Endoplasmic reticulum stress responses

被引:716
作者
Schroeder, M. [1 ]
机构
[1] Univ Durham, Sch Biol & Biomed Sci, Durham DH1 3LE, England
基金
英国惠康基金; 英国生物技术与生命科学研究理事会;
关键词
apoptosis; Ca2+ store; cholesterol; endoplasmic reticulum; membrane fluidity; molecular chaperone; protein folding; unfolded protein response;
D O I
10.1007/s00018-007-7383-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
In homeostasis, cellular processes are in a dynamic equilibrium. Perturbation of homeostasis causes stress. In this review I summarize how perturbation of three major functions of the endoplasmic reticulum (ER) in eukaryotic cells-protein folding, lipid and sterol biosynthesis, and storing intracellular Ca2+ - causes ER stress and activates signaling pathways collectively termed the unfolded protein response (UPR). I discuss how the UPR reestablishes homeostasis, and summarize our current understanding of how the transition from protective to apoptotic UPR signaling is controlled, and how the UPR induces inflammatory signaling.
引用
收藏
页码:862 / 894
页数:33
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