Endoplasmic reticulum stress-mediated induction of SESTRIN 2 potentiates cell survival
| العنوان: | Endoplasmic reticulum stress-mediated induction of SESTRIN 2 potentiates cell survival |
|---|---|
| المؤلفون: | Patricia Cleary, John B. Patterson, Afshin Samali, Susan E. Logue, Svetlana Saveljeva, Karolina Pakos-Zebrucka, Katarzyna Mnich, Abiodun Ayo |
| المصدر: | Oncotarget |
| بيانات النشر: | Impact Journals, LLC, 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | X-Box Binding Protein 1, 0301 basic medicine, autophagy, Programmed cell death, XBP1, Cell Survival, UPR, mTORC1, carcinoma, Mechanistic Target of Rapamycin Complex 1, Protein Serine-Threonine Kinases, eIF-2 Kinase, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, death, Cell Line, Tumor, Endoribonucleases, Research Paper: Autophagy and Cell Death, Humans, transcriptional regulation, Chemistry, Endoplasmic reticulum, ATF4, Autophagy, apoptosis, Nuclear Proteins, unfolded protein response, Endoplasmic Reticulum Stress, HCT116 Cells, er-stress, Up-Regulation, Cell biology, perk, cell death, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, MCF-7 Cells, Unfolded protein response, SESTRIN 2, biological phenomena, cell phenomena, and immunity, ER stress |
| الوصف: | Upregulation of SESTRIN 2 (SESN2) has been reported in response to diverse cellular stresses. In this study we demonstrate SESTRIN 2 induction following endoplasmic reticulum (ER) stress. ER stress-induced increases in SESTRIN 2 expression were dependent on both PERK and IRE1/XBP1 arms of the unfolded protein response (UPR). SESTRIN 2 induction, post ER stress, was responsible for mTORC1 inactivation and contributed to autophagy induction. Conversely, knockdown of SESTRIN 2 prolonged mTORC1 signaling, repressed autophagy and increased ER stress-induced cell death. Unexpectedly, the increase in ER stress-induced cell death was not linked to autophagy inhibition. Analysis of UPR pathways identified prolonged eIF2 alpha, ATF4 and CHOP signaling in SESTRIN 2 knockdown cells following ER stress. SESTRIN 2 regulation enables UPR derived signals to indirectly control mTORC1 activity shutting down protein translation thus preventing further exacerbation of ER stress. |
| تدمد: | 1949-2553 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::48e2f717b77af4be6b4fea98cff418caTest https://doi.org/10.18632/oncotarget.7601Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....48e2f717b77af4be6b4fea98cff418ca |
| قاعدة البيانات: | OpenAIRE |
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