groups. These genes were involved in inflammatory and immune response, xenobiotics, and lipid and glucose metabolism. To identify the genes responsible for the different regenerative response, 10-week and 18-month-old mice subjected to PH were sacrificed at different time intervals after surgery. The results showed that 2463 transcripts had significantly different expression post PH between the two groups. However, in spite of impaired liver regeneration in old mice, cell cycle genes were similarly modified in both groups, the only exception being cyclin D1 gene which was up-regulated soon after PH in young mice, but mostly down-regulated in aged animals. Surprisingly, while in young hepatectomized mice, Yap messenger RNA (mRNA) expression was not significantly enhanced and protein expression essentially reflected the progression into cell cycle, its mRNA and protein levels were robustly increased in the liver of aged animals. Furthermore, a significant change of the age-related expression of the size regulator Yes-associated protein (YAP) was observed. Unexpectedly, while in young hepatectomized mice, Yap mRNA expression was not significantly enhanced and protein expression essentially reflected the progression into cell cycle, its mRNA and protein levels were robustly increased in the liver of aged animals. Moreover, when PH was performed on mitogen-induced enlarged livers, the earlier restoration of the original liver mass compared to animals subjected to PH only led to YAP down-regulation concomitantly with cyclin D1 up-regulation. Our data suggest that YAP activation is a size-dependent homeostatic mechanism that does not necessarily reflect cell cycle progression.
BibTeX:
@article{Pibiri2015,
  author = {Pibiri, Monica and Sulas, Pia and Leoni, Vera Piera and Perra, Andrea and Kowalik, Marta Anna and Cordella, Angela and Saggese, Pasquale and Nassa, Giovanni and Ravo, Maria},
  title = {Global gene expression profile of normal and regenerating liver in young and old mice},
  journal = {AGE},
  year = {2015},
  volume = {37},
  number = {3},
  pages = {1--14},
  url = {http://link.springer.com/article/10.1007/s11357-015-9796-7},
  doi = {http://doi.org/10.1007/s11357-015-9796-7}
}
Pilcher, C.M., Jones, C.K., Schroyen, M., Severin, A.J., Patience, J.F., Tuggle, C.K. and Koltes, J.E. Transcript profiles in longissimus dorsi muscle and subcutaneous adipose tissue: A comparison of pigs with different postweaning growth rates 2015 Journal of Animal Science
Vol. 0(0), pp. 0 
article DOI URL 
BibTeX:
@article{Pilcher2015,
  author = {Pilcher, C M and Jones, C K and Schroyen, M and Severin, A J and Patience, J F and Tuggle, C K and Koltes, J E},
  title = {Transcript profiles in longissimus dorsi muscle and subcutaneous adipose tissue: A comparison of pigs with different postweaning growth rates},
  journal = {Journal of Animal Science},
  year = {2015},
  volume = {0},
  number = {0},
  pages = {0},
  url = {https://dl.sciencesocieties.org/publications/jas/abstracts/0/0/jas.2014-8593},
  doi = {http://doi.org/10.2527/jas.2014-8593}
}
Pinto, C.L., Kalasekar, S.M., McCollum, C.W., Riu, A., Jonsson, P., Lopez, J., Swindell, E., Bouhlatouf, A., Balaguer, P., Bondesson, M. and Gustafsson, J.-Å. Lxr regulates lipid metabolic and visual perception pathways during zebrafish development 2015 Molecular and Cellular Endocrinology  article DOI URL 
Abstract: The Liver X Receptors (LXRs) play important roles in multiple metabolic pathways, including fatty acid, cholesterol, carbohydrate and energy metabolism. To expand the knowledge of the functions of LXR signaling during embryonic development, we performed a whole-genome microarray analysis of Lxr target genes in zebrafish larvae treated with either one of the synthetic LXR ligands T0901317 or GW3965. Assessment of the biological processes enriched by differentially expressed genes revealed a prime role for Lxr in regulating lipid metabolic processes, similarly to the function of LXR in mammals. In addition, exposure to the Lxr ligands induced changes in expression of genes in the neural retina and lens of the zebrafish eye, including the photoreceptor guanylate cyclase activators and lens gamma crystallins, suggesting a potential novel role for Lxr in modulating the transcription of genes associated with visual function in zebrafish. The regulation of expression of metabolic genes was phenotypically reflected in an increased absorption of yolk in the zebrafish larvae, and changes in the expression of genes involved in visual perception were associated with morphological alterations in the retina and lens of the developing zebrafish eye. The regulation of expression of both lipid metabolic and eye specific genes was sustained in 1 month old fish. The transcriptional networks demonstrated several conserved effects of LXR activation between zebrafish and mammals, and also identified potential novel functions of Lxr, supporting zebrafish as a promising model for investigating the role of Lxr during development.
BibTeX:
@article{Pinto2015,
  author = {Pinto, Caroline Lucia and Kalasekar, Sharanya Maanasi and McCollum, Catherine W and Riu, Anne and Jonsson, Philip and Lopez, Justin and Swindell, Eric and Bouhlatouf, Abdel and Balaguer, Patrick and Bondesson, Maria and Gustafsson, Jan-Åke},
  title = {Lxr regulates lipid metabolic and visual perception pathways during zebrafish development},
  journal = {Molecular and Cellular Endocrinology},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S0303720715300964},
  doi = {http://doi.org/10.1016/j.mce.2015.09.030}
}
Puqiang Yang, Ashley Chorath, W.J., Wang, B., Gao, J., Liu, R., Hong, J., Wang, W., Gu, W. and Ning, G. Article Identification and Validation Novel Risk Genes for Type 1 Diabetes – A Meta-Analysis 2015 Journal of diabetes
Vol. 7(2), pp. 158-65 
article DOI URL 
Abstract: Background: Type 1 diabetes (T1D) cannot be explained by environmental factors alone and gene mutations in T1D should be also taken seriously. The aim of this study was to investigate the novel genetic risk of T1D by systematically reviewing the published literature and performing a meta-analysis.
Method: A comprehensive search of electronic databases was completed using Illumina BioEngine. Seven T1D case/control bio-sets from four different studies were selected, including 286 T1D cases and 162 controls. The selected top T1D risk genes were further analyzed integrating an online open source T1D genetic database. Pathway enrichment analysis (PEA) and network connectivity analysis (NCA) were conducted to identify potential functional association between target genes and T1D.
Results: Six genes were identified through the meta-analysis as top target genes for T1D: HLA-DQB1, OAS1, CMKLR1, NFE2, MNDA and GPR56. These genes play roles within multiple T1D genetic pathways and demonstrate solid connections with known T1D target genes. NCA results also revealed strong functional association between these genes and T1D.
Conclusion: This study identified known as well as novel T1D target genes and their functional pathways that influence the T1D pathogenesis. Our results may provide new insights for the understanding of the genetic mechanisms of T1D
BibTeX:
@article{PuqiangYangAshleyChorath2015,
  author = {Puqiang Yang, Ashley Chorath, Wenjuan Jiang and Wang, Bokai and Gao, Jie and Liu, Ruixin and Hong, Jie and Wang, Weiqing and Gu, Weiqiong and Ning, Guang},
  title = {Article Identification and Validation Novel Risk Genes for Type 1 Diabetes – A Meta-Analysis},
  journal = {Journal of diabetes},
  year = {2015},
  volume = {7},
  number = {2},
  pages = {158--65},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/24796653},
  doi = {http://doi.org/10.1111/1753-0407.12163}
}
Qiao, S., Koyutürk, M. and Özsoyoğlu, Z.M. Integrated Querying of Disparate Association and Interaction Data in Biomedical Applications 2015 , pp. 146-155  inproceedings DOI URL 
Abstract: In biomedical applications, network models are commonly used to represent interactions and higher-level associations among biological entities. Integrated analyses of these interaction and association data has proven useful in extracting knowledge, and generating novel hypotheses for biomedical research. For example, integrated mining of clinical similarity among diseases, known disease-gene associations, and molecular interactions among proteins provide insight on prioritizing candidate disease genes. However, since most datasets provide their own schema and query interface, opportunities for exploratory and integrative querying of disparate data are currently limited. In this study, we capitalize on RDF-based representations of biomedical interaction and association data to develop a querying framework that enables efficient processing and flexible specification of graph template matching queries. The proposed framework enables integrative querying of biomedical databases to discover complex patterns of associations among a diverse range of biological entities, including biomolecules, biological processes, organisms, and phenotypes. Our experimental results on the UniProt dataset show the proposed framework can be used to efficiently process complex queries, and identify biologically relevant patterns of associations that cannot be readily obtained by querying each dataset independently.
BibTeX:
@inproceedings{Qiao2015,
  author = {Qiao, Shi and Koyutürk, Mehmet and Özsoyoğlu, Z Meral},
  title = {Integrated Querying of Disparate Association and Interaction Data in Biomedical Applications},
  publisher = {ACM},
  year = {2015},
  pages = {146--155},
  url = {http://doi.acm.org/10.1145/2808719.2808734},
  doi = {http://doi.org/10.1145/2808719.2808734}
}
Rafiei, F., Torabi, Z. and Ebrahimie, E. "Type A" response regulators are involved in the plant-microbe interaction 2015 Plant Omics Journal
Vol. 8(2), pp. 178-182 
article  
BibTeX:
@article{Rafiei2015,
  author = {Rafiei, Fariba and Torabi, Zohreh and Ebrahimie, Esmaeil},
  title = {"Type A" response regulators are involved in the plant-microbe interaction},
  journal = {Plant Omics Journal},
  year = {2015},
  volume = {8},
  number = {2},
  pages = {178--182}
}
Rahman, M.S., Kwon, W.-S., Lee, J.-S., Yoon, S.-J., Ryu, B.-Y. and Pang, M.-G. Bisphenol-A Affects Male Fertility via Fertility-related Proteins in Spermatozoa 2015 Scientific Reports
Vol. 5, pp. 9169 
article DOI URL 
Abstract: The xenoestrogen bisphenol-A (BPA) is a widespread environmental contaminant that has been studied for its impact on male fertility in several species of animals and humans. Growing evidence suggests that xenoestrogens can bind to receptors on spermatozoa and thus alter sperm function. The objective of the study was to investigate the effects of varying concentrations of BPA (0.0001, 0.01, 1, and 100 μM for 6 h) on sperm function, fertilization, embryonic development, and on selected fertility-related proteins in spermatozoa. Our results showed that high concentrations of BPA inhibited sperm motility and motion kinematics by significantly decreasing ATP levels in spermatozoa. High BPA concentrations also increased the phosphorylation of tyrosine residues on sperm proteins involved in protein kinase A-dependent regulation and induced a precocious acrosome reaction, which resulted in poor fertilization and compromised embryonic development. In addition, BPA induced the down-regulation of β-actin and up-regulated peroxiredoxin-5, glutathione peroxidase 4, glyceraldehyde-3-phosphate dehydrogenase, and succinate dehydrogenase. Our results suggest that high concentrations of BPA alter sperm function, fertilization, and embryonic development via regulation and/or phosphorylation of fertility-related proteins in spermatozoa. We conclude that BPA-induced changes in fertility-related protein levels in spermatozoa may be provided a potential cue of BPA-mediated disease conditions.
BibTeX:
@article{Rahman2015,
  author = {Rahman, Md Saidur and Kwon, Woo-Sung and Lee, June-Sub and Yoon, Sung-Jae and Ryu, Buom-Yong and Pang, Myung-Geol},
  title = {Bisphenol-A Affects Male Fertility via Fertility-related Proteins in Spermatozoa},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  pages = {9169},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/25772901},
  doi = {http://doi.org/10.1038/srep09169}
}
Rai, A., Singh, R., Shirke, P.A., Tripathi, R.D., Trivedi, P.K. and Chakrabarty, D. Expression of Rice CYP450-Like Gene (Os08g01480) in Arabidopsis Modulates Regulatory Network Leading to Heavy Metal and Other Abiotic Stress Tolerance. 2015 PloS one
Vol. 10(9), pp. e0138574 
article URL 
Abstract: Heavy metal (HM) toxicity has become a grave problem in the world since it leads to hazardous effects on living organisms. Transcriptomic/proteomic studies in plants have identified a large number of metal-responsive gene families. Of these, cytochrome-P450 (CYPs) family members are composed of enzymes carrying out detoxification of exogenous molecules. Here, we report a CYP-like protein encoded by Os08g01480 locus in rice that helps the plant to combat HM and other abiotic stresses. To functionally characterize CYP-like gene, cDNA and promoter were isolated from rice to develop Arabidopsis transgenic lines. Heterologous expression of Os08g01480 in Arabidopsis provided significant tolerance towards abiotic stresses. In silico analysis reveals that Os08g01480 might help plants to combat environmental stress via modulating auxin metabolism. Transgenic lines expressing reporter gene under control of Os08g01480 promoter demonstrated differential promoter activity in different tissues during environmental stresses. These studies indicated that differential expression of Os08g01480 might be modulating response of plants towards environmental stresses as well as in different developmental stages.
BibTeX:
@article{Rai2015,
  author = {Rai, Arti and Singh, Ruchi and Shirke, Pramod Arvind and Tripathi, Rudra Deo and Trivedi, Prabodh Kumar and Chakrabarty, Debasis},
  title = {Expression of Rice CYP450-Like Gene (Os08g01480) in Arabidopsis Modulates Regulatory Network Leading to Heavy Metal and Other Abiotic Stress Tolerance.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2015},
  volume = {10},
  number = {9},
  pages = {e0138574},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0138574}
}
Randles, M. and Lennon, R. Applying Proteomics to Investigate Extracellular Matrix in Health and Disease 2015   incollection URL 
Abstract: The molecular composition of basement membranes (BMs) has traditionally been investigated by candidate-based approaches leading to the identification of key structural components as described in previous chapters. Laminins, collagen IV, nidogens, perlecan, and type XV/XVIII collagen are integral to BMs with isoforms showing tissue specificity. More recently the application of mass spectrometry (MS)-based proteomics has led to the discovery of many more structural and regulatory components of BMs and more broadly, extracellular matrix (ECM). These investigations have revealed tissue-specific signatures of between 100 and 150 ECM components, demonstrating the complexity of the extracellular niche. In addition to providing a structural scaffold for cells, ECM is a dynamic extracellular environment capable of regulating the physical properties of tissues. Global investigations of ECM with proteomics in turn enable systems level analyses and when applied to health and disease states these investigations provide insights into pathways regulating matrix dysregulation. This chapter focuses on the methods used to extract ECM and on the analysis of its composition using MS-based proteomics, and it provides examples of how these approaches have been used to investigate health and disease states.
BibTeX:
@incollection{Randles2015,
  author = {Randles, Michael and Lennon, Rachel},
  title = {Applying Proteomics to Investigate Extracellular Matrix in Health and Disease},
  publisher = {Academic Press},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S1063582315000587}
}
Rannou, E., François, A., Toullec, A., Guipaud, O., Buard, V., Tarlet, G., Mintet, E., Jaillet, C., Iruela-Arispe, M.L., Benderitter, M., Sabourin, J.-C. and Milliat, F. In vivo evidence for an endothelium-dependent mechanism in radiation-induced normal tissue injury 2015 Scientific Reports
Vol. 5 
article DOI URL 
Abstract: The pathophysiological mechanism involved in side effects of radiation therapy, and especially the role of the endothelium remains unclear. Previous results showed that plasminogen activator inhibitor-type 1 (PAI-1) contributes to radiation-induced intestinal injury and suggested that this role could be driven by an endothelium-dependent mechanism. We investigated whether endothelial-specific PAI-1 deletion could affect radiation-induced intestinal injury. We created a mouse model with a specific deletion of PAI-1 in the endothelium (PAI-1KOendo) by a Cre-LoxP system. In a model of radiation enteropathy, survival and intestinal radiation injury were followed as well as intestinal gene transcriptional profile and inflammatory cells intestinal infiltration. Irradiated PAI-1KOendo mice exhibited increased survival, reduced acute enteritis severity and attenuated late fibrosis compared with irradiated PAI-1flx/flx mice. Double E-cadherin/TUNEL labeling confirmed a reduced epithelial cell apoptosis in irradiated PAI-1KOendo. High-throughput gene expression combined with bioinformatic analyses revealed a putative involvement of macrophages. We observed a decrease in CD68+cells in irradiated intestinal tissues from PAI-1KOendo mice as well as modifications associated with M1/M2 polarization. This work shows that PAI-1 plays a role in radiation-induced intestinal injury by an endothelium-dependent mechanism and demonstrates in vivo that the endothelium is directly involved in the progression of radiation-induced enteritis.
