粒体自噬
帕金
品脱1
生物
线粒体
自噬
细胞生物学
泛素连接酶
泛素
帕金森病
遗传学
基因
疾病
医学
病理
细胞凋亡
作者
Thanh Ngoc Nguyen,Benjamin Scott Padman,Michael Lazarou
标识
DOI:10.1016/j.tcb.2016.05.008
摘要
Functional mitochondria are critically important for the maintenance of cellular integrity and survival. Mitochondrial dysfunction is a major contributor to neurodegenerative diseases including Parkinson's disease (PD). Two gene products mutated in familial Parkinsonism, PINK1 and Parkin, function together to degrade damaged mitochondria through a selective form of autophagy termed mitophagy. PINK1 accumulates on the surface of dysfunctional mitochondria where it simultaneously recruits and activates Parkin's E3 ubiquitin ligase activity. This forms the basis of multiple signaling events that culminate in engulfment of damaged mitochondria within autophagosomes and degradation by lysosomes. This review discusses the molecular signals of PINK1/Parkