摘要
整合应激反应(integrated stress response,ISR)指细胞在氧化应激、氨基酸剥夺和内质网应激等情况下,通过真核细胞起始因子2(eukaryotic translation initiator factor 2α,eIF2α)所介导的细胞适应反应。近年来研究发现,eIF2α的上游激酶——蛋白激酶R样内质网激酶(protein ki-nase R-like ER kinase,PERK)是整合应激反应的关键分子,并调控另外两条内质网应激信号途径——需肌醇酶-1(inositol-requiring enzyme-1,IRE1)和活化转录因子6(activating transcriptionfactor 6,ATF6)途径,调控蛋白质合成、折叠、细胞自噬与凋亡,并启动与整合细胞核、线粒体和高尔基体等亚细胞器反应,决定应激细胞的转归。本文综述内质网整合应激反应的诱发因素、细胞信号途径及其生理和病理生理作用的研究进展。
Integrated stress response（ISR） is a high conserved cell adaptive response,which is induced by oxidative stress,deprivation of acid aminos,and endoplasmic reticulum（ER） stress through eukaryotic translation initiator factor 2α（eIF2α） pathway.Recently,it is reported that protein kinase R-like ER kinase（PERK）,the upstream of eIF2α is the key molecule in ISR.PERK regulates protein synthesis,folding,autophagy and apoptosis through cross-talking with inositol-requiring enzyme-1（IRE1） and activating transcription factor 6（ATF6）,another two signaling pathways in ER stress.We reviewed the factors induced ISR and its signaling pathways,summarized the physiological and pathophysiological role of endoplasmic reticulum-mediated integrated stress response.
出处
《生理科学进展》
CAS
CSCD
北大核心
2013年第4期241-246,共6页
Progress in Physiological Sciences