BibTeX:
@article{Rannou2015,
  author = {Rannou, Emilie and François, Agnès and Toullec, Aurore and Guipaud, Olivier and Buard, Valérie and Tarlet, Georges and Mintet, Elodie and Jaillet, Cyprien and Iruela-Arispe, Maria Luisa and Benderitter, Marc and Sabourin, Jean-Christophe and Milliat, Fabien},
  title = {In vivo evidence for an endothelium-dependent mechanism in radiation-induced normal tissue injury},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625166/ files/4002/Rannou et al. - 2015 - In vivo evidence for an endothelium-dependent mech.pdf},
  doi = {http://doi.org/10.1038/srep15738}
}
Rekaik, H., Blaudin De Thé, F.-X., Fuchs, J., Massiani-Beaudoin, O., Prochiantz, A., Joshi, R.L., Blaudin de Thé, F.-X., Fuchs, J., Massiani-Beaudoin, O., Prochiantz, A. and Joshi, R.L. Engrailed Homeoprotein Protects Mesencephalic Dopaminergic Neurons from Oxidative Stress 2015 Cell Reports  article DOI URL 
Abstract: Summary Engrailed homeoproteins are expressed in adult dopaminergic neurons of the substantia nigra. In Engrailed1 heterozygous mice, these neurons start dying at 6 weeks, are more sensitive to oxidative stress, and progressively develop traits similar to those observed following an acute and strong oxidative stress inflected to wild-type neurons. These changes include DNA strand breaks and the modification (intensity and distribution) of several nuclear and nucleolar heterochromatin marks. Engrailed1 and Engrailed2 are biochemically equivalent transducing proteins previously used to antagonize dopaminergic neuron death in Engrailed1 heterozygous mice and in mouse models of Parkinson disease. Accordingly, we show that, following an acute oxidative stress, a single Engrailed2 injection restores all nuclear and nucleolar heterochromatin marks, decreases the number of DNA strand breaks, and protects dopaminergic neurons against apoptosis.
BibTeX:
@article{Rekaik2015,
  author = {Rekaik, Hocine and Blaudin De Thé, François-Xavier and Fuchs, Julia and Massiani-Beaudoin, Olivia and Prochiantz, Alain and Joshi, Rajiv L. L and Blaudin de Thé, François-Xavier and Fuchs, Julia and Massiani-Beaudoin, Olivia and Prochiantz, Alain and Joshi, Rajiv L. L},
  title = {Engrailed Homeoprotein Protects Mesencephalic Dopaminergic Neurons from Oxidative Stress},
  journal = {Cell Reports},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S2211124715009894 http://www.ncbi.nlm.nih.gov/pubmed/26411690},
  doi = {http://doi.org/10.1016/j.celrep.2015.08.076}
}
Rengaraj, D., Kwon, W.-S. and Pang, M.-G. Bioinformatics Annotation of Human Y Chromosome-Encoded Protein Pathways and Interactions 2015 Journal of Proteome Research
Vol. 14(9), pp. 3503-3518 
article DOI URL 
Abstract: We performed a comprehensive analysis of human Y chromosome-encoded proteins, their pathways, and their interactions using bioinformatics tools. From the NCBI annotation release 107 of human genome, we retrieved a total of 66 proteins encoded on Y chromosome. Most of the retrieved proteins were also matched with the proteins listed in the core databases of the Human Proteome Project including neXtProt, PeptideAtlas, and the Human Protein Atlas. When we examined the pathways of human Y-encoded proteins through KEGG database and Pathway Studio software, many of proteins fall into the categories related to cell signaling pathways. Using the STRING program, we found a total of 49 human Y-encoded proteins showing strong/medium interaction with each other. While using the Pathway studio software, we found that a total of 16 proteins interact with other chromosome-encoded proteins. In particular, the SRY protein interacted with 17 proteins encoded on other chromosomes. Additionally, we aligned the sequences of human Y-encoded proteins with the sequences of chimpanzee and mouse Y-encoded proteins using the NCBI BLAST program. This analysis resulted in a significant number of orthologous proteins between human, chimpanzee, and mouse. Collectively, our findings provide the scientific community with additional information on the human Y chromosome-encoded proteins.
BibTeX:
@article{Rengaraj2015,
  author = {Rengaraj, Deivendran and Kwon, Woo-Sung and Pang, Myung-Geol},
  title = {Bioinformatics Annotation of Human Y Chromosome-Encoded Protein Pathways and Interactions},
  journal = {Journal of Proteome Research},
  year = {2015},
  volume = {14},
  number = {9},
  pages = {3503--3518},
  url = {http://dx.doi.org/10.1021/acs.jproteome.5b00491 http://pubs.acs.org/doi/full/10.1021/acs.jproteome.5b00491},
  doi = {http://doi.org/10.1021/acs.jproteome.5b00491}
}
Robison, F.M., Heuberger, A.L., Brick, M.A. and Prenni, J.E. Proteome Characterization of Leaves in Common Bean 2015 Proteomes
Vol. 3(3), pp. 236-248 
article DOI URL 
Abstract: Dry edible bean (Phaseolus vulgaris L.) is a globally relevant food crop. The bean genome was recently sequenced and annotated allowing for proteomics investigations aimed at characterization of leaf phenotypes important to agriculture. The objective of this study was to utilize a shotgun proteomics approach to characterize the leaf proteome and to identify protein abundance differences between two bean lines with known variation in their physiological resistance to biotic stresses. Overall, 640 proteins were confidently identified. Among these are proteins known to be involved in a variety of molecular functions including oxidoreductase activity, binding peroxidase activity, and hydrolase activity. Twenty nine proteins were found to significantly vary in abundance (p-value textless 0.05) between the two bean lines, including proteins associated with biotic stress. To our knowledge, this work represents the first large scale shotgun proteomic analysis of beans and our results lay the groundwork for future studies designed to investigate the molecular mechanisms involved in pathogen resistance.
BibTeX:
@article{Robison2015,
  author = {Robison, Faith M and Heuberger, Adam L and Brick, Mark A and Prenni, Jessica E},
  title = {Proteome Characterization of Leaves in Common Bean},
  journal = {Proteomes},
  year = {2015},
  volume = {3},
  number = {3},
  pages = {236--248},
  url = {http://www.mdpi.com/2227-7382/3/3/236 http://www.mdpi.com/2227-7382/3/3/236/htm},
  doi = {http://doi.org/10.3390/proteomes3030236}
}
Rodriguez, A., Crespo, I., Androsova, G. and del Sol, A. Discrete Logic Modelling Optimization to Contextualize Prior Knowledge Networks Using PRUNET 2015 PLoS ONE
Vol. 10(6), pp. e0127216 
article DOI URL 
Abstract: High-throughput technologies have led to the generation of an increasing amount of data in different areas of biology. Datasets capturing the cell's response to its intra- and extra-cellular microenvironment allows such data to be incorporated as signed and directed graphs or influence networks. These prior knowledge networks (PKNs) represent our current knowledge of the causality of cellular signal transduction. New signalling data is often examined and interpreted in conjunction with PKNs. However, different biological contexts, such as cell type or disease states, may have distinct variants of signalling pathways, resulting in the misinterpretation of new data. The identification of inconsistencies between measured data and signalling topologies, as well as the training of PKNs using context specific datasets (PKN contextualization), are necessary conditions to construct reliable, predictive models, which are current challenges in the systems biology of cell signalling. Here we present PRUNET, a user-friendly software tool designed to address the contextualization of a PKNs to specific experimental conditions. As the input, the algorithm takes a PKN and the expression profile of two given stable steady states or cellular phenotypes. The PKN is iteratively pruned using an evolutionary algorithm to perform an optimization process. This optimization rests in a match between predicted attractors in a discrete logic model (Boolean) and a Booleanized representation of the phenotypes, within a population of alternative subnetworks that evolves iteratively. We validated the algorithm applying PRUNET to four biological examples and using the resulting contextualized networks to predict missing expression values and to simulate well-characterized perturbations. PRUNET constitutes a tool for the automatic curation of a PKN to make it suitable for describing biological processes under particular experimental conditions. The general applicability of the implemented algorithm makes PRUNET suitable for a variety of biological processes, for instance cellular reprogramming or transitions between healthy and disease states.
BibTeX:
@article{Rodriguez2015,
  author = {Rodriguez, Ana and Crespo, Isaac and Androsova, Ganna and del Sol, Antonio},
  title = {Discrete Logic Modelling Optimization to Contextualize Prior Knowledge Networks Using PRUNET},
  journal = {PLoS ONE},
  year = {2015},
  volume = {10},
  number = {6},
  pages = {e0127216},
  url = {http://dx.doi.org/10.1371/journal.pone.0127216},
  doi = {http://doi.org/10.1371/journal.pone.0127216}
}
Rodriguez-Jorquera, I.A., Kroll, K.J., Toor, G.S. and Denslow, N.D. Transcriptional and physiological response of fathead minnows (Pimephales promelas) exposed to urban waters entering into wildlife protected areas 2015 Environmental Pollution
Vol. 199, pp. 155-165 
article DOI URL 
Abstract: The mission of protected areas is to conserve biodiversity and improve human welfare. To assess the effect of urban waters entering into protected areas, we performed 48-h whole-effluent exposures with fathead minnows, analyzing changes in steady state levels of mRNAs in the livers of exposed fish. Raw wastewater, treated city wastewater, and treated wastewater from a university were collected for exposures. All exposed fish showed altered mRNA levels of DNA damage-repair genes. Fish exposed to raw and treated wastewaters showed down-regulation of transcripts for key intermediates of cholesterol biosynthesis and elevated plasma cholesterol. The type of wastewater treatment influenced the response of gene transcription. Because of the relevance of some of the altered cellular pathways, we suggest that these effluents may cause deleterious effects on fish inside protected areas that receive these waters. Inclusion of research and mitigation efforts for this type of threat in protected areas management is advised.
BibTeX:
@article{Rodriguez-Jorquera2015,
  author = {Rodriguez-Jorquera, Ignacio A and Kroll, Kevin J and Toor, Gurpal S and Denslow, Nancy D},
  title = {Transcriptional and physiological response of fathead minnows (Pimephales promelas) exposed to urban waters entering into wildlife protected areas},
  journal = {Environmental Pollution},
  year = {2015},
  volume = {199},
  pages = {155--165},
  url = {http://www.sciencedirect.com/science/article/pii/S0269749115000408 http://www.sciencedirect.com/science/article/pii/S0269749115000408/pdfft?md5=f1d8f39b20a434e34c57ef97abce54bf&pid=1-s2.0-S0269749115000408-main.pdf},
  doi = {http://doi.org/10.1016/j.envpol.2015.01.021}
}
Rogée, S., Gall, M.L., Chafey, P., Bouquet, J., Cordonnier, N., Frederici, C. and Pavio, N. Quantitative proteomics identifies host factors modulated during acute hepatitis E infection in swine model 2015 Journal of Virology
Vol. 89(1), pp. 129-143 
article DOI URL 
Abstract: Hepatitis E virus (HEV) causes acute enterically-transmitted hepatitis. In industrialized countries, it is a zoonotic disease, swine being the major reservoir of human HEV contaminations. The occurrence and severity of the disease are variable, ranging from asymptomatic to self-limiting acute hepatitis, chronic infection or fulminant hepatitis. In the absence of a robust cell culture system or small animal models, the HEV life cycle and pathological process remain unclear. To characterize HEV pathogenesis and virulence mechanisms, a quantitative proteomic analysis was carried out to identify cellular factors and pathways modulated during acute infection of swine. Three groups of pigs were inoculated with 3 different strains of swine HEV to evaluate the possible role of viral determinants in pathogenesis. Liver samples were analyzed by a differential proteomic approach, 2D-DIGE and 61 modulated proteins were identified by mass spectroscopy. The results obtained show that the 3 HEV strains replicate similarly in swine and that they modulate several cellular pathways suggesting that HEV impairs several cellular processes, which can account for various disease expressions. Several proteins such as Heterogeneous nuclear ribonucleoprotein K, Apolipoprotein E and Prohibitin, known to be involved in other viral life cycles, were up-regulated in HEV-infected livers. Some differences were observed between the 3 strains, suggesting that HEV's genetic variability may induce variation in pathogenesis. This comparative analysis of liver proteome modulated during HEV infection with 3 different strains of genotype 3 provides an important basis for further investigations on factors involved in HEV replication and the mechanism of HEV pathogenesis. Importance Hepatitis E virus (HEV) is responsible for acute hepatitis—ranging from asymptomatic to self-limiting acute hepatitis—chronic infection, or fulminant hepatitis. In industrialized countries, HEV is considered an emerging zoonotic disease, swine being the principal reservoir for human contaminations. The viral and cellular factors involved in the replication and/or pathogenesis of HEV are still not fully known. Here we report that several cellular pathways involved in cholesterol, lipid metabolism or cell survival were modulated during HEV infection in swine model. Moreover, we observed a difference between the different swine strains, suggesting that HEV's genetic variability could play a role in pathogenesis. We also identified some proteins known to be involved in other viral cycles. Our study provides insight into the mechanisms modulated during HEV infection and constitutes a useful reference for future work on HEV pathogenesis and virulence.
BibTeX:
@article{Rogee2015,
  author = {Rogée, Sophie and Gall, Morgane Le and Chafey, Philippe and Bouquet, Jérôme and Cordonnier, Nathalie and Frederici, Christian and Pavio, Nicole},
  title = {Quantitative proteomics identifies host factors modulated during acute hepatitis E infection in swine model},
  journal = {Journal of Virology},
  year = {2015},
  volume = {89},
  number = {1},
  pages = {129--143},
  url = {http://jvi.asm.org/content/early/2014/10/09/JVI.02208-14 http://www.ncbi.nlm.nih.gov/pubmed/25320303},
  doi = {http://doi.org/10.1128/JVI.02208-14}
}
Rungoe, C., Nyboe Andersen, N. and Jess, T. Inflammatory bowel disease and risk of coronary heart disease 2015 Trends in Cardiovascular Medicine  article DOI URL 
BibTeX:
@article{Rungoe2015,
  author = {Rungoe, Christine and Nyboe Andersen, Nynne and Jess, Tine},
  title = {Inflammatory bowel disease and risk of coronary heart disease},
  journal = {Trends in Cardiovascular Medicine},
  year = {2015},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S1050173815001061},
  doi = {http://doi.org/10.1016/j.tcm.2015.03.010}
}
Schulze, S., Henkel, S.G., Driesch, D., Guthke, R. and Linde, J. Computational prediction of molecular pathogen-host interactions based on dual transcriptome data 2015 Frontiers in Microbiology: Infectious Diseases
Vol. 6, pp. 65 
article DOI URL 
BibTeX:
@article{Schulze2015,
  author = {Schulze, Sylvie and Henkel, Sebastian Gerhard and Driesch, Dominik and Guthke, Reinhard and Linde, Jörg},
  title = {Computational prediction of molecular pathogen-host interactions based on dual transcriptome data},
  journal = {Frontiers in Microbiology: Infectious Diseases},
  year = {2015},
  volume = {6},
  pages = {65},
  url = {http://journal.frontiersin.org/Journal/10.3389/fmicb.2015.00065/abstract},
  doi = {http://doi.org/10.3389/fmicb.2015.00065}
}
Seok, J., Davis, R.W. and Xiao, W. A hybrid approach of gene sets and single genes for the prediction of survival risks with gene expression data. 2015 PloS one
Vol. 10(5), pp. e0122103 
article URL 
Abstract: Accumulated biological knowledge is often encoded as gene sets, collections of genes associated with similar biological functions or pathways. The use of gene sets in the analyses of high-throughput gene expression data has been intensively studied and applied in clinical research. However, the main interest remains in finding modules of biological knowledge, or corresponding gene sets, significantly associated with disease conditions. Risk prediction from censored survival times using gene sets hasn't been well studied. In this work, we propose a hybrid method that uses both single gene and gene set information together to predict patient survival risks from gene expression profiles. In the proposed method, gene sets provide context-level information that is poorly reflected by single genes. Complementarily, single genes help to supplement incomplete information of gene sets due to our imperfect biomedical knowledge. Through the tests over multiple data sets of cancer and trauma injury, the proposed method showed robust and improved performance compared with the conventional approaches with only single genes or gene sets solely. Additionally, we examined the prediction result in the trauma injury data, and showed that the modules of biological knowledge used in the prediction by the proposed method were highly interpretable in biology. A wide range of survival prediction problems in clinical genomics is expected to benefit from the use of biological knowledge.
BibTeX:
@article{Seok2015,
  author = {Seok, Junhee and Davis, Ronald W and Xiao, Wenzhong},
  title = {A hybrid approach of gene sets and single genes for the prediction of survival risks with gene expression data.},
  journal = {PloS one},
  publisher = {Public Library of Science},
  year = {2015},
  volume = {10},
  number = {5},
  pages = {e0122103},
  url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0122103}
}
Shamloo-Dashtpagerdi, R., Razi, H. and Ebrahimie, E. Mining expressed sequence tags of rapeseed (Brassica napus L.) to predict the drought responsive regulatory network 2015 Physiology and Molecular Biology of Plants, pp. 1-12  article DOI URL 
Abstract: It is of great significance to understand the regulatory mechanisms by which plants deal with drought stress. Two EST libraries derived from rapeseed (Brassica napus) leaves in non-stressed and drought stress conditions were analyzed in order to obtain the transcriptomic landscape of drought-exposed B. napus plants, and also to identify and characterize significant drought responsive regulatory genes and microRNAs. The functional ontology analysis revealed a substantial shift in the B. napus transcriptome to govern cellular drought responsiveness via different stress-activated mechanisms. The activity of transcription factor and protein kinase modules generally increased in response to drought stress. The 26 regulatory genes consisting of 17 transcription factor genes, eight protein kinase genes and one protein phosphatase gene were identified showing significant alterations in their expressions in response to drought stress. We also found the six microRNAs which were differentially expressed during drought stress supporting the involvement of a post-transcriptional level of regulation for B. napus drought response. The drought responsive regulatory network shed light on the significance of some regulatory components involved in biosynthesis and signaling of various plant hormones (abscisic acid, auxin and brassinosteroids), ubiquitin proteasome system, and signaling through Reactive Oxygen Species (ROS). Our findings suggested a complex and multi-level regulatory system modulating response to drought stress in B. napus.
