دورية أكاديمية
Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization.
| العنوان: | Mechanisms of ER Stress-Mediated Mitochondrial Membrane Permeabilization. |
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| المؤلفون: | Gupta, Sanjeev, Cuffe, Lorraine, Szegezdi, Eva, Logue, Susan E, Neary, Catherine, Healy, Sandra, Samali, Afshin |
| المصدر: | Rowan-Virtua School of Osteopathic Medicine Faculty Scholarship |
| بيانات النشر: | Rowan Digital Works |
| سنة النشر: | 2010 |
| المجموعة: | Rowan University: Rowan Digital Works |
| مصطلحات موضوعية: | apoptosis, mitochondrial permeability, caspases, mitochondrial outer membrane permeabilization, Cell and Developmental Biology, Cell Biology, Life Sciences, Medicine and Health Sciences |
| الوصف: | During apoptosis, the process of mitochondrial outer membrane permeabilization (MOMP) represents a point-of-no-return as it commits the cell to death. Here we have assessed the role of caspases, Bcl-2 family members and the mitochondrial permeability transition pore on ER stress-induced MOMP and subsequent cell death. Induction of ER stress leads to upregulation of several genes such as Grp78, Edem1, Erp72, Atf4, Wars, Herp, p58ipk, and ERdj4 and leads to caspase activation, release of mitochondrial intermembrane proteins and dissipation of mitochondrial transmembrane potential (DeltaPsim). Mouse embryonic fibroblasts (MEFs) from caspase-9, -2 and, -3 knock-out mice were resistant to ER stress-induced apoptosis which correlated with decreased processing of pro-caspase-3 and -9. Furthermore, pretreatment of cells with caspase inhibitors (Boc-D.fmk and DEVD.fmk) attenuated ER stress-induced loss of DeltaPsim. However, only deficiency of caspase-9 and -2 could prevent ER stress-mediated loss of DeltaPsim. Bcl-2 overexpression or pretreatment of cells with the cell permeable BH4 domain (BH4-Tat) or the mitochondrial permeability transition pore inhibitors, bongkrekic acid or cyclosporine A, attenuated the ER stress-induced loss of DeltaPsim. These data suggest a role for caspase-9 and -2, Bcl-2 family members and the mitochondrial permeability transition pore in loss of mitochondrial membrane potential during ER stress-induced apoptosis. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | unknown |
| العلاقة: | https://rdw.rowan.edu/som_facpub/162Test; https://rdw.rowan.edu/context/som_facpub/article/1161/viewcontent/Neary___Mechanisms_of_Stress.pdfTest |
| DOI: | 10.1155/2010/170215 |
| الإتاحة: | https://doi.org/10.1155/2010/170215Test https://rdw.rowan.edu/som_facpub/162Test https://rdw.rowan.edu/context/som_facpub/article/1161/viewcontent/Neary___Mechanisms_of_Stress.pdfTest |
| حقوق: | http://creativecommons.org/licenses/by/4.0Test/ |
| رقم الانضمام: | edsbas.8E379E45 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1155/2010/170215 |
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