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.
Endoplasmic reticulam is an imprtant organdie 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-l-mediated activation of ASK1/JNK, cleavage and activation of procaspase-12 and Bcl-2-regulated Ca^2＋ release from the ER.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2007年第11期1136-1141,共6页
Progress In Biochemistry and Biophysics
基金
国家自然科学基金资助项目(30370348和30770491)~~
关键词
内质网应激
未折叠蛋白响应
细胞凋亡
endoplasmic reticulum stress, unfolded protein response, cell apoptosis