BibTeX:
@article{Shamloo-Dashtpagerdi2015,
  author = {Shamloo-Dashtpagerdi, Roohollah and Razi, Hooman and Ebrahimie, Esmaeil},
  title = {Mining expressed sequence tags of rapeseed (Brassica napus L.) to predict the drought responsive regulatory network},
  journal = {Physiology and Molecular Biology of Plants},
  year = {2015},
  pages = {1--12},
  url = {http://link.springer.com/article/10.1007/s12298-015-0311-5},
  doi = {http://doi.org/10.1007/s12298-015-0311-5}
}
Shao, B., Guo, Y., Wang, L., Zhou, Q., Gao, T., Zheng, B., Zheng, H., Zhou, T., Zhou, Z., Guo, X., Huang, X. and Sha, J. Unraveling the proteomic profile of mice testis during the initiation of meiosis 2015 Journal of Proteomics
Vol. 120, pp. 35-43 
article DOI URL 
Abstract: In mice, once primordial germ cells (PGCs) are generated, they continue to proliferate and migrate to eventually reach the future gonads. They initiate sexual differentiation after their colonization of the gonads. During this process, retinoic acid (RA) induces meiosis in the female germ cells, which proceeds to the diplotene stage of meiotic prophase I, whereas the male germ cells initiate growth arrest. After birth, meiosis is initiated in mice spermatogonia by their conversion to preleptotene spermatocytes. There are evidences showing the roles of RA in the regulation of spermatogonial differentiation and meiosis initiation. However, it is still not well known on what responds to RA and how RA signaling engages meiosis. Thus, we constructed a proteomic profile of proteins associated with meiosis onset during testis development in mouse and identified 104 differentially expressed proteins (≥ 1.5 folds). Bioinformatic analysis showed proteins functioning in specific cell processes. The expression patterns of five selected proteins were verified via Western blot, of which we found that Tfrc gene was RA responsive, with a RA responsive element, and could be up regulated by RA in spermatogonial stem cell (SSC) line. Taken together, the results provide an important reference profile for further functional study of meiosis initiation. Biological significance Spermatogenesis involves mitosis of spermatogonia, meiosis of spermatocytes and spermiogenesis, in which meiosis is a unique event to germ cells, and not in the somatic cells. Till now, the detailed molecular mechanisms of the transition from mitosis to meiosis are still not elucidated. With high-throughput proteomic technology, it is now possible to systemically identify proteins possibly involved. With TMT-6plex based quantification, we identified 104 proteins differentially between testes without meiosis (day 8.5) and those that were meiosis initiated (day 10.5). And a well-known protein essential for meiosis initiation, stra8, was identified to be differentially expressed in the study. And bioinformatic analysis and functional studies revealed several proteins regulated by retinoic acid, a chemical known to regulate the meiosis initiation. Thus, this quantitative proteomic approach can identify meiosis initiation regulating proteins, and further functional studies of these proteins will help elucidate the mechanisms of meiosis initiation.
BibTeX:
@article{Shao2015,
  author = {Shao, Binbin and Guo, Yueshuai and Wang, Lei and Zhou, Quan and Gao, Tingting and Zheng, Bo and Zheng, Haoyu and Zhou, Tao and Zhou, Zuomin and Guo, Xuejiang and Huang, Xiaoyan and Sha, Jiahao},
  title = {Unraveling the proteomic profile of mice testis during the initiation of meiosis},
  journal = {Journal of Proteomics},
  year = {2015},
  volume = {120},
  pages = {35--43},
  url = {http://www.sciencedirect.com/science/article/pii/S1874391915000792},
  doi = {http://doi.org/10.1016/j.jprot.2015.02.015}
}
Sharov, A.A., Schlessinger, D. and Ko, M.S.H. ExAtlas: An interactive online tool for meta-analysis of gene expression data 2015 Journal of Bioinformatics and Computational Biology, pp. 1550019  article DOI URL 
Abstract: We have developed ExAtlas, an on-line software tool for meta-analysis and visualization of gene expression data. In contrast to existing software tools, ExAtlas compares multi-component data sets and generates results for all combinations (e.g. all gene expression profiles versus all Gene Ontology annotations). ExAtlas handles both users' own data and data extracted semi-automatically from the public repository (GEO/NCBI database). ExAtlas provides a variety of tools for meta-analyses: (1) standard meta-analysis (fixed effects, random effects, z-score, and Fisher's methods); (2) analyses of global correlations between gene expression data sets; (3) gene set enrichment; (4) gene set overlap; (5) gene association by expression profile; (6) gene specificity; and (7) statistical analysis (ANOVA, pairwise comparison, and PCA). ExAtlas produces graphical outputs, including heatmaps, scatter-plots, bar-charts, and three-dimensional images. Some of the most widely used public data sets (e.g. GNF/BioGPS, Gene Ontology, KEGG, GAD phenotypes, BrainScan, ENCODE ChIP-seq, and protein–protein interaction) are pre-loaded and can be used for functional annotations.
BibTeX:
@article{Sharov2015,
  author = {Sharov, Alexei A and Schlessinger, David and Ko, Minoru S H},
  title = {ExAtlas: An interactive online tool for meta-analysis of gene expression data},
  journal = {Journal of Bioinformatics and Computational Biology},
  year = {2015},
  pages = {1550019},
  url = {http://www.worldscientific.com/doi/abs/10.1142/S0219720015500195 http://www.worldscientific.com/doi/abs/10.1142/S0219720015500195?journalCode=jbcb},
  doi = {http://doi.org/10.1142/S0219720015500195}
}
Shimada, Y., Kuninaga, S., Ariyoshi, M., Zhang, B., Shiina, Y., Takahashi, Y., Umemoto, N., Nishimura, Y., Enari, H. and Tanaka, T. E2F8 promotes hepatic steatosis through FABP3 expression in diet-induced obesity in zebrafish 2015 Nutrition & Metabolism
Vol. 12(1), pp. 17 
article DOI URL 
BibTeX:
@article{Shimada2015,
  author = {Shimada, Yasuhito and Kuninaga, Shisei and Ariyoshi, Michiko and Zhang, Beibei and Shiina, Yasuhiko and Takahashi, Yoshinori and Umemoto, Noriko and Nishimura, Yuhei and Enari, Hiroyuki and Tanaka, Toshio},
  title = {E2F8 promotes hepatic steatosis through FABP3 expression in diet-induced obesity in zebrafish},
  journal = {Nutrition & Metabolism},
  year = {2015},
  volume = {12},
  number = {1},
  pages = {17},
  url = {http://www.nutritionandmetabolism.com/content/12/1/17/abstract http://www.nutritionandmetabolism.com/content/pdf/s12986-015-0012-7.pdf},
  doi = {http://doi.org/10.1186/s12986-015-0012-7}
}
So Youn Won, J.H.O. Computational Identification of Anthocyanin-Related Genes Using Transcriptome Data from Black Rice Plants 2015 Cell & Developmental Biology
Vol. 04(02) 
article DOI URL 
BibTeX:
@article{SoYounWon2015,
  author = {So Youn Won, Jae Hyeon Oh},
  title = {Computational Identification of Anthocyanin-Related Genes Using Transcriptome Data from Black Rice Plants},
  journal = {Cell & Developmental Biology},
  year = {2015},
  volume = {04},
  number = {02},
  url = {http://www.omicsgroup.org/journals/computational-identification-of-anthocyaninrelated-genes-using-transcriptome-data-from-black-rice-plants-2168-9296-1000157.php?aid=59107},
  doi = {http://doi.org/10.4172/2168-9296.1000157}
}
Subramani, S., Kalpana, R., Monickaraj, P.M. and Natarajan, J. HPIminer: A text mining system for building and visualizing human protein interaction networks and pathways 2015 Journal of Biomedical Informatics  article DOI URL 
Abstract: The knowledge on protein–protein interactions (PPI) and their related pathways are equally important to understand the biological functions of the living cell. Such information on human proteins is highly desirable to understand the mechanism of several diseases such as cancer and Alzheimer's disease. Because much of that information is buried in biomedical literature, an automated text mining system for visualizing human PPI and pathways is highly desirable. In this paper, we present HPIminer, a text mining system for visualizing human protein interactions and pathways from biomedical literature. HPIminer extracts human PPI information and PPI pairs from biomedical literature, and visualize their associated interactions, networks and pathways using two curated databases HPRD and KEGG. To our knowledge, HPIminer is the first system to build interaction networks from literature as well as curated databases. Further, the new interactions mined only from literature and not reported earlier in databases are highlighted as new. A comparative study with other similar tools shows that the resultant network is more informative and provides additional information on interacting proteins and their associated networks.
BibTeX:
@article{Subramani2015,
  author = {Subramani, Suresh and Kalpana, Raja and Monickaraj, Pankaj Moses and Natarajan, Jeyakumar},
  title = {HPIminer: A text mining system for building and visualizing human protein interaction networks and pathways},
  journal = {Journal of Biomedical Informatics},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S1532046415000088},
  doi = {http://doi.org/10.1016/j.jbi.2015.01.006}
}
Svetlov, S.I., Prima, V., Zhang, Z., Curley, K.C., Kobeissy, F., Moghieb, A. and Wang, K.K.W. Acute and Subacute Differential Gene Expression in Rat Midbrain Following Blast Exposure Compared to Mechanical Brain Trauma 2015 Journal of Neurology and Neurobiology
Vol. 1(1) 
article  
Abstract: In this study, we employed two models of traumatic brain injury (TBI) in rats: head-directed blast overpressure exposure (OBI) and mechanical controlled cortical impact (CCI). Two groups of animals served as controls: naïve rats and rats exposed to blast noise. A genomics neurosystems biology approach was used to analyze differential gene expression between experimental groups. Midbrain RNA was isolated 24 hours (acute) and 7 days (subacute) after traumatic insult, probed with Affymetrix array containing 31,100 gene sequences, and quantified by Agilent Technologies. Differentially expressed genes were grouped into functional clusters and the significance of gene expression changes at 24 h and 7 days was further assessed using parametric and nonparametric t- test with Welch correction. Then, gene interactions in pathological pathways following blast exposures vs. mechanical impact were created and analysed using neurosystems biology tools. According to ANOVA (ptextless0.05), there was a significant difference in expression of 994 genes within blast exposure groups (vs. control) and in 1532 genes within CCI group (vs. control) with an overall overlap of 579 genes. Parametric and nonparametric t-tests revealed significant differences in temporal profile of changes in various genes at 24 hours vs. 7 days in blast exposed animals compared to CCI. Specifically, genes involved in neural development and repair, such as ROBO1 and NEDD4 were up-regulated in CCI, while they were shown to be down-regulated following blast exposure. These results demonstrate several differences as well as overlaps in the expression of genes between the two brain insults. This will help to reveal specific molecular signatures of each brain insult and assist in developing diagnostics of chronic posttraumatic encephalopathy.
BibTeX:
@article{Svetlov2015,
  author = {Svetlov, Stanislav I and Prima, Victor and Zhang, Zhiqun and Curley, Kenneth C and Kobeissy, Firas and Moghieb, Ahmed and Wang, Kevin K W},
  title = {Acute and Subacute Differential Gene Expression in Rat Midbrain Following Blast Exposure Compared to Mechanical Brain Trauma},
  journal = {Journal of Neurology and Neurobiology},
  year = {2015},
  volume = {1},
  number = {1}
}
Thompson, P., Madan, J.C. and Moore, J.H. Prediction of relevant biomedical documents: a human microbiome case study 2015 BioData Mining
Vol. 8(1), pp. 28 
article DOI URL 
Abstract: BACKGROUND: Retrieving relevant biomedical literature has become increasingly difficult due to the large volume and rapid growth of biomedical publication. A query to a biomedical retrieval system often retrieves hundreds of results. Since the searcher will not likely consider all of these documents, ranking the documents is important. Ranking by recency, as PubMed does, takes into account only one factor indicating potential relevance. This study explores the use of the searcher's relevance feedback judgments to support relevance ranking based on features more general than recency.

RESULTS: It was found that the researcher's relevance judgments could be used to accurately predict the relevance of additional documents: both using tenfold cross-validation and by training on publications from 2008-2010 and testing on documents from 2011.

CONCLUSIONS: This case study has shown the promise for relevance feedback to improve biomedical document retrieval. A researcher's judgments as to which initially retrieved documents are relevant, or not, can be leveraged to predict additional relevant documents.
BibTeX:
@article{Thompson2015,
  author = {Thompson, Paul and Madan, Juliette C and Moore, Jason H},
  title = {Prediction of relevant biomedical documents: a human microbiome case study},
  journal = {BioData Mining},
  publisher = {BioMed Central},
  year = {2015},
  volume = {8},
  number = {1},
  pages = {28},
  url = {http://www.biodatamining.org/content/8/1/28/abstract http://www.biodatamining.org/content/8/1/28 http://biodatamining.biomedcentral.com/articles/10.1186/s13040-015-0061-5},
  doi = {http://doi.org/10.1186/s13040-015-0061-5}
}
To, C., Ringelberg, C.S., Royce, D.B., Williams, C.R., Risingsong, R., Sporn, M.B. and Liby, K.T. Dimethyl fumarate and the oleanane triterpenoids, CDDO-Imidazolide and CDDO-Methyl Ester, both activate the Nrf2 pathway but have opposite effects in the A/J model of lung 2015 Carcinogenesis, pp. bgv061  article DOI URL 
Abstract: Lung cancer accounts for the highest number of cancer-related deaths in the United States, highlighting the need for better prevention and therapy. Activation of the Nrf2 pathway detoxifies harmful insults and reduces oxidative stress, thus preventing carcinogenesis in various preclinical models. However, constitutive activation of the Nrf2 pathway has been detected in numerous cancers, which confers a survival advantage to tumor cells and a poor prognosis. In our study, we compared the effects of two clinically relevant classes of Nrf2 activators, dimethyl fumarate (DMF) and the synthetic oleanane triterpenoids, CDDO-Imidazolide (CDDO-Im) and CDDO-Methyl ester (CDDO-Me) in RAW 264.7 mouse macrophage-like cells, in VC1 lung cancer cells, and in the A/J model of lung cancer. Although the triterpenoids and DMF both activated the Nrf2 pathway, CDDO-Im and CDDOMe were markedly more potent than DMF. All of these drugs reduced the production of reactive oxygen species and inhibited nitric oxide production in RAW264.7 cells, but the triterpenoids were 100 times more potent than DMF in these assays. Microarray analysis revealed that only 52 of 99 Nrf2 target genes were induced by all three compounds, and each drug regulated a unique subset of Nrf2 genes. These drugs also altered the expression of other genes important in lung cancer independent of Nrf2. Although all three compounds enhanced the phosphorylation of CREB, only DMF increased the phosphorylation of Akt. CDDO-Me, at either 12.5-50 mg/kg of diet, was the most effective drug in our lung cancer mouse model. Specifically, CDDO-Me significantly reduced the average tumor number, size and burden compared to the control group (Ptextless0.05). Additionally, 52% of the tumors in the control group were high grade tumors compared to only 14% in the CDDO-Me group. Though less potent, CDDO-Im had similar activity as CDDO-Me. In contrast, 61-63% of the tumors in the DMF groups (400-1200 mg/kg diet) were high-grade tumors compared to 52% for the controls (Ptextless0.05). Additionally, DMF significantly increased the average number of tumors compared to the controls (Ptextless0.05). Thus, in contrast to the triterpenoids, which effectively reduced pathogenesis in A/J mice, DMF enhanced the severity of lung carcinogenesis in these mice. Collectively, these results suggest that although CDDO-Im, CDDO-Me and DMF all activate the Nrf2 pathway, they target distinct genes and signaling pathways, resulting in opposite effects for the prevention of experimental lung cancer.
