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内质网是细胞内蛋白质合成、折叠的重要场所。低氧、葡萄糖饥饿、氧化和糖基化作用紊乱等刺激下,未折叠或折叠错误的蛋白质会积聚于内质网内,导致内质网应激反应。上调内质网伴侣蛋白表达、减轻内质网负担等机制可以恢复细胞内环境的稳态,但严重或持久的内质网应激反应通过caspase-12、JNK及CHOP等机制启动细胞凋亡程序。本文综述了细胞保护反应中内质网未折叠蛋白反应及其诱导凋亡信号的研究进展。
Endoplasmic reticulum is an important site for protein synthesis and folding in cells. Hypoxia, glucose starvation, oxidative and glycosylation disorders and other stimuli, unfolded or folded wrong protein will accumulate in the endoplasmic reticulum, leading to endoplasmic reticulum stress response. Upregulation of endoplasmic reticulum chaperone protein expression and the mechanism of reducing endoplasmic reticulum burden can restore the homeostasis of the cellular environment, but severe or long-lasting endoplasmic reticulum stress response initiates the apoptosis program through mechanisms such as caspase-12, JNK and CHOP . This review summarizes the advances in the cellular responses to the unfolded protein response of endoplasmic reticulum and its induction of apoptosis.