Dergi makalesi Açık Erişim
Tang, Zhi; Baykal, Ahmet Tank; Gao, Hui; Quezada, Hernan Concha; Zhang, Haiyan; Bereczki, Erika; Serhatli, Muge; Baykal, Betul; Acioglu, Cigdem; Wang, Shan; Ioja, Eniko; Ji, Xinying; Zhang, Yan; Guan, Zhizhong; Winblad, Bengt; Pei, Jin-Jing
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> <dc:creator>Tang, Zhi</dc:creator> <dc:creator>Baykal, Ahmet Tank</dc:creator> <dc:creator>Gao, Hui</dc:creator> <dc:creator>Quezada, Hernan Concha</dc:creator> <dc:creator>Zhang, Haiyan</dc:creator> <dc:creator>Bereczki, Erika</dc:creator> <dc:creator>Serhatli, Muge</dc:creator> <dc:creator>Baykal, Betul</dc:creator> <dc:creator>Acioglu, Cigdem</dc:creator> <dc:creator>Wang, Shan</dc:creator> <dc:creator>Ioja, Eniko</dc:creator> <dc:creator>Ji, Xinying</dc:creator> <dc:creator>Zhang, Yan</dc:creator> <dc:creator>Guan, Zhizhong</dc:creator> <dc:creator>Winblad, Bengt</dc:creator> <dc:creator>Pei, Jin-Jing</dc:creator> <dc:date>2014-01-01</dc:date> <dc:description>mTor plays a central role in controlling protein homeostasis and cell survival. Recently, we have demonstrated that perturbations of mTor signaling are implicated in Alzheimer's disease (AD) and that mTor complex 1 (mTorC1) is involved in the formation of toxic phospho-tau. Therefore, we employed mass-spectrometry-based proteomics to identify specific protein expression changes in relation with cell survival in human neuroblastoma SH-SYSY cells expressing genetically modified mTor. Cell death in SH-SYSY cells was induced by moderate serum deprivation. Using flow cytometry we observed that up-regulated mTor complex 2 (mTorC2) increases the number of viable cells. By using a combination approach of proteomic and enrichment analysis we have identified several proteins (Thioredoxin-dependent peroxide reductase, Peroxiredoxin-5, Cofilin 1 (non-muscle), Annexin A5, Mortalin, and 14-3-3 protein zeta/delta) involved in mitochondrial integrity, apoptotosis, and pro-survival functions (caspase inhibitor activity and anti-apoptosis) that were significantly altered by mTor activity modulation. The major findings of this study are the implication of mTorC2 but not mTorC1 in cell viability modulation by activating the pro-survival machinery. Taken together, these results suggest that up-regulated mTorC2 might be playing an important role in promoting cell survival by suppressing the mitochondria-caspase-apoptotic pathway in vitro.</dc:description> <dc:identifier>https://aperta.ulakbim.gov.trrecord/99259</dc:identifier> <dc:identifier>oai:zenodo.org:99259</dc:identifier> <dc:rights>info:eu-repo/semantics/openAccess</dc:rights> <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights> <dc:source>JOURNAL OF PROTEOME RESEARCH 13(5) 2433-2444</dc:source> <dc:title>mTor Is a Signaling Hub in Cell Survival: A Mass-Spectrometry-Based Proteomics Investigation</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> <dc:type>publication-article</dc:type> </oai_dc:dc>
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