mTor Is a signaling hub in cell survival: A mass-spectrometry-based proteomics investigation
Erişim
info:eu-repo/semantics/closedAccessTarih
2014Yazar
Tang, ZhiBaykal, Ahmet Tarık
Gao, Hui
Quezada, Hernan Concha
Zhang, Haiyan
Bereczki, Erika
Serhatlı, Müge
Baykal, Betül
Acıoğlu, Çiğdem
Wang, Shan
Ioja, Eniko
Ji, Xinying
Zhang, Yan
Guan, Zhizhong
Winblad, Bengt
Pei, Jin-Jing
Üst veri
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Tang, Z., Baykal, A. T., Gao, H., Quezada, H. C., Zhang, H., Bereczki, E. ... Pei, J.-J. (2014). mTor Is a signaling hub in cell survival: A mass-spectrometry-based proteomics investigation. Journal of Proteome Research, 13(5), 2433-2444. https://dx.doi.org/10.1021/pr500192gÖzet
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.
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Journal of Proteome ResearchCilt
13Sayı
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