BibTeX:
@article{To2015,
  author = {To, Ciric and Ringelberg, Carol S and Royce, Darlene B and Williams, Charlotte R and Risingsong, Renee and Sporn, Michael B and Liby, Karen T},
  title = {Dimethyl fumarate and the oleanane triterpenoids, CDDO-Imidazolide and CDDO-Methyl Ester, both activate the Nrf2 pathway but have opposite effects in the A/J model of lung},
  journal = {Carcinogenesis},
  year = {2015},
  pages = {bgv061},
  url = {http://carcin.oxfordjournals.org/content/early/2015/05/04/carcin.bgv061 http://www.ncbi.nlm.nih.gov/pubmed/25939751 http://carcin.oxfordjournals.org/content/early/2015/05/04/carcin.bgv061.short},
  doi = {http://doi.org/10.1093/carcin/bgv061}
}
Tormo, E., Pineda, B., Serna, E., Guijarro, A., Ribas, G., Fores, J., Chirivella, E., Climent, J., Lluch, A. and Eroles, P. MicroRNA profile in response to doxorubicin treatment in breast cancer 2015 Journal of Cellular Biochemistry  article DOI URL 
Abstract: Chemotherapy treatment is the standard in triple negative breast cancers, a cancer subgroup which lacks a specific target. The mechanisms leading to the response, as well as any markers that allow the differentiation between responder and non-responder groups prior to treatment are unknown. In parallel, miRNAs can act as oncogenes or tumor suppressors and there is evidence of their involvement in promoting resistance to anticancer drugs. Therefore we hypothesized that changes in miRNA expression after doxorubicin treatment may also be relevant in treatment response. OBJECTIVE: To study miRNAs that are differentially expressed in response to doxorubicin treatment. METHODS: One luminal-A and two triple negative, breast cancer cell lines were exposed to doxorubicin. Microarray analysis was performed to identify the common and differentially modified miRNAs. Genes and pathways that are theoretically regulated by these miRNAs were analyzed. RESULTS: Thirteen miRNAs common to all three lines were modified, in addition to 25 that were specific to triple negative cell lines, and 69 that changed only in the luminal-A cell line. This altered expression pattern seemed to be more strongly related to the breast cancer subgroup than to the treatment. The analysis of target genes revealed that cancer related pathways were the most affected by these miRNAs, moreover many of them had been previously related to chemotherapy resistance; thus suggesting follow-up studies. Additionally, through functional assays, we showed that miR-548c-3p is implicated in doxorubicin-treated MCF-7 cell viability, suggesting a role for this miRNA in resistance. This article is protected by copyright. All rights reserved.
BibTeX:
@article{Tormo2015,
  author = {Tormo, Eduardo and Pineda, Begoña and Serna, Eva and Guijarro, Alba and Ribas, Gloria and Fores, Jaume and Chirivella, Enrique and Climent, Joan and Lluch, Ana and Eroles, Pilar},
  title = {MicroRNA profile in response to doxorubicin treatment in breast cancer},
  journal = {Journal of Cellular Biochemistry},
  year = {2015},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/25802200},
  doi = {http://doi.org/10.1002/jcb.25162}
}
Van den Hof, W.F.P.M., Ruiz-Aracama, A., Summeren, A.V., Jennen, D.G.J., Gaj, S., Coonen, M.L.J., Brauers, K., Wodzig, W.K.W.H., van Delft, J.H.M. and Kleinjans, J.C.S. Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro 2015 Toxicology in Vitro  article DOI URL 
Abstract: In order to improve attrition rates of candidate-drugs there is a need for a better understanding of the mechanisms underlying drug-induced hepatotoxicity. We aim to further unravel the toxicological response of hepatocytes to a prototypical cholestatic compound by integrating transcriptomic and metabonomic profiling of HepG2 cells exposed to Cyclosporin A. Cyclosporin A exposure induced intracellular cholesterol accumulation and diminished intracellular bile acid levels. Performing pathway analyses of significant mRNAs and metabolites separately and integrated, resulted in more relevant pathways for the latter. Integrated analyses showed pathways involved in cell cycle and cellular metabolism to be significantly changed. Moreover, pathways involved in protein processing of the endoplasmic reticulum, bile acid biosynthesis and cholesterol metabolism were significantly affected. Our findings indicate that an integrated approach combining metabonomics and transcriptomics data derived from representative in vitro models, with bioinformatics can improve our understanding of the mechanisms of action underlying drug-induced hepatotoxicity. Furthermore, we showed that integrating multiple omics and thereby analyzing genes, microRNAs and metabolites of the opposed model for drug-induced cholestasis can give valuable information about mechanisms of drug-induced cholestasis in vitro and therefore could be used in toxicity screening of new drug candidates at an early stage of drug discovery.
BibTeX:
@article{VandenHof2015,
  author = {Van den Hof, Wim F P M and Ruiz-Aracama, Ainhoa and Summeren, Anke Van and Jennen, Danyel G J and Gaj, Stan and Coonen, Maarten L J and Brauers, Karen and Wodzig, Will K W H and van Delft, Joost H M and Kleinjans, Jos C S},
  title = {Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro},
  journal = {Toxicology in Vitro},
  year = {2015},
  url = {http://www.sciencedirect.com/science/article/pii/S0887233314002653},
  doi = {http://doi.org/10.1016/j.tiv.2014.12.016}
}
Vathipadiekal, V., Wang, X.V., Wei, W., Waldron, L., Drapkin, R., Gillette, M., Skates, S.J. and Birrer, M.J. Creation of a human Secretome: Novel Composite Library of Human Secreted Proteins: Validation using Ovarian Cancer Gene Expression Data and Virtual Secretome Array 2015 Clinical Cancer Research, pp. clincanres.3173.2014  article DOI URL 
Abstract: Purpose: To generate a comprehensive "Secretome" of proteins potentially found in the blood and derive a virtual Affymetrix array. To validate the utility of this database for the discovery of novel serum-based biomarkers using ovarian cancer transcriptomic data. Experimental Design: The secretome was constructed by aggregating the data from databases of known secreted proteins, transmembrane or membrane proteins, signal peptides, G-protein coupled receptors, or proteins existing in the extracellular region, and the virtual array was generated by mapping them to Affymetrix probeset identifiers. Whole genome microarray data from ovarian cancer, normal ovarian surface epithelium and fallopian tube epithelium were used to identify transcripts up-regulated in ovarian cancer. Results: We established the sercretome from 8 public databases and a virtual array consisting of 16,521 Affymetrix U133 Plus 2.0 probesets. Using ovarian cancer transcriptomic data, we identified candidate blood -based biomarkers for ovarian cancer and performed bioinformatic validation by demonstrating re-discovery of known biomarkers including CA125 and HE4. Two novel top biomarker (FGF18 and GPR172A) were validated in serum samples from an independent patient cohort. Conclusions: We present the secretome, comprising the most comprehensive resource available for protein products that are potentially found in the blood. The associated virtual array can be used to translate gene expression data into cancer biomarker discovery. A list of blood-based biomarkers for ovarian cancer detection is reported and includes CA125 and HE4. FGF18 and GPR172A were identified and validated by ELISA as being differentially expressed in the serum of ovarian cancer patients compared to controls.
BibTeX:
@article{Vathipadiekal2015,
  author = {Vathipadiekal, Vinod and Wang, Xin Victoria and Wei, Wei and Waldron, Levi and Drapkin, Ronny and Gillette, Michael and Skates, Steven J and Birrer, Michael J},
  title = {Creation of a human Secretome: Novel Composite Library of Human Secreted Proteins: Validation using Ovarian Cancer Gene Expression Data and Virtual Secretome Array},
  journal = {Clinical Cancer Research},
  year = {2015},
  pages = {clincanres.3173.2014},
  url = {http://clincancerres.aacrjournals.org/content/early/2015/05/05/1078-0432.CCR-14-3173 http://clincancerres.aacrjournals.org/content/early/2015/05/05/1078-0432.CCR-14-3173.full.pdf http://www.ncbi.nlm.nih.gov/pubmed/25944803 http://clincancerres.aacrjournal},
  doi = {http://doi.org/10.1158/1078-0432.CCR-14-3173}
}
Vladislavovna, N., Ekaterina Karenovna, E., Natalia Sergeevna, S., Zarema Grigorievna, K. and Anastasia, K. Platelet-Activating Factor-Acetylhydrolase Gene (PLA2G7) Expression in Children with a History of Food Anaphylaxis 2015 Journal of Allergy & Therapy
Vol. 06(01) 
article DOI  
BibTeX:
@article{Vladislavovna2015,
  author = {Vladislavovna, Natalia and Ekaterina Karenovna, Esakova and Natalia Sergeevna, Saakyan and Zarema Grigorievna, Kondratieva and Anastasia, Kokaeva},
  title = {Platelet-Activating Factor-Acetylhydrolase Gene (PLA2G7) Expression in Children with a History of Food Anaphylaxis},
  journal = {Journal of Allergy & Therapy},
  year = {2015},
  volume = {06},
  number = {01},
  doi = {http://doi.org/10.4172/2155-6121.1000211}
}
Wang, Y.-D., Rajanbabu, V. and Chen, J.-Y. Transcriptome analysis of medaka following epinecidin-1 and TH1-5 treatment of NNV infection 2015 Fish & Shellfish Immunology
Vol. 42(1), pp. 121-131 
article DOI URL 
Abstract: Nervous necrosis virus (NNV) infects a wide range of larval and juvenile fish species, thereby causing enormous economic losses in the aquaculture industry. Possible solutions to this problem include the use of antimicrobial peptides (AMPs), which directly inhibit bacterial growth, and also modulate host signaling mechanisms. The AMPs epinecidin (Epi)-1 and Tilapia hepcidin (TH) 1-5 have been demonstrated to be effective against Nervous necrosis virus infection in medaka (Oryzias latipes). However, the underlying molecular mechanisms are yet to be explored. Here, microarray analyses were performed to examine how NNV infection and/or epinecidin-1 or TH1-5 treatment affects gene expression in medaka; such analyses enabled the prediction of host signaling pathways affected by virus infection and/or regulated by epinecidin-1 and TH1-5. Transcriptome analysis revealed altered expression of genes involved in B cell activation, T cell activation, adipocytokine signaling, and mast cell activation. We subsequently used real-time PCR to analyze expression of key genes involved in these signaling mechanisms. Medaka infected with NNV exhibited up-regulation of PVALB, CEBPA, IFIM, IFN, IL-6ST, NF-kB2, SOC3, SP1, and TGFB1, and such increases were prevented by pre-treatment with epinecidin-1 or TH1-5. Immunohistochemistry using the anti-NNV antibody to stain brain and eye sections revealed that epinecidin-1 treatment during or after infection clears viral load, while TH1-5 treatment only reduces viral numbers if applied during infection. These observations demonstrate that epinecidin-1 and TH1-5 modulate NNV-induced host signaling mechanisms, thereby preventing viral multiplication in host organisms.
BibTeX:
@article{Wang2015,
  author = {Wang, Yi-Da and Rajanbabu, Venugopal and Chen, Jyh-Yih},
  title = {Transcriptome analysis of medaka following epinecidin-1 and TH1-5 treatment of NNV infection},
  journal = {Fish & Shellfish Immunology},
  year = {2015},
  volume = {42},
  number = {1},
  pages = {121--131},
  url = {http://www.sciencedirect.com/science/article/pii/S1050464814004148 http://www.ncbi.nlm.nih.gov/pubmed/25449377},
  doi = {http://doi.org/10.1016/j.fsi.2014.10.040}
}
Wang, J., Zuo, Y., Man, Y.-g., Avital, I., Stojadinovic, A., Liu, M., Yang, X., Varghese, R.S., Tadesse, M.G. and Ressom, H.W. Pathway and Network Approaches for Identification of Cancer Signature Markers from Omics Data 2015 Journal of Cancer
Vol. 6(1), pp. 54-65 
article  
BibTeX:
@article{Wang2015a,
  author = {Wang, Jinlian and Zuo, Yiming and Man, Yan-gao and Avital, Itzhak and Stojadinovic, Alexander and Liu, Meng and Yang, Xiaowei and Varghese, Rency S and Tadesse, Mahlet G and Ressom, Habtom W},
  title = {Pathway and Network Approaches for Identification of Cancer Signature Markers from Omics Data},
  journal = {Journal of Cancer},
  year = {2015},
  volume = {6},
  number = {1},
  pages = {54--65}
}
Wang, X.-F., Zhang, X.-Y., Gao, X., Liu, X.-X. and Wang, Y.-H. Proteomic Profiling of the Respiratory Syncytial Virus-Infected Rat Pneumonia Model 2015 Japanese Journal of Infectious Diseases
Vol. advpub 
article DOI  
Abstract: Respiratory syncytial virus (RSV) is a major cause of pediatric lower respiratory tract disease. Our goal was to obtain a detailed understanding of the molecular pathogenesis of RSV infections by studying the protein expression profiles in rats with pneumonia. First, we successfully established the pneumonia rat model by intranasal injection with RSV. The differentially expressed proteins of lung tissues of RSV-infected rats compared with those of the controls were analyzed by using two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) and MALDI-TOF/TOF MS. A total of 41 differentially expressed protein spots representing 20 unique proteins were successfully identified. Classification analysis showed that most of the proteins are implicated in metabolic processes, cellular processes, cellular component organization or biogenesis, and immune system process. The significantly elevated expressions of four proteins T-kininogen 1 (KNT1), T-kininogen 2 (KNT2), haptoglobin (HP), and hemopexin (HPX) were further validated in RSV-infected rats using western blot and immunohistochemistry, which might serve as the potential biomarkers of RSV-infected pneumonia. These results provide new insights into the pathogenesis of RSV infection-induced pneumonia, and provide important directions for functional studies and therapeutic design in the future.
BibTeX:
@article{Wang2015b,
  author = {Wang, Xue-Feng and Zhang, Xiu-Ying and Gao, Xuejuan and Liu, Xiao-Xue and Wang, Yi-Huan},
  title = {Proteomic Profiling of the Respiratory Syncytial Virus-Infected Rat Pneumonia Model},
  journal = {Japanese Journal of Infectious Diseases},
  year = {2015},
  volume = {advpub},
  doi = {http://doi.org/10.7883/yoken.JJID.2015.244}
}
Wu, H., Ng, R., Chen, X., Steer, C.J. and Song, G. MicroRNA-21 is a potential link between non-alcoholic fatty liver disease and hepatocellular carcinoma via modulation of the HBP1-p53-Srebp1c pathway 2015 Gut, pp. gutjnl-2014-308430  article DOI URL 
Abstract: Background Non-alcoholic fatty liver disease (NAFLD) is a major risk factor for hepatocellular carcinoma (HCC). However, the mechanistic pathways that link both disorders are essentially unknown. Objective Our study was designed to investigate the role of microRNA-21 in the pathogenesis of NAFLD and its potential involvement in HCC. Methods Wildtype mice maintained on a high fat diet (HFD) received tail vein injections of microRNA-21-anti-sense oligonucleotide (ASO) or miR-21 mismatched ASO for 4 or 8 weeks. Livers were collected after that time period for lipid content and gene expression analysis. Human hepatoma HepG2 cells incubated with oleate were used to study the role of miR-21 in lipogenesis and analysed with Nile-Red staining. microRNA-21 function in carcinogenesis was determined by soft-agar colony formation, cell cycle analysis and xenograft tumour assay using HepG2 cells. Results The expression of microRNA-21 was increased in the livers of HFD-treated mice and human HepG2 cells incubated with fatty acid. MicroRNA-21 knockdown in those mice and HepG2 cells impaired lipid accumulation and growth of xenograft tumour. Further studies revealed that Hbp1 was a novel target of microRNA-21 and a transcriptional activator of p53. It is well established that p53 is a tumour suppressor and an inhibitor of lipogenesis by inhibiting Srebp1c. As expected, microRNA-21 knockdown led to increased HBP1 and p53 and subsequently reduced lipogenesis and delayed G1/S transition, and the additional treatment of HBP1-siRNA antagonised the effect of microRNA-21-ASO, suggesting that HBP1 mediated the inhibitory effects of microRNA-21-ASO on both hepatic lipid accumulation and hepatocarcinogenesis. Mechanistically, microRNA-21 knockdown induced p53 transcription, which subsequently reduced expression of genes controlling lipogenesis and cell cycle transition. In contrast, the opposite result was observed with overexpression of microRNA-21, which prevented p53 transcription. Conclusions Our findings reveal a novel mechanism by which microRNA-21, in part, promotes hepatic lipid accumulation and cancer progression by interacting with the Hbp1-p53-Srebp1c pathway and suggest the potential therapeutic value of microRNA-21-ASO for both disorders.
