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蛋白质正确折叠需要一套复杂的内质网蛋白复合体的调节机制。在缺氧、氧化应激、异常糖基化反应以及钙离子稳态失衡等情况下,非折叠蛋白质增多。当超出内质网的处理能力时,可导致内质网应激(ERS)]。细胞自身通过改变其转录和翻译过程,减少蛋白质的合成,降低进入内质网内蛋白质的数量,同时上调内质网中分子伴侣和蛋白折叠的表达,增强内质网的蛋白折叠功能;还可以通过上调内质网蛋白降解通路上相关基因的表达,加速非折叠蛋白的降解过
Correct folding of proteins requires a complex set of regulatory mechanisms of the endoplasmic reticulum protein complex. In hypoxia, oxidative stress, abnormal glycosylation and calcium homeostasis imbalances, non-folded protein increased. Endoplasmic reticulum stress (ERS) can result when it exceeds the processing capacity of the endoplasmic reticulum). By changing its transcriptional and translational processes, the cell itself reduces protein synthesis, reduces the amount of protein that enters the endoplasmic reticulum, increases the expression of molecular chaperones and protein folds in the endoplasmic reticulum, and enhances the protein folding function of the endoplasmic reticulum; Accelerate the degradation of unfolded proteins by up-regulating the expression of related genes on the endoplasmic reticulum protein degradation pathway