钙连接素
内质网相关蛋白降解
内质网
蛋白质折叠
糖蛋白
细胞生物学
折叠(DSP实现)
化学
未折叠蛋白反应
生物
生物化学
钙网蛋白
电气工程
工程类
作者
Maurizio Molinari,Verena Calanca,Carmela Galli,Paola Lucca,Paolo Paganetti
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2003-02-27
卷期号:299 (5611): 1397-1400
被引量:463
标识
DOI:10.1126/science.1079474
摘要
The mechanisms that determine how folding attempts are interrupted to target folding-incompetent proteins for endoplasmic reticulum–associated degradation (ERAD) are poorly defined. Here the α-mannosidase I–like protein EDEM was shown to extract misfolded glycoproteins, but not glycoproteins undergoing productive folding, from the calnexin cycle. EDEM overexpression resulted in faster release of folding-incompetent proteins from the calnexin cycle and earlier onset of degradation, whereas EDEM down-regulation prolonged folding attempts and delayed ERAD. Up-regulation of EDEM during ER stress may promote cell recovery by clearing the calnexin cycle and by accelerating ERAD of terminally misfolded polypeptides.
科研通智能强力驱动
Strongly Powered by AbleSci AI