BibTeX:
@article{Wu2015,
  author = {Wu, Heng and Ng, Raymond and Chen, Xin and Steer, Clifford J and Song, Guisheng},
  title = {MicroRNA-21 is a potential link between non-alcoholic fatty liver disease and hepatocellular carcinoma via modulation of the HBP1-p53-Srebp1c pathway},
  journal = {Gut},
  year = {2015},
  pages = {gutjnl--2014--308430},
  url = {http://gut.bmj.com/content/early/2015/08/17/gutjnl-2014-308430 http://www.ncbi.nlm.nih.gov/pubmed/26282675 http://gut.bmj.com/content/early/2015/08/17/gutjnl-2014-308430.full},
  doi = {http://doi.org/10.1136/gutjnl-2014-308430}
}
Yan, S., Zhang, H., Zheng, F., Sheng, N., Guo, X. and Dai, J. Perfluorooctanoic acid exposure for 28 days affects glucose homeostasis and induces insulin hypersensitivity in mice 2015 Scientific Reports
Vol. 5 
article DOI URL 
Abstract: Perfluoroalkyl acids (PFAAs) are widely used in many applications due to their unique physical and chemical characteristics. Because of the increasing prevalence of metabolic syndromes, including obesity, dyslipidemia and insulin resistance, concern has arisen about the roles of environmental pollutants in such diseases. Earlier epidemiologic studies showed a potential association between perfluorooctanoic acid (PFOA) and glucose metabolism, but how PFOA influences glucose homeostasis is still unknown. Here, we report on the modulation of the phosphatidylinositol 3-kinase-serine/threonine protein kinase (PI3K-AKT) signaling pathway in the livers of mice after 28 d of exposure to PFOA. Compared with normal mice, PFOA exposure significantly decreased the expression of the phosphatase and tensin homologue (PTEN) protein and affected the PI3K-AKT signaling pathway in the liver. Tolerance tests further indicated that PFOA exposure induced higher insulin sensitivity and glucose tolerance in mice. Biochemical analysis revealed that PFOA exposure reduced hepatic glycogen synthesis, which might be attributed to gluconeogenesis inhibition. The levels of several circulating proteins were altered after PFOA exposure, including proteins potentially related to diabetes and liver disease. Our results suggest that PFOA affected glucose metabolism and induced insulin hypersensitivity in mice.
BibTeX:
@article{Yan2015,
  author = {Yan, Shengmin and Zhang, Hongxia and Zheng, Fei and Sheng, Nan and Guo, Xuejiang and Dai, Jiayin},
  title = {Perfluorooctanoic acid exposure for 28 days affects glucose homeostasis and induces insulin hypersensitivity in mice},
  journal = {Scientific Reports},
  year = {2015},
  volume = {5},
  url = {http://www.nature.com/srep/2015/150612/srep11029/full/srep11029.htmlaffil-auth},
  doi = {http://doi.org/10.1038/srep11029}
}
Yang, X., Koltes, J.E., Park, C.A., Chen, D. and Reecy, J.M. Gene Co-Expression Network Analysis Provides Novel Insights into Myostatin Regulation at Three Different Mouse Developmental Timepoints 2015 PLoS ONE
Vol. 10(2), pp. e0117607 
article DOI URL 
Abstract: Myostatin (Mstn) knockout mice exhibit large increases in skeletal muscle mass. However, relatively few of the genes that mediate or modify MSTN effects are known. In this study, we performed co-expression network analysis using whole transcriptome microarray data from MSTN-null and wild-type mice to identify genes involved in important biological processes and pathways related to skeletal muscle and adipose development. Genes differentially expressed between wild-type and MSTN-null mice were further analyzed for shared DNA motifs using DREME. Differentially expressed genes were identified at 13.5 d.p.c. during primary myogenesis and at d35 during postnatal muscle development, but not at 17.5 d.p.c. during secondary myogenesis. In total, 283 and 2034 genes were differentially expressed at 13.5 d.p.c. and d35, respectively. Over-represented transcription factor binding sites in differentially expressed genes included SMAD3, SP1, ZFP187, and PLAGL1. The use of regulatory (RIF) and phenotypic (PIF) impact factor and differential hubbing co-expression analyses identified both known and potentially novel regulators of skeletal muscle growth, including Apobec2, Atp2a2, and Mmp13 at d35 and Sox2, Tmsb4x, and Vdac1 at 13.5 d.p.c. Among the genes with the highest PIF scores were many fiber type specifying genes. The use of RIF, PIF, and differential hubbing analyses identified both known and potentially novel regulators of muscle development. These results provide new details of how MSTN may mediate transcriptional regulation as well as insight into novel regulators of MSTN signal transduction that merit further study regarding their physiological roles in muscle and adipose development.
BibTeX:
@article{Yang2015,
  author = {Yang, Xuerong and Koltes, James E and Park, Carissa A and Chen, Daiwen and Reecy, James M},
  title = {Gene Co-Expression Network Analysis Provides Novel Insights into Myostatin Regulation at Three Different Mouse Developmental Timepoints},
  journal = {PLoS ONE},
  year = {2015},
  volume = {10},
  number = {2},
  pages = {e0117607},
  url = {http://dx.doi.org/10.1371/journal.pone.0117607 http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0117607&representation=PDF},
  doi = {http://doi.org/10.1371/journal.pone.0117607}
}
Yang, M., Ye, L., Wang, B., Gao, J., Liu, R., Hong, J., Wang, W., Gu, W. and Ning, G. Decreased miR-146 expression in peripheral blood mononuclear cells is correlated with ongoing islet autoimmunity in type 1 diabetes patients 1miR-146. 2015 Journal of diabetes
Vol. 7(2), pp. 158-65 
article DOI URL 
Abstract: BACKGROUND Type 1 diabetes mellitus (T1D) is a common autoimmune disease mediated by autoimmune attack against pancreatic β-cells. It has been reported that dysregulation of microRNAs (miRNAs) may contribute to the pathogenesis of autoimmune diseases, including T1D. The aim of the present study was to identify pathogenic miRNAs in peripheral blood mononuclear cells (PBMC) of T1D patients. METHODS Global miRNA and mRNA expression was profiled in PBMC from 12 patients with newly diagnosed T1D and 10 normal controls. Differently expressed miRNAs were validated in an independent set of patients and controls. The dynamic changes in miRNA and target gene expression were analyzed in T1D patients treated with either a short (6 months) or long (12-24 months) course of insulin. The association between miRNA expression and serum glutamic acid decarboxylase antibody (GADA) titers was also investigated. RESULTS Compared with normal controls, there were 26 miRNAs and 1218 genes differently expressed in PBMC of patients with newly diagnosed T1D. The greatest downregulation was for miR-146a (48% decrease; P textless 0.05). Expression of its target genes, predicted to be tumor necrosis factor receptor-associated factor 6 (TRAF6), B cell CLL/lymphoma 11A (BCL11A), syntaxin 3 (STX3) and numb homolog (NUMB), was upregulated. Moreover, T1D patients on long-course insulin and optimized glucose control had sustained low expression of miR-146. Interestingly, decreased miR-146a expression was significantly associated with high serum GADA titers (P textless 0.05). CONCLUSIONS The results suggest that dysregulation of miR-146 expression in PBMC may be associated with the ongoing autoimmune imbalance in T1D patients.
BibTeX:
@article{Yang2015a,
  author = {Yang, Minglan and Ye, Lei and Wang, Bokai and Gao, Jie and Liu, Ruixin and Hong, Jie and Wang, Weiqing and Gu, Weiqiong and Ning, Guang},
  title = {Decreased miR-146 expression in peripheral blood mononuclear cells is correlated with ongoing islet autoimmunity in type 1 diabetes patients 1miR-146.},
  journal = {Journal of diabetes},
  year = {2015},
  volume = {7},
  number = {2},
  pages = {158--65},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/24796653},
  doi = {http://doi.org/10.1111/1753-0407.12163}
}
Yong, H.E.J., Melton, P.E., Johnson, M.P., Freed, K.A., Kalionis, B., Murthi, P., Brennecke, S.P., Keogh, R.J. and Moses, E.K. [81-OR]: Genome-wide transcriptome directed pathway analysis of maternal preeclampsia susceptibility genes 2015 Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health
Vol. 5(1), pp. 43-44 
article DOI URL 
Abstract: Objectives Preeclampsia (PE) is a common and serious pregnancy disorder with a strong genetic component. Numerous genetic studies performed, including our own, have yielded many susceptibility genes from distinct functional groups. Additionally, transcriptome profiling at the maternal-fetal interface has likewise yielded many differentially expressed genes. Often there is little overlap between the two approaches, although both are significantly informative with respect to PE. We have thus taken a novel approach by analysing pathways common to the susceptibility genes and the PE transcriptome. Methods Using Illumina Human Ht12v4 and Wg6v3 BeadChips, transcriptome profiling was conducted on n = 65 normotensive and n = 60 PE decidua basalis tissues collected at delivery. R software was used to pre-process transcript data for pathway analysis. Pathways were analysed and constructed using Ariadne Pathway Studio 9. We examined the following susceptibility genes: ACVR1, ACVR1C, ACVR2A, COL4A1, COL4A2, ERAP1, ERAP2, INHA, INHBB and LNPEP (Yong et al., 2014). Significance was set at p textless 0.05. Results Major common targets/regulators of these susceptibility genes were AGT, IFNG, IL6, INHBA, SERPINE1, TGFB1 and VEGFA (Fig. 1). The top downstream pathway categories of susceptibility genes that were significantly altered in the PE decidual transcriptome were apoptosis and cell signalling. Conclusions Susceptibility genes from distinct functional groups have similar downstream pathways through common targets/regulators. Several of these pathways matched those altered in PE. This study contributes to a better understanding on how susceptibility genes may interact in the development of PE. With this knowledge, more targeted functional analyses of PE susceptibility genes in these key pathways can be performed to examine their contributions to the pathogenesis and severity of PE. Disclosures H.E. Yong: None. P.E. Melton: None. M.P. Johnson: None. K.A. Freed: None. B. Kalionis: None. P. Murthi: None. S.P. Brennecke: None. R.J. Keogh: None. E.K. Moses: None.
BibTeX:
@article{Yong2015,
  author = {Yong, Hannah E J and Melton, Phillip E and Johnson, Matthew P and Freed, Katy A and Kalionis, Bill and Murthi, Padma and Brennecke, Shaun P and Keogh, Rosemary J and Moses, Eric K},
  title = {[81-OR]: Genome-wide transcriptome directed pathway analysis of maternal preeclampsia susceptibility genes},
  journal = {Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health},
  year = {2015},
  volume = {5},
  number = {1},
  pages = {43--44},
  url = {http://www.sciencedirect.com/science/article/pii/S221077891400186X http://www.sciencedirect.com/science/article/pii/S221077891400186X/pdfft?md5=96e74a1cb10c9dd68b1f0a7d3a30cd33&pid=1-s2.0-S221077891400186X-main.pdf},
  doi = {http://doi.org/10.1016/j.preghy.2014.10.085}
}
Yoshimura, K., Okanoue, T., Ebise, H., Iwasaki, T., Mizuno, M., Shima, T., Ichihara, J. and Yamazaki, K. Identification of novel noninvasive markers for diagnosing nonalcoholic steatohepatitis and related fibrosis by data mining 2015 Hepatology, pp. n/a-n/a  article DOI URL 
Abstract: It is important that patients with nonalcoholic steatohepatitis (NASH) are diagnosed and treated early to prevent serious complications, such as liver cirrhosis or hepatocellular carcinoma. However, current methods for NASH diagnosis are invasive as they rely on liver biopsy, making early diagnosis difficult. In this study, we developed novel noninvasive markers for the diagnosis of NASH and NASH-related fibrosis. A total of 132 Japanese patients with nonalcoholic fatty liver disease were included in this study. Blood samples were collected, and 261 biomolecules were quantified in the serum. Using cluster and pathway analyses, we identified biomolecule modules connected to biological events that occur with disease progression to NASH. The modules were used as variables for diagnosis, leading to a NASH diagnostic marker associated with 2 biological events, i.e., protective response to hepatic steatosis and hepatitis-causing innate immune response. Regarding the NASH-related fibrosis marker, immunological responses to hepatocyte injury were identified as a biological event. To develop diagnostic markers for NASH and NASH-related fibrosis, specific biomolecules were selected from each biomolecule module. The former marker was obtained by averaging the levels of 4 biomolecules, whereas the latter was obtained by averaging the levels of 2 biomolecules. Both markers achieved a diagnostic accuracy of almost 0.9 of the area under the receiver operating characteristic curve, and the latter exhibited equivalent performance in an independent group of 62 prospectively recruited patients. Conclusion: We developed highly accurate markers for the diagnosis of both NASH and NASH-related fibrosis (i.e., FM-NASH index and FM-fibro index, respectively). These markers may be used as an alternative diagnostic tool to liver biopsy. This article is protected by copyright. All rights reserved.
BibTeX:
@article{Yoshimura2015,
  author = {Yoshimura, Keito and Okanoue, Takeshi and Ebise, Hayao and Iwasaki, Tsuyoshi and Mizuno, Masayuki and Shima, Toshihide and Ichihara, Junji and Yamazaki, Kazuto},
  title = {Identification of novel noninvasive markers for diagnosing nonalcoholic steatohepatitis and related fibrosis by data mining},
  journal = {Hepatology},
  year = {2015},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.1002/hep.28226/abstract},
  doi = {http://doi.org/10.1002/hep.28226}
}
Zavoronkovs, A., Buzdin, A., Borisov, N. and Aliper, A. System, Method and Software for Improved Drug Efficacy and Safety in a Patient 2015   misc URL 
BibTeX:
@misc{Zavoronkovs2015,
  author = {Zavoronkovs, Aleksandrs and Buzdin, Anton and Borisov, Nikolay and Aliper, Alexander},
  title = {System, Method and Software for Improved Drug Efficacy and Safety in a Patient},
  year = {2015},
  url = {http://www.freepatentsonline.com/y2016/0132632.html}
}
Zhang, B., Shimada, Y., Kuroyanagi, J., Ariyoshi, M., Nomoto, T., Shintou, T., Umemoto, N., Nishimura, Y., Miyazaki, T. and Tanaka, T. In vivo selective imaging and inhibition of leukemia stem-like cells using the fluorescent carbocyanine derivative, DiOC5(3) 2015 Biomaterials
Vol. 52, pp. 14-25 
article DOI URL 
Abstract: Elimination of leukemia stem cells (LSCs) is necessary for the destruction of malignant cell populations. Owing to the very small number of LSCs in leukemia cells, xenotransplantation studies are difficult in terms of functionally and pathophysiologically replicating clinical conditions of cell culture experiments. There is currently a limited number of lead compounds that target LSCs. Using the LSC-xenograft zebrafish screening method we previously developed, we found that the fluorescent compound 3,3′-dipentyloxacarbocyanine iodide (DiOC5(3)) selectively marked LSCs and suppressed their proliferation in vivo and in vitro. DiOC5(3) had no obvious toxicity to human umbilical cord blood CD34+ progenitor cells and normal zebrafish. It accumulated in mitochondria through organic anion transporter polypeptides that are overexpressed in the plasma membrane of LSCs, and induced apoptosis via ROS overproduction. DiOC5(3) also inhibited the nuclear translocation of NF-κB through the downregulation of LSC-selective pathways, as indicated from DNA microarray analysis. In summary, DiOC5(3) is a new type of anti-LSC compound available for diagnostic imaging and therapeutics that has the advantage of being a single fluorescent chemical.
BibTeX:
@article{Zhang2015,
  author = {Zhang, Beibei and Shimada, Yasuhito and Kuroyanagi, Junya and Ariyoshi, Michiko and Nomoto, Tsuyoshi and Shintou, Taichi and Umemoto, Noriko and Nishimura, Yuhei and Miyazaki, Takeshi and Tanaka, Toshio},
  title = {In vivo selective imaging and inhibition of leukemia stem-like cells using the fluorescent carbocyanine derivative, DiOC5(3)},
  journal = {Biomaterials},
  year = {2015},
  volume = {52},
  pages = {14--25},
  url = {http://www.sciencedirect.com/science/article/pii/S0142961215001192 http://www.sciencedirect.com/science/article/pii/S0142961215001192/pdfft?md5=aa600439847f722cfdee9860377a2f7b&pid=1-s2.0-S0142961215001192-main.pdf},
  doi = {http://doi.org/10.1016/j.biomaterials.2015.02.009}
}
Zhang, J., Koch, I., Gibson, L.A., Loughery, J.R., Martyniuk, C.J., Button, M., Caumette, G., Reimer, K.J., Cullen, W.R. and Langlois, V.S. Transcriptomic responses during early development following arsenic exposure in Western clawed frogs, Silurana tropicalis 2015 Toxicological Sciences, pp. kfv207  article DOI URL 
Abstract: Arsenic compounds are widespread environmental contaminants and exposure elicits serious health issues, including early developmental anomalies. Depending on the oxidation state, the intermediates of arsenic metabolism interfere with a range of subcellular events, but the fundamental molecular events that lead to speciation-dependent arsenic toxicity are not fully elucidated. The present study therefore assesses the impact of arsenic exposure on early development by measuring speciation and gene expression profiles in the developing Western clawed frog (Silurana tropicalis) larvae following the environmental relevant 0.5 and 1 ppm arsenate exposure. Using HPLC-ICP-MS, arsenate, dimethylarsenic acid, arsenobetaine, arsenocholine, and tetramethylarsonium ion were detected. Microarray and pathway analyses were utilized to characterize the comprehensive transcriptomic responses to arsenic exposure. Clustering analysis of expression data showed distinct gene expression patterns in arsenate treated groups when compared with the control. Pathway enrichment revealed common biological themes enriched in both treatments, including cell signal transduction, cell survival, and developmental pathways. Moreover, the 0.5 ppm exposure led to the enrichment of pathways and biological processes involved in arsenic intake or efflux, as well as histone remodelling. These compensatory responses are hypothesized to be responsible for maintaining an in-body arsenic level comparable to control animals. With no appreciable changes observed in malformation and mortality between control and exposed larvae, this is the first study to suggest that the underlying transcriptomic regulations related to signal transduction, cell survival, developmental pathways, and histone remodelling may contribute to maintaining ongoing development while coping with the potential arsenic toxicity in S.tropicalis during early development.
