粒体自噬
生物
细胞生物学
帕金
自噬
阻抑素
线粒体
内膜转移酶
神经退行性变
线粒体分裂
线粒体融合
线粒体内膜
品脱1
线粒体膜转运蛋白
外膜转位酶
膜间隙
线粒体载体
电压依赖性阴离子通道
生物化学
细胞凋亡
病理
医学
疾病
帕金森病
作者
Yongjie Wei,Wei Chung Chiang,Rhea Sumpter,Prashant Mishra,Beth Levine
出处
期刊:Cell
[Elsevier]
日期:2017-01-12
卷期号:168 (1-2): 224-238.e10
被引量:430
标识
DOI:10.1016/j.cell.2016.11.042
摘要
The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identify the inner mitochondrial membrane protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria for autophagic degradation. PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans. Our findings pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 that may underlie its roles in physiology, aging, and disease.
科研通智能强力驱动
Strongly Powered by AbleSci AI