内质网相关蛋白降解
高尔基体
内质网
甘露糖苷酶
细胞生物学
生物
糖蛋白
蛋白酶体
甘露糖
分子生物学
生物化学
未折叠蛋白反应
作者
Nobuko Hosokawa,Zhipeng You,Lucie Tremblay,Kazuhiro Nagata,Annetté Herscovics
标识
DOI:10.1016/j.bbrc.2007.08.057
摘要
Terminally misfolded or unassembled proteins are degraded by the cytoplasmic ubiquitin-proteasome pathway in a process known as ERAD (endoplasmic reticulum-associated protein degradation). Overexpression of ER alpha1,2-mannosidase I and EDEMs target misfolded glycoproteins for ERAD, most likely due to trimming of N-glycans. Here we demonstrate that overexpression of Golgi alpha1,2-mannosidase IA, IB, and IC also accelerates ERAD of terminally misfolded human alpha1-antitrypsin variant null (Hong Kong) (NHK), and mannose trimming from the N-glycans on NHK in 293 cells. Although transfected NHK is primarily localized in the ER, some NHK also co-localizes with Golgi markers, suggesting that mannose trimming by Golgi alpha1,2-mannosidases can also contribute to NHK degradation.
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