BibTeX:
@article{Zhang2015a,
  author = {Zhang, Jing and Koch, Iris and Gibson, Laura A and Loughery, Jennifer R and Martyniuk, Christopher J and Button, Mark and Caumette, Guilhem and Reimer, Kenneth J and Cullen, William R and Langlois, Valerie S},
  title = {Transcriptomic responses during early development following arsenic exposure in Western clawed frogs, Silurana tropicalis},
  journal = {Toxicological Sciences},
  year = {2015},
  pages = {kfv207},
  url = {http://toxsci.oxfordjournals.org/content/early/2015/10/01/toxsci.kfv207 http://www.ncbi.nlm.nih.gov/pubmed/26427749 http://toxsci.oxfordjournals.org/content/early/2015/10/01/toxsci.kfv207.abstract},
  doi = {http://doi.org/10.1093/toxsci/kfv207}
}
Zhou, Q., Chen, T., Zhang, W., Bozkanat, M., Li, Y., Xiao, L., van Breemen, R.B., Christman, J.W., Sznajder, J.I. and Zhou, G. Suppression of Von Hippel-Lindau Protein in Fibroblasts Protects Against Bleomycin-induced Pulmonary Fibrosis 2015 American Journal of Respiratory Cell and Molecular Biology  article DOI URL 
Abstract: We have reported that von Hippel-Lindau protein (pVHL) expression is elevated in human and mouse fibrotic lungs and that overexpression of pVHL stimulates fibroblast proliferation. We sought to determine whether loss of pVHL in fibroblasts prevents injury and fibrosis in mice that are treated with bleomycin. We generated heterozygous fibroblast-specific pVHL knockdown mice (Fsp-VHL+/-) and homozygous fibroblast-specific pVHL knockout mice (Fsp-VHL-/-) by crossbreeding vhlh 2-lox mice (VHL+/+) with Fsp-Cre mice. Our data show that Fsp-VHL-/- but not Fsp-VHL+/- mice have elevated red blood cell counts, hematocrit, hemoglobin content, and expression of HIF targets, indicating HIF activation. To examine the role of pVHL in bleomycin-induced lung injury and fibrosis in vivo, we administered PBS or bleomycin to age-, sex-, and strain-matched 8-week-old VHLfl/fl, Fsp-VHL+/-, and Fsp-VHL-/- mice. In Fsp-VHL+/- and Fsp-VHL-/- mice, bleomycin-induced collagen accumulation, fibroblast proliferation, differentiation, and matrix protein dysregulation were markedly attenuated. Suppression of pVHL also decreased bleomycin-induced Wnt signaling and PGE2 signaling but did not affect bleomycin-induced initial acute lung injury and lung inflammation. These results indicate that pVHL has a pivotal role in bleomycin-induced pulmonary fibrosis, possibly via a HIF-independent pathway. Paradoxically pVHL does not affect bleomycin-induced lung injury and inflammation, indicating a separation of the mechanisms involved in injury/inflammation from those involved in pulmonary fibrosis.
BibTeX:
@article{Zhou2015,
  author = {Zhou, Qiyuan and Chen, Tianji and Zhang, Wei and Bozkanat, Melike and Li, Yongchao and Xiao, Lei and van Breemen, Richard B and Christman, John W and Sznajder, Jacob I and Zhou, Guofei},
  title = {Suppression of Von Hippel-Lindau Protein in Fibroblasts Protects Against Bleomycin-induced Pulmonary Fibrosis},
  journal = {American Journal of Respiratory Cell and Molecular Biology},
  year = {2015},
  url = {http://www.atsjournals.org/doi/abs/10.1165/rcmb.2015-0111OC},
  doi = {http://doi.org/10.1165/rcmb.2015-0111OC}
}
Zhu, J., Zhao, C., Zhuang, T., Jonsson, P., Sinha, I., Williams, C., Strömblad, S. and Dahlman-Wright, K. RING finger protein 31 promotes p53 degradation in breast cancer cells 2015 Oncogene  article DOI URL 
Abstract: The atypical E3 ubiquitin ligase RNF31 is highly expressed in human breast cancer, the most frequent neoplastic lethality among women. Here, RNF31 depletion in breast cancer cells in combination with global gene expression profiling revealed p53 (TP53) signaling as a potential RNF31 target. Interestingly, RNF31 decreased p53 stability, whereas depletion of RNF31 in breast cancer cells caused cell cycle arrest and cisplatin-induced apoptosis in a p53-dependent manner. Furthermore, RNF31 associated with the p53/MDM2 complex and facilitated p53 polyubiquitination and degradation by stabilizing MDM2, suggesting a molecular mechanism by which RNF31 regulates cell death. Analysis of publically available clinical data sets displayed a negative correlation between RNF31 and p53 target genes, including IGFBP3 and BTG1, consistent with RNF31 regulating p53 function in vivo as well. Together, our findings suggest RNF31 as a potential therapeutic target to restore p53 function in breast cancer.
BibTeX:
@article{Zhu2015,
  author = {Zhu, J and Zhao, C and Zhuang, T and Jonsson, P and Sinha, I and Williams, C and Strömblad, S and Dahlman-Wright, K},
  title = {RING finger protein 31 promotes p53 degradation in breast cancer cells},
  journal = {Oncogene},
  year = {2015},
  url = {http://www.nature.com/onc/journal/vaop/ncurrent/full/onc2015260a.html},
  doi = {http://doi.org/10.1038/onc.2015.260}
}
Elsevier Helps Biologists Understand Disease Biology More Quickly with the Launch of... -- NEW YORK, December 9, 2015 /PRNewswire/ -- 2015   misc URL 
BibTeX:
@misc{,,
  title = {Elsevier Helps Biologists Understand Disease Biology More Quickly with the Launch of... -- NEW YORK, December 9, 2015 /PRNewswire/ --},
  year = {2015},
  url = {http://www.prnewswire.com/news-releases/elsevier-helps-biologists-understand-disease-biology-more-quickly-with-the-launch-of-pathway-studio-web-561199271.html}
}
Ahmed, N.U., Jung, H.-J., Park, J.-I., Cho, Y.-G., Hur, Y. and Nou, I.-S. Identification and expression analysis of cold and freezing stress responsive genes of Brassica oleracea 2014 Gene  article DOI URL 
Abstract: Cold and freezing stress is a major environmental constraint to the production of Brassica crops. Enhancement of tolerance by exploiting cold and freezing tolerance related genes offers the most efficient approach to address this problem. Cold-induced transcriptional profiling is a promising approach to the identification of potential genes related to cold and freezing stress tolerance. In this study, 99 highly expressed genes were identified from a whole genome microarray dataset of Brassica rapa. Blast search analysis of the Brassica oleracea database revealed the corresponding homologous genes. To validate their expression, pre-selected cold tolerant and susceptible cabbage lines were analyzed. Out of 99 BoCRGs, 43 were differentially expressed in response to varying degrees of cold and freezing stress in the contrasting cabbage lines. Among the differentially expressed genes, 18 were highly up-regulated in the tolerant lines, which is consistent with their microarray expression. Additionally, 12 BoCRGs were expressed differentially after cold stress treatment in two contrasting cabbage lines, and BoCRG54, 56, 59, 62, 70, 72 and 99 were predicted to be involved in cold regulatory pathways. Taken together, the cold-responsive genes identified in this study provide additional direction for elucidating the regulatory network of low temperature stress tolerance and developing cold and freezing stress resistant Brassica crops.
BibTeX:
@article{Ahmed2014,
  author = {Ahmed, Nasar Uddin and Jung, Hee-Jeong and Park, Jong-In and Cho, Yong-Gu and Hur, Yoonkang and Nou, Ill-Sup},
  title = {Identification and expression analysis of cold and freezing stress responsive genes of Brassica oleracea},
  journal = {Gene},
  year = {2014},
  url = {http://www.sciencedirect.com/science/article/pii/S0378111914012104},
  doi = {http://doi.org/10.1016/j.gene.2014.10.050}
}
Alam, S., Phan, H.T., Okazaki, M., Takagi, M., Kawahara, K., Tsukahara, T. and Suzuki, H. Computational extraction of a neural molecular network through alternative splicing 2014 BMC research notes
Vol. 7(1), pp. 934 
article DOI URL 
Abstract: BACKGROUND: Generally, the results of high throughput analyses contain information about gene expressions, and about exon expressions. Approximately 90% of primary protein-coding transcripts undergo alternative splicing in mammals. However, changes induced by alternative exons have not been properly analyzed for their impact on important molecular networks or their biological events. Even when alternative exons are identified, they are usually subjected to bioinformatics analysis in the same way as the gene ignoring the possibility of functionality change because of the alteration of domain caused by alternative exon. Here, we reveal an effective computational approach to explore an important molecular network based on potential changes of functionality induced by alternative exons obtained from our comprehensive analysis of neuronal cell differentiation. RESULTS: From our previously identified 262 differentially alternatively spliced exons during neuronal cell differentiations, we extracted 241 sets that changed the amino acid sequences between the alternatively spliced sequences. Conserved domain searches indicated that annotated domain(s) were changed in 128 sets. We obtained 49 genes whose terms overlapped between domain description and gene annotation. Thus, these 49 genes have alternatively differentially spliced in exons that affect their main functions. We performed pathway analysis using these 49 genes and identified the EGFR (epidermal growth factor receptor) and mTOR (mammalian target of rapamycin) signaling pathway as being involved frequently. Recent studies reported that the mTOR pathway is associated with neuronal cell differentiation, vindicating that our approach extracted an important molecular network successfully. CONCLUSIONS: Effective informatics approaches for exons should be more complex than those for genes, because changes in alternative exons affect protein functions via alterations of amino acid sequences and functional domains. Our method extracted alterations of functional domains and identified key alternative splicing events. We identified the EGFR and mTOR signaling pathway as the most affected pathway. The mTOR pathway is important for neuronal differentiation, suggesting that this in silico extraction of alternative splicing networks is useful. This preliminary analysis indicated that automated analysis of the effects of alternative splicing would provide a rich source of biologically relevant information.
BibTeX:
@article{Alam2014,
  author = {Alam, Shafiul and Phan, Huong Thi and Okazaki, Mio and Takagi, Masahiro and Kawahara, Kozo and Tsukahara, Toshifumi and Suzuki, Hitoshi},
  title = {Computational extraction of a neural molecular network through alternative splicing},
  journal = {BMC research notes},
  year = {2014},
  volume = {7},
  number = {1},
  pages = {934},
  url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320441/pdf/131042014Article3461.pdf http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320441/ http://www.ncbi.nlm.nih.gov/pubmed/25523101},
  doi = {http://doi.org/10.1186/1756-0500-7-934}
}
Alawieh, A., Sabra, Z., Nokkari, A., El-Assaad, A., Mondello, S., Zaraket, F., Fadlallah, B. and Kobeissy, F.H. Bioinformatics approach to understanding interacting pathways in neuropsychiatric disorders 2014 Methods in molecular biology (Clifton, N.J.)
Vol. 1168, pp. 157-172 
article DOI URL 
Abstract: Bioinformatics-based applications have been incorporated into several medical disciplines, including cancer, neuroscience, and recently psychiatry. Both the increasing interest in the molecular aspect of neuropsychiatry and the availability of high-throughput discovery and analysis tools have encouraged the incorporation of bioinformatics and neurosystems biology techniques into psychiatry and neuroscience research. As applied to neuropsychiatry, systems biology involves the acquisition and processing of high-throughput datasets to infer new information. A major component in bioinformatics output is pathway analysis that provides an insight into and prediction of possible underlying pathogenic processes which may help understand disease pathogenesis. In addition, this analysis serves as a tool to identify potential biomarkers implicated in these disorders. In this chapter, we summarize the different tools and algorithms used in pathway analysis along with their applications to the different layers of molecular investigations, from genomics to proteomics.
BibTeX:
@article{Alawieh2014,
  author = {Alawieh, Ali and Sabra, Zahraa and Nokkari, Amaly and El-Assaad, Atlal and Mondello, Stefania and Zaraket, Fadi and Fadlallah, Bilal and Kobeissy, Firas H},
  title = {Bioinformatics approach to understanding interacting pathways in neuropsychiatric disorders},
  journal = {Methods in molecular biology (Clifton, N.J.)},
  year = {2014},
  volume = {1168},
  pages = {157--172},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/24870135},
  doi = {http://doi.org/10.1007/978-1-4939-0847-9_9}
}
Alisoltani, A., Fallahi, H., Ebrahimi, M., Ebrahimi, M. and Ebrahimie, E. Prediction of Potential Cancer-Risk Regions Based on Transcriptome Data: Towards a Comprehensive View 2014 PLoS ONE
Vol. 9(5), pp. e96320 
article DOI URL 
Abstract: A novel integrative pipeline is presented for discovery of potential cancer-susceptibility regions (PCSRs) by calculating the number of altered genes at each chromosomal region, using expression microarray datasets of different human cancers (HCs). Our novel approach comprises primarily predicting PCSRs followed by identification of key genes in these regions to obtain potential regions harboring new cancer-associated variants. In addition to finding new cancer causal variants, another advantage in prediction of such risk regions is simultaneous study of different types of genomic variants in line with focusing on specific chromosomal regions. Using this pipeline we extracted numbers of regions with highly altered expression levels in cancer condition. Regulatory networks were also constructed for different types of cancers following the identification of altered mRNA and microRNAs. Interestingly, results showed that GAPDH, LIFR, ZEB2, mir-21, mir-30a, mir-141 and mir-200c, all located at PCSRs, are common altered factors in constructed networks. We found a number of clusters of altered mRNAs and miRNAs on predicted PCSRs (e.g.12p13.31) and their common regulators including KLF4 and SOX10. Large scale prediction of risk regions based on transcriptome data can open a window in comprehensive study of cancer risk factors and the other human diseases.
BibTeX:
@article{Alisoltani2014,
  author = {Alisoltani, Arghavan and Fallahi, Hossein and Ebrahimi, Mahdi and Ebrahimi, Mansour and Ebrahimie, Esmaeil},
  title = {Prediction of Potential Cancer-Risk Regions Based on Transcriptome Data: Towards a Comprehensive View},
  journal = {PLoS ONE},
  year = {2014},
  volume = {9},
  number = {5},
  pages = {e96320},
  url = {http://dx.doi.org/10.1371/journal.pone.0096320 http://www.ncbi.nlm.nih.gov/pubmed/24796549},
  doi = {http://doi.org/10.1371/journal.pone.0096320}
}
An, F., Fan, J., Li, J., Li, Q.X., Li, K., Zhu, W., Wen, F., Carvalho, L.J.C.B. and Chen, S. Comparison of Leaf Proteomes of Cassava (Manihot esculenta Crantz) Cultivar NZ199 Diploid and Autotetraploid Genotypes 2014 PLoS ONE
Vol. 9(4), pp. e85991 
article DOI URL 
Abstract: Cassava polyploid breeding has drastically improved our knowledge on increasing root yield and its significant tolerance to stresses. In polyploid cassava plants, increases in DNA content highly affect cell volumes and anatomical structures. However, the mechanism of this effect is poorly understood. The purpose of the present study was to compare and validate the changes between cassava cultivar NZ199 diploid and autotetraploid at proteomic levels. The results showed that leaf proteome of cassava cultivar NZ199 diploid was clearly differentiated from its autotetraploid genotype using 2-DE combined MS technique. Sixty-five differential protein spots were seen in 2-DE image of autotetraploid genotype in comparison with that of diploid. Fifty-two proteins were identified by MALDI-TOF-MS/MS, of which 47 were up-regulated and 5 were down-regulated in autotetraploid genotype compared with diploid genotype. The classified functions of 32 up-regulated proteins were associated with photosynthesis, defense system, hydrocyanic acid (HCN) metabolism, protein biosynthesis, chaperones, amino acid metabolism and signal transduction. The remarkable variation in photosynthetic activity, HCN content and resistance to salt stress between diploid and autotetraploid genotypes is closely linked with expression levels of proteomic profiles. The analysis of protein interaction networks indicated there are direct interactions between the 15 up-regulation proteins involved in the pathways described above. This work provides an insight into understanding the protein regulation mechanism of cassava polyploid genotype, and gives a clue to improve cassava polyploidy breeding in increasing photosynthesis and resistance efficiencies.
