帕金
品脱1
MFN2型
粒体自噬
线粒体
泛素连接酶
细胞生物学
生物
张力素
线粒体融合
泛素
线粒体DNA
生物化学
自噬
PTEN公司
内科学
信号转导
医学
PI3K/AKT/mTOR通路
帕金森病
细胞凋亡
疾病
基因
作者
Yun Chen,Gerald W. Dorn
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2013-04-26
卷期号:340 (6131): 471-475
被引量:1125
标识
DOI:10.1126/science.1231031
摘要
Where Parkin Parks Damaged mitochondria are removed from cells in a process known as mitophagy. Failure of this quality-control mechanism contributes to Parkinson's disease. When damaged mitochondria lose membrane depolarization, the protein kinase, PINK1, accumulates on the mitochondrial surface, recruits Parkin, and promotes mitophagy. Chen and Dorn (p. 471 ) describe another component of this process, mitofusin 2, which appears to function as the receptor for Parkin on the surface of damaged mitochondria.
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