| 内质网应激介导的细胞凋亡 |
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| 引用本文： | 关丽英,许彩民,潘华珍.内质网应激介导的细胞凋亡[J].生物化学与生物物理进展,2007,34(11):1136-1141. |
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| 作者姓名： | 关丽英 许彩民 潘华珍 |
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| 作者单位： | 中国医学科学院,中国协和医科大学,基础医学研究所,生物化学与分子生物学国家重点实验室,北京,100005 |
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| 摘 要： | 内质网是细胞内重要的细胞器,内质网功能的损伤引起ER应激(ERS).内质网通过激活未折叠蛋白质反应(UPR)以保护由内质网应激所引起的细胞损伤,恢复细胞功能,包括暂停早期蛋白质合成、内质网分子伴侣和折叠酶的转录激活、内质网相关性降解(ERAD)的诱导.长期过强的内质网应激诱导内质网相关性细胞凋亡,清除受损细胞,包括内质网应激诱导CHOP/GADD153表达、JNK的激活以及caspase-12蛋白水解酶的活化等一系列生物学效应.
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| 关 键 词： | 内质网应激 未折叠蛋白响应 细胞凋亡 |
| 收稿时间： | 2007/3/15 0:00:00 |
| 修稿时间： | 2007-03-15 |
Endoplasmic Reticulam Stress-induced Apoptosis |
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| GUAN Li-Ying,XU Cai-Min and PAN Hua-Zhen.Endoplasmic Reticulam Stress-induced Apoptosis[J].Progress In Biochemistry and Biophysics,2007,34(11):1136-1141. |
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| Authors: | GUAN Li-Ying XU Cai-Min and PAN Hua-Zhen |
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| Institution: | National Laboratory of Medical Molecular Biology, Basic Insititute of Medical Science,The Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China;National Laboratory of Medical Molecular Biology, Basic Insititute of Medical Science,The Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China;National Laboratory of Medical Molecular Biology, Basic Insititute of Medical Science,The Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China |
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| Abstract: | Endoplasmic reticulam is an imprtant organelle in cells. Normal functions of the ER could be impaired and that causes endoplasmic reticulam stress (ERS). ERS activates unfolded protein response (UPR), including immediate stoppage of new protein synthesis, up-regulation of ER chaperones and folding enzymes, and inducement of ER-associated degradation as a self-protective mechanism and induces rescue or adaptive response. If stress is prolonged and functions of the ER are severely impaired, to protect the organism by eliminating the damaged cells, apoptotic signals are generated through several mechanisms including: induction of C/EBP homologous protein CHOP, IRE-1-mediated activation of ASK1/JNK, cleavage and activation of procaspase-12 and Bcl-2-regulated Ca2 release from the ER. |
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| Keywords: | endoplasmic reticulum stress unfolded protein response cell apoptosis |
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