BibTeX:
@article{An2014,
  author = {An, Feifei and Fan, Jie and Li, Jun and Li, Qing X and Li, Kaimian and Zhu, Wenli and Wen, Feng and Carvalho, Luiz J C B and Chen, Songbi},
  title = {Comparison of Leaf Proteomes of Cassava (Manihot esculenta Crantz) Cultivar NZ199 Diploid and Autotetraploid Genotypes},
  journal = {PLoS ONE},
  year = {2014},
  volume = {9},
  number = {4},
  pages = {e85991},
  url = {http://dx.plos.org/10.1371/journal.pone.0085991},
  doi = {http://doi.org/10.1371/journal.pone.0085991}
}
Anderson, J.L., Smith, S.C. and Taylor, R.L. The pigeon (Columba livia) model of spontaneous atherosclerosis 2014 Poultry Science  article DOI URL 
Abstract: Multiple animal models have been employed to study human atherosclerosis, the principal cause of mortality in the United States. Each model has individual advantages related to specific pathologies. Initiation, the earliest disease phase, is best modeled by the White Carneau (WC-As) pigeon. Atherosclerosis develops spontaneously in the WC-As without either external manipulation or known risk factors. Furthermore, susceptibility is caused by a single gene defect inherited in an autosomal recessive manner. The Show Racer (SR-Ar) pigeon is resistant to atherosclerosis. Breed differences in the biochemistry and metabolism of celiac foci cells have been described. For example, WC-As have lower oxidative metabolism but higher amounts of chondroitin-6-sulfate and nonesterified fatty acids compared with SR-Ar. Gene expression in aortic smooth muscle cells was compared between breeds using representational difference analysis and microarray analysis. Energy metabolism and cellular phenotype were the chief gene expression differences. Glycolysis and synthetic cell types were related to the WC-As but oxidative metabolism and contractile cell types were related to the SR-Ar. Rosiglitazone, a PPARγ agonist, blocked RNA binding motif (RBMS1) expression in WC-As cells. The drug may act through the c-myc oncogene as RBMS1 is a c-myc target. Proteomic tests of aortic smooth muscle cells supported greater glycosylation in the WC-As and a transforming growth factor β effect in SR-Ar. Unoxidized fatty acids build up in WC-As cells because of their metabolic deficiency, ultimately preventing the contractile phenotype in these cells. The single gene responsible for the disease is likely regulatory in nature.
BibTeX:
@article{Anderson2014,
  author = {Anderson, J L and Smith, S C and Taylor, R L},
  title = {The pigeon (Columba livia) model of spontaneous atherosclerosis},
  journal = {Poultry Science},
  year = {2014},
  url = {http://ps.oxfordjournals.org/cgi/doi/10.3382/ps.2014-04280},
  doi = {http://doi.org/10.3382/ps.2014-04280}
}
Andrew, A.S., Gui, J., Hu, T., Wyszynski, A., Marsit, C.J., Kelsey, K.T., Schned, A.R., Tanyos, S.A., Pendleton, E.M., Ekstrom, R.M., Li, Z., Zens, M.S., Borsuk, M., Moore, J.H. and Karagas, M.R. Genetic polymorphisms modify bladder cancer recurrence and survival in a USA population-based prognostic study: Genetics modify bladder cancer prognosis 2014 BJU International, pp. n/a-n/a  article DOI URL 
Abstract: Objective To identify genetic variants that modify bladder cancer prognosis focusing on genes involved in major biological carcinogenesis processes (apoptosis, proliferation, DNA repair, hormone regulation, immune surveillance, and cellular metabolism), as nearly half of patients with bladder cancer experience recurrences reliable predictors of this recurrent phenotype are needed to guide surveillance and treatment. Patients and methods We analysed variant genotypes hypothesised to modify these processes in 563 patients with urothelial-cell carcinoma enrolled in a population-based study of incident bladder cancer conducted in New Hampshire, USA. After diagnosis, patients were followed over time to ascertain recurrence and survival status, making this one of the first population-based studies with detailed prognosis data. Cox proportional hazards regression was used to assess the relationship between single nucleotide polymorphisms (SNPs) and prognosis endpoints. Results Patients with aldehyde dehydrogenase 2 (ALDH2) variants had a shorter time to first recurrence (adjusted non-invasive hazard ratio [HR] 1.90, 95% confidence interval [CI] 1.29–2.78). There was longer survival among patients with non-invasive tumours associated with DNA repair X-ray repair cross-complementing protein 4 (XRCC4) heterozygous genotype compared with wild-type (adjusted HR 0.53, 95% CI 0.38–0.74). Time to recurrence was shorter for patients who had a variant allele in vascular cellular adhesion molecule 1 (VCAM1) and were treated with immunotherapy (P interaction textless 0.001). Conclusions Our analysis suggests candidate prognostic SNPs that could guide personalised bladder cancer surveillance and treatment.
BibTeX:
@article{Andrew2014,
  author = {Andrew, Angeline S and Gui, Jiang and Hu, Ting and Wyszynski, Asaf and Marsit, Carmen J and Kelsey, Karl T and Schned, Alan R and Tanyos, Sam A and Pendleton, Eben M and Ekstrom, Rebecca M and Li, Zhongze and Zens, Michael S and Borsuk, Mark and Moore, Jason H and Karagas, Margaret R},
  title = {Genetic polymorphisms modify bladder cancer recurrence and survival in a USA population-based prognostic study: Genetics modify bladder cancer prognosis},
  journal = {BJU International},
  year = {2014},
  pages = {n/a--n/a},
  url = {http://doi.wiley.com/10.1111/bju.12641},
  doi = {http://doi.org/10.1111/bju.12641}
}
Arnold, C., Abdelmoez, A., Thurner, G., Debagge, P., Lukas, P., Skvortsov, S. and Skvortsova, I. Rac1 as a multifunctional therapeutic target to prevent and combat cancer metastasis 2014 Oncoscience  article  
Abstract: Metastatic progression of malignant tumors resistant to conventional therapeutic approaches is an ultimate challenge in clinical oncology. Despite the efforts of basic and clinical researchers, there is still no effective treatment schedule to prevent or combat metastatic spread of malignant tumors. This report presents recent findings that could help in the development of targeted therapeutics directed against the most aggressive and treatment-resistant carcinoma cells. It was demonstrated that HNSCC carcinoma cell lines with acquired treatment resistance possessed increased number of cells with carcinoma stem cell (CSC) properties. Furthermore, resistant cells were characterized by increased expression of Rac1, enhanced cell migration, and accelerated release of proangio- and vasculogenic factors (VEGF-A) and influence on endothelial cell (HMEC-1) migration. Inhibition of Rac1 signaling in the treatment-resistant carcinoma cells can interrupt metastatic process due to anoikis restoration and decrease of cell migration. It is also suggested that carcinoma cells with repressed survival capacities will be characterized by reduced release of proangiogenic factors, resulting in the decrease of endothelial cell migration. Therefore targeting of Rac1-related pathways may be considered as a promising therapeutic approach to prevent or combat metastatic lesions.
BibTeX:
@article{Arnold2014,
  author = {Arnold, Christoph and Abdelmoez, Alshaimaa and Thurner, Gudrun and Debagge, Paul and Lukas, Peter and Skvortsov, Sergej and Skvortsova, Ira},
  title = {Rac1 as a multifunctional therapeutic target to prevent and combat cancer metastasis},
  journal = {Oncoscience},
  year = {2014}
}
Ayoglu, B., Chaouch, A., Lochmüller, H., Politano, L., Bertini, E., Spitali, P., Hiller, M., Niks, E., Gualandi, F., Pontén, F., Bushby, K., Aartsma-Rus, A., Schwartz, E., Le Priol, Y., Straub, V., Uhlén, M., Cirak, S., ‘t Hoen, P.A.C., Muntoni, F., Ferlini, A., Schwenk, J.M., Nilsson, P. and Al-Khalili Szigyarto, C. Affinity proteomics within rare diseases: a BIO-NMD study for blood biomarkers of muscular dystrophies 2014 EMBO Molecular Medicine, pp. n/a-n/a  article DOI URL 
Abstract: Despite the recent progress in the broad-scaled analysis of proteins in body fluids, there is still a lack in protein profiling approaches for biomarkers of rare diseases. Scarcity of samples is the main obstacle hindering attempts to apply discovery driven protein profiling in rare diseases. We addressed this challenge by combining samples collected within the BIO-NMD consortium from four geographically dispersed clinical sites to identify protein markers associated with muscular dystrophy using an antibody bead array platform with 384 antibodies. Based on concordance in statistical significance and confirmatory results obtained from analysis of both serum and plasma, we identified eleven proteins associated with muscular dystrophy, among which four proteins were elevated in blood from muscular dystrophy patients: carbonic anhydrase III (CA3) and myosin light chain 3 (MYL3), both specifically expressed in slow-twitch muscle fibers and mitochondrial malate dehydrogenase 2 (MDH2) and electron transfer flavoprotein A (ETFA). Using age-matched sub-cohorts, 9 protein profiles correlating with disease progression and severity were identified, which hold promise for the development of new clinical tools for management of dystrophinopathies.
BibTeX:
@article{Ayoglu2014,
  author = {Ayoglu, Burcu and Chaouch, Amina and Lochmüller, Hanns and Politano, Luisa and Bertini, Enrico and Spitali, Pietro and Hiller, Monika and Niks, Eric and Gualandi, Francesca and Pontén, Fredrik and Bushby, Kate and Aartsma-Rus, Annemieke and Schwartz, Elena and Le Priol, Yannick and Straub, Volker and Uhlén, Mathias and Cirak, Sebahattin and ‘t Hoen, Peter A C and Muntoni, Francesco and Ferlini, Alessandra and Schwenk, Jochen M and Nilsson, Peter and Al-Khalili Szigyarto, Cristina},
  title = {Affinity proteomics within rare diseases: a BIO-NMD study for blood biomarkers of muscular dystrophies},
  journal = {EMBO Molecular Medicine},
  year = {2014},
  pages = {n/a--n/a},
  url = {http://onlinelibrary.wiley.com/doi/10.15252/emmm.201303724/abstract http://www.ncbi.nlm.nih.gov/pubmed/24920607},
  doi = {http://doi.org/10.15252/emmm.201303724}
}
Babgohari, M.Z., Ebrahimie, E. and Niazi, A. In silico analysis of high affinity potassium transporter (HKT) isoforms in different plants 2014 Aquatic Biosystems
Vol. 10(1), pp. 9 
article DOI URL 
Abstract: High affinity potassium transporters (HKTs) are located in the plasma membrane of the vessels and have significant influence on salt tolerance in some plants. They exclude Na+ from the parenchyma cells to reduce Na+ concentration. Despite many studies, the underlying regulatory mechanisms and the exact functions of HKTs within different genomic backgrounds are relatively unknown. In this study, various bioinformatics techniques, including promoter analysis, identification of HKT-surrounding genes, and construction of gene networks, were applied to investigate the HKT regulatory mechanism.
BibTeX:
@article{Babgohari2014,
  author = {Babgohari, Mahbobeh Zamani and Ebrahimie, Esmaeil and Niazi, Ali},
  title = {In silico analysis of high affinity potassium transporter (HKT) isoforms in different plants},
  journal = {Aquatic Biosystems},
  year = {2014},
  volume = {10},
  number = {1},
  pages = {9},
  url = {http://www.aquaticbiosystems.org/content/10/1/9/abstract},
  doi = {http://doi.org/10.1186/2046-9063-10-9}
}
Bahamonde, P.A., Tetreault, G.R., McMaster, M.E., Servos, M.R., Martyniuk, C.J. and Munkittrick, K.R. Molecular signatures in rainbow darter (Etheostoma caeruleum) inhabiting an urbanized river reach receiving wastewater effluents 2014 Aquatic Toxicology (Amsterdam, Netherlands)
Vol. 148, pp. 211-220 
article DOI URL 
Abstract: Rainbow darter (Etheostoma caeruleum) is a small benthic fish species found in North America that are abundant and distributed throughout the Grand River watershed, ON, Canada. Rainbow darter exhibit intersex in males at sites adjacent to municipal wastewater effluents (MWWE). In October 2010, female and male rainbow darter were collected at 3 sites (1 upstream reference and 2 downstream exposed sites) in the Grand River near the cities of Kitchener and Waterloo. The primary objectives of this research were (1) to characterize the responses of whole organism endpoints (i.e. condition factor (K), liversomatic (LSI) and gonadosomatic index (GSI), histopathology) to MWWEs and (2) to identify transcripts showing altered steady state abundance with exposure to MWWE in fish inhabiting municipal wastewater effluent-exposed areas. Genes measured in this study included vitellogenin, Sry-box containing protein 9 (sox9), forkhead box L2 (foxl2), doublesex and mab-3 related transcription factor 1 (dmrt1), cytochrome P450, family 11, subfamily A, polypeptide 1 (cyp11a) as well as estrogen (esr1, esrb) and androgen (ar) receptors. There were no changes in condition factor; however, there was a significant increase in LSI and a decrease in GSI in fish inhabiting downstream environments when compared with fish collected from the reference site. Males had a high incidence (∼ 70%) of intersex in downstream sites; characterized by the presence of oocytes within the testis. In the gonad, there were sex specific differences for genes related to sexual differentiation; dmrt1 was only expressed in males whereas foxl2 and sox9 were highly expressed in females compared to males. Expression levels of ar and esr1 were higher in females than males. Conversely, esrb was not differentially expressed between sexes or among sites. There were no differences detected for the genes investigated within sex among sites. This study is the first to report on gene expression changes in the rainbow darter, with emphasis on the differences in transcript abundance between sexes and how these changes relate to exposures to MWWEs. Molecular approaches are being investigated for their potential application to field ecotoxicology, and molecular bioassays for relevant, sentinel species in environmental monitoring programs are required to better understand the impact of anthropogenic impacts on species at risk in river systems.
BibTeX:
@article{Bahamonde2014,
  author = {Bahamonde, P A and Tetreault, G R and McMaster, M E and Servos, M R and Martyniuk, C J and Munkittrick, K R},
  title = {Molecular signatures in rainbow darter (Etheostoma caeruleum) inhabiting an urbanized river reach receiving wastewater effluents},
  journal = {Aquatic Toxicology (Amsterdam, Netherlands)},
  year = {2014},
  volume = {148},
  pages = {211--220},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/24513783},
  doi = {http://doi.org/10.1016/j.aquatox.2014.01.010}
}
Bechah, Y., Verneau, J., Ben Amara, A., Barry, A.O., Lépolard, C., Achard, V., Panicot-Dubois, L., Textoris, J., Capo, C., Ghigo, E. and Mege, J.-L. Persistence of Coxiella burnetii, the Agent of Q Fever, in Murine Adipose Tissue 2014 PLoS ONE
Vol. 9(5), pp. e97503 
article DOI URL 
Abstract: Coxiella burnetii, the agent of Q fever, is known to persist in humans and rodents but its cellular reservoir in hosts remains undetermined. We hypothesized that adipose tissue serves as a C. burnetii reservoir during bacterial latency. BALB/c and C57BL/6 mice were infected with C. burnetii by the intraperitoneal route or the intracheal route. Adipose tissue was tested for the presence of C. burnetii several months after infection. C. burnetii was detected in abdominal, inguinal and dorsal adipose tissue 4 months post-infection, when no bacteria were detected in blood, liver, lungs and spleen, regardless of the inoculation route and independently of mouse strain. The transfer of abdominal adipose tissue from convalescent BALB/c mice to naïve immunodeficient mice resulted in the infection of the recipient animals. It is likely that C. burnetii infects adipocytes in vivo because bacteria were found in adipocytes within adipose tissue and replicated within in vitro-differentiated adipocytes. In addition, C. burnetii induced a specific transcriptional program in in-vivo and in vitro-differentiated adipocytes, which was enriched in categories associated with inflammatory response, hormone response and cytoskeleton. These changes may account for bacterial replication in in-vitro and chronic infection in-vivo. Adipose tissue may be the reservoir in which C. burnetii persists for prolonged periods after apparent clinical cure. The mouse model of C. burnetii infection may be used to understand the relapses of Q fever and provide new perspectives to the follow-up of patients.
BibTeX:
@article{Bechah2014,
  author = {Bechah, Yassina and Verneau, Johanna and Ben Amara, Amira and Barry, Abdoulaye O and Lépolard, Catherine and Achard, Vincent and Panicot-Dubois, Laurence and Textoris, Julien and Capo, Christian and Ghigo, Eric and Mege, Jean-Louis},
  title = {Persistence of Coxiella burnetii, the Agent of Q Fever, in Murine Adipose Tissue},
  journal = {PLoS ONE},
  year = {2014},
  volume = {9},
  number = {5},
  pages = {e97503},
  url = {http://dx.doi.org/10.1371/journal.pone.0097503},
  doi = {http://doi.org/10.1371/journal.pone.0097503}
}
Bissegger, S., Martyniuk, C.J. and Langlois, V. Transcriptomic profiling in Silurana tropicalis testes exposed to finasteride 2014 General and Comparative Endocrinology  article DOI URL 
Abstract: Investigations of endocrine disrupting chemicals found in aquatic ecosystems with estrogenic and androgenic modes of action have increased over the past two decades due to a surge of evidence of adverse effects in wildlife. Chemicals that disrupt androgen signalling and steroidogenesis can result in an imbalanced conversion of testosterone (T) into 17β-estradiol (E2) and other androgens such as 5α-dihydrotestosterone (5α-DHT). Therefore, a better understanding of how chemicals perturb these pathways is warranted. In this study, the brain, liver, and testes of Silurana tropicalis were exposed ex vivo to the human drug finasteride, a potent steroid 5α-reductase inhibitor and a model compound to study the inhibition of the conversion of T into 5α-DHT. These experiments were conducted (1) to determine organ specific changes in sex steroid production after treatment, and (2) to elucidate the transcriptomic response to finasteride in testicular tissue. Enzyme-linked immunosorbent assays were used to measure hormone levels in media following finasteride incubation for 6h. Finasteride significantly increased T levels in the media of liver and testis tissue, but did not induce any changes in E2 and 5α-DHT production. Gene expression analysis was performed in frog testes and data revealed that finasteride treatment significantly altered 1,434 gene probes. Gene networks associated with male reproduction such as meiosis, hormone biosynthesis, sperm entry, gonadotropin releasing hormone were affected by finasteride exposure as well as other pathways such as oxysterol synthesis, apoptosis, and epigenetic regulation. For example, this study suggests that the mode of action by which finasteride induces cellular damage in testicular tissue as reported by others, is via oxidative stress in testes. This data also suggests that 5-reductase inhibition disrupts the expression of genes related to reproduction. It is proposed that androgen-disrupting chemicals may mediate their action via 5-reductases and that the effects of environmental pollutants are not limited to the androgen receptor signalling.
BibTeX:
@article{Bissegger2014,
  author = {Bissegger, Sonja and Martyniuk, Christopher J and Langlois, Valérie},
  title = {Transcriptomic profiling in Silurana tropicalis testes exposed to finasteride},
  journal = {General and Comparative Endocrinology},
  year = {2014},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S0016648014000446},
  doi = {http://doi.org/10.1016/j.ygcen.2014.01.018}
}
Borotkanics, R. and Lehmann, H. Network motifs that recur across species, including gene regulatory and protein-protein interaction networks 2014 Archives of toxicology  article DOI URL 
Abstract: Cellular molecules interact in complex ways, giving rise to a cell's functional outcomes. Conscientious efforts have been made in recent years to better characterize these patterns of interactions. It has been learned that many of these interactions can be represented abstractly as a network and within a network there in many instances are network motifs. Network motifs are subgraphs that are statistically overrepresented within networks. To date, specific network motifs have been experimentally identified across various species and also within specific, intracellular networks; however, motifs that recur across species and major network types have not been systematically characterized. We reason that recurring network motifs could potentially have important implications and applications for toxicology and, in particular, toxicity testing. Therefore, the goal of this study was to determine the set of intracellular, network motifs found to recur across species of both gene regulatory and protein-protein interaction networks. We report the recurrence of 13 intracellular, network motifs across species. Ten recurring motifs were found across both protein-protein interaction networks and gene regulatory networks. The significant pair motif was found to recur only in gene regulatory networks. The diamond and one-way cycle reversible step motifs were found to recur only in protein-protein interaction networks. This study is the first formal review of recurring, intracellular network motifs across species. Within toxicology, combining our understanding of recurring motifs with mechanism and mode of action knowledge could result in more robust and efficient toxicity testing models. We are sure that our results will support research in applying network motifs to toxicity testing.
BibTeX:
@article{Borotkanics2014,
  author = {Borotkanics, Robert and Lehmann, Harold},
  title = {Network motifs that recur across species, including gene regulatory and protein-protein interaction networks},
  journal = {Archives of toxicology},
  year = {2014},
  url = {http://www.ncbi.nlm.nih.gov/pubmed/24847787},
  doi = {http://doi.org/10.1007/s00204-014-1274-y}
}
Brockmeier, E.K., Jayasinghe, B.S., Pine, W.E., Wilkinson, K.A. and Denslow, N.D. Exposure to Paper Mill Effluent at a Site in North Central Florida Elicits Molecular-Level Changes in Gene Expression Indicative of Progesterone and Androgen Exposure 2014 PLoS ONE
Vol. 9(9), pp. e106644 
article DOI URL 
Abstract: Endocrine disrupting compounds (EDCs) are chemicals that negatively impact endocrine system function, with effluent from paper mills one example of this class of chemicals. In Florida, female Eastern mosquitofish (Gambusia holbrooki) have been observed with male secondary sexual characteristics at three paper mill-impacted sites, indicative of EDC exposure, and are still found at one site on the Fenholloway River. The potential impacts that paper mill effluent exposure has on the G. holbrooki endocrine system and the stream ecosystem are unknown. The objective of this study was to use gene expression analysis to determine if exposure to an androgen receptor agonist was occurring and to couple this analysis with in vitro assays to evaluate the presence of androgen and progesterone receptor active chemicals in the Fenholloway River. Focused gene expression analyses of masculinized G. holbrooki from downstream of the Fenholloway River paper mill were indicative of androgen exposure, while genes related to reproduction indicated potential progesterone exposure. Hepatic microarray analysis revealed an increase in the expression of metabolic genes in Fenholloway River fish, with similarities in genes and biological processes compared to G. holbrooki exposed to androgens. Water samples collected downstream of the paper mill and at a reference site indicated that progesterone and androgen receptor active chemicals were present at both sites, which corroborates previous chemical analyses. Results indicate that G. holbrooki downstream of the Fenholloway River paper mill are impacted by a mixture of both androgens and progesterones. This research provides data on the mechanisms of how paper mill effluents in Florida are acting as endocrine disruptors.
BibTeX:
@article{Brockmeier2014,
  author = {Brockmeier, Erica K and Jayasinghe, B Sumith and Pine, William E and Wilkinson, Krystan A and Denslow, Nancy D},
  title = {Exposure to Paper Mill Effluent at a Site in North Central Florida Elicits Molecular-Level Changes in Gene Expression Indicative of Progesterone and Androgen Exposure},
  journal = {PLoS ONE},
  year = {2014},
  volume = {9},
  number = {9},
  pages = {e106644},
  url = {http://dx.doi.org/10.1371/journal.pone.0106644},
  doi = {http://doi.org/10.1371/journal.pone.0106644}
}
Burch, T., Yu, L., Nyalwidhe, J., Horcajadas, J.A., Bocca, S., Swanson, R.J. and Oehninger, S. Characterization of secreted proteins of 2-cell mouse embryos cultured in vitro to the blastocyst stage with and without protein supplementation 2014 Journal of Assisted Reproduction and Genetics  article DOI URL 
BibTeX:
@article{Burch2014,
  author = {Burch, Tanya and Yu, Liang and Nyalwidhe, Julius and Horcajadas, Jose A and Bocca, Silvina and Swanson, R James and Oehninger, Sergio},
  title = {Characterization of secreted proteins of 2-cell mouse embryos cultured in vitro to the blastocyst stage with and without protein supplementation},
  journal = {Journal of Assisted Reproduction and Genetics},
  year = {2014},
  url = {http://link.springer.com/10.1007/s10815-014-0207-2},
  doi = {http://doi.org/10.1007/s10815-014-0207-2}
}
Butz, H., Szabó, P.M., Nofech-Mozes, R., Rotondo, F., Kovacs, K., Mirham, L., Girgis, H., Boles, D., Patocs, A. and Yousef, G.M. Integrative Bioinformatics Analysis Reveals New Prognostic Biomarkers of Clear Cell Renal Cell Carcinoma 2014 Clinical Chemistry, pp. clinchem.2014.225854  article DOI URL 
Abstract: background: The outcome of clear cell renal cell carcinoma (ccRCC) is still unpredictable. Even with new targeted therapies, the average progression-free survival is dismal. Markers for early detection and progression could improve disease outcome. Methods: To identify efficient and hitherto unrecognized pathogenic factors of the disease, we performed a uniquely comprehensive pathway analysis and built a gene interaction network based on large publicly available data sets assembled from 28 publications, comprising a 3-prong approach with high-throughput mRNA, microRNA, and protein expression profiles of 593 ccRCC and 389 normal kidney samples. We validated our results on 2 different data sets of 882 ccRCC and 152 normal tissues. Functional analyses were done by proliferation, migration, and invasion assays following siRNA (small interfering RNA) knockdown. Results: After integration of multilevel data, we identified aryl-hydrocarbon receptor (AHR), grainyhead-like-2 (GRHL2), and KIAA0101 as new pathogenic factors. GRHL2 expression was associated with higher chances for disease relapse and retained prognostic utility after controlling for grade and stage [hazard ratio (HR), 3.47, P = 0.012]. Patients with KIAA0101-positive expression suffered worse disease-free survival (HR, 3.64, P textless 0.001), and in multivariate analysis KIAA0101 retained its independent prognostic significance. Survival analysis showed that GRHL2- and KIAA0101-positive patients had significantly lower disease-free survival (P = 0.002 and P textless 0.001). We also found that KIAA0101 silencing decreased kidney cancer cell migration and invasion in vitro. Conclusions: Using an integrative system biology approach, we identified 3 novel factors not previously linked to kidney cancer (AHR, GRHL2, and KIAA0101) that are involved in ccRCC pathogenesis and are potential biomarkers.
BibTeX:
@article{Butz2014,
  author = {Butz, Henriett and Szabó, Peter M and Nofech-Mozes, Roy and Rotondo, Fabio and Kovacs, Kalman and Mirham, Lorna and Girgis, Hala and Boles, Dina and Patocs, Attila and Yousef, George M},
  title = {Integrative Bioinformatics Analysis Reveals New Prognostic Biomarkers of Clear Cell Renal Cell Carcinoma},
  journal = {Clinical Chemistry},
  year = {2014},
  pages = {clinchem.2014.225854},
  url = {http://www.clinchem.org/content/early/2014/08/14/clinchem.2014.225854 http://www.ncbi.nlm.nih.gov/pubmed/25139457},
  doi = {http://doi.org/10.1373/clinchem.2014.225854}
}
Buzdin, A.A., Zhavoronkov, A.A., Korzinkin, M.B., Roumiantsev, S.A., Aliper, A.M., Venkova., L., Smirnov, P.Y., Borisov, N.N.M., Venkova, L.S., Smirnov, P.Y. and Borisov, N.N.M. The OncoFinder algorithm for minimizing the errors introduced by the high-throughput methods of transcriptome analysis 2014 Frontiers in Molecular Biosciences
Vol. 1 
article DOI URL 
Abstract: The diversity of the installed sequencing and microarray equipment make it increasingly difficult to compare and analyze the gene expression datasets obtained using the different methods. Many applications requiring high-quality and low error rates can not make use of available data using traditional analytical approaches. Recently, we proposed a new concept of signalome-wide analysis of functional changes in the intracellular pathways termed OncoFinder, a bioinformatic tool for quantitative estimation of the signaling pathway activation (SPA). We also developed methods to compare the gene expression data obtained using multiple platforms and minimizing the error rates by mapping the gene expression data onto the known and custom signaling pathways. This technique for the first time makes it possible to analyze the functional features of intracellular regulation on a mathematical basis. In this study we show that the OncoFinder method significantly reduces the errors introduced by transcriptome-wide experimental techniques. We compared the gene expression data for the same biological samples obtained by both the next generation sequencing (NGS) and microarray methods. For these different techniques we demonstrate that there is virtually no correlation between the gene expression values for all datasets analyzed (R2 textless 0.1). In contrast, when the OncoFinder algorithm is applied to the data we observed clear-cut correlations between the NGS and microarray gene expression datasets. The signaling pathway activation profiles obtained using NGS and microarray techniques were almost identical for the same biological samples allowing for the platform-agnostic analytical applications. We conclude that this feature of the OncoFinder enables to characterize the functional states of the transcriptomes and interactomes more accurately as before, which makes OncoFinder a method of choice for many applications including genetics, physiology, biomedicine and molecular diagnostics.
BibTeX:
@article{Buzdin2014,
  author = {Buzdin, Anton A. and Zhavoronkov, Alex A. and Korzinkin, Mikhail B. and Roumiantsev, Sergey A. and Aliper, Alexander M. and Venkova., L and Smirnov, Philip Y. and Borisov, Nicolay Nikolay M. and Venkova, Larisa S. and Smirnov, Philip Y. and Borisov, Nicolay Nikolay M.},
  title = {The OncoFinder algorithm for minimizing the errors introduced by the high-throughput methods of transcriptome analysis},
  journal = {Frontiers in Molecular Biosciences},
  year = {2014},
  volume = {1},
  url = {http://journal.frontiersin.org/article/10.3389/fmolb.2014.00008/abstract http://journal.frontiersin.org/Journal/105110/abstract},
  doi = {http://doi.org/10.3389/fmolb.2014.00008}
}
Buzdin, A.A., Zhavoronkov, A.A., Korzinkin, M.B., Venkova, L.S., Zenin, A.A., Smirnov, P.Y. and Borisov, N.M. Oncofinder, a new method for the analysis of intracellular signaling pathway activation using transcriptomic data 2014 Frontiers in Genetics
Vol. 5 
article DOI URL 
BibTeX:
@article{Buzdin2014b,
  author = {Buzdin, Anton A. and Zhavoronkov, Alex A. and Korzinkin, Mikhail B. and Venkova, Larisa S. and Zenin, Alexander A. and Smirnov, Philip Yu. and Borisov, Nikolay M.},
  title = {Oncofinder, a new method for the analysis of intracellular signaling pathway activation using transcriptomic data},
  journal = {Frontiers in Genetics},
  year = {2014},
  volume = {5},
  url = {http://journal.frontiersin.org/article/10.3389/fgene.2014.00055/abstract},
  doi = {http://doi.org/10.3389/fgene.2014.00055}
}
Cadinu, D., Hooda, J., Alam, M.M., Balamurugan, P., Henke, R.M. and Zhang, L. Comparative proteomic analysis reveals characteristic molecular changes accompanying the transformation of nonmalignant to cancer lung cells 2014 EuPA Open Proteomics  article DOI URL 
Abstract: To identify changes in proteins accompanying transformation of normal lung epithelial cells to cancer cells, we performed a comparative proteomic study using two cell lines representing matching normal and cancer cells. Strikingly, a good number of detected actin cytoskeletal proteins were preferentially downregulated in cancer cells, while similar numbers of proteins in other organelles were up or downregulated. We also found that the formation of stress fibers and focal adhesions were substantially decreased in cancer cells. Protein network analysis showed that the altered proteins are highly connected. These results provide novel insights into the molecular mechanism promoting lung cancer progression.
BibTeX:
@article{Cadinu2014,
  author = {Cadinu, Daniela and Hooda, Jagmohan and Alam, Md Maksudul and Balamurugan, Parimaladevi and Henke, Robert M and Zhang, Li},
  title = {Comparative proteomic analysis reveals characteristic molecular changes accompanying the transformation of nonmalignant to cancer lung cells},
  journal = {EuPA Open Proteomics},
  year = {2014},
  url = {http://linkinghub.elsevier.com/retrieve/pii/S2212968514000026},
  doi = {http://doi.org/10.1016/j.euprot.2014.01.001}
}
Candelaria, N.R., Addanki, S., Zheng, J., Nguyen-Vu, T., Karaboga, H., Dey, P., Gabbi, C., Vedin, L.-L., Liu, K., Wu, W., Jonsson, P.K., Lin, J.Z., Su, F., Bollu, L.R., Hodges, S.E., McElhany, A.L., Issazadeh, M.A., Fisher, W.E., Ittmann, M.M., Steffensen, K.R., Gustafsson, J.-Å. and Lin, C.-Y. Antiproliferative Effects and Mechanisms of Liver X Receptor Ligands in Pancreatic Ductal Adenocarcinoma Cells 2014 PLoS ONE
Vol. 9(9), pp. e106289 
article DOI URL 
Abstract: Pancreatic ductal adenocarcinoma (PDAC) is difficult to detect early and is often resistant to standard chemotherapeutic options, contributing to extremely poor disease outcomes. Members of the nuclear receptor superfamily carry out essential biological functions such as hormone signaling and are successfully targeted in the treatment of endocrine-related malignancies. Liver X receptors (LXRs) are nuclear receptors that regulate cholesterol homeostasis, lipid metabolism, and inflammation, and LXR agonists have been developed to regulate LXR function in these processes. Intriguingly, these compounds also exhibit antiproliferative activity in diverse types of cancer cells. In this study, LXR agonist treatments disrupted proliferation, cell-cycle progression, and colony-formation of PDAC cells. At the molecular level, treatments downregulated expression of proteins involved in cell cycle progression and growth factor signaling. Microarray experiments further revealed changes in expression profiles of multiple gene networks involved in biological processes and pathways essential for cell growth and proliferation following LXR activation. These results establish the antiproliferative effects of LXR agonists and potential mechanisms of action in PDAC cells and provide evidence for their potential application in the prevention and treatment of PDAC.
BibTeX:
@article{Candelaria2014,
  author = {Candelaria, Nicholes R and Addanki, Sridevi and Zheng, Jine and Nguyen-Vu, Trang and Karaboga, Husna and Dey, Prasenjit and Gabbi, Chiara and Vedin, Lise-Lotte and Liu, Ka and Wu, Wanfu and Jonsson, Philip K and Lin, Jean Z and Su, Fei and Bollu, Lakshmi Reddy and Hodges, Sally E and McElhany, Amy L and Issazadeh, Mehdi A and Fisher, William E and Ittmann, Michael M and Steffensen, Knut R and Gustafsson, Jan-Åke and Lin, Chin-Yo},
  title = {Antiproliferative Effects and Mechanisms of Liver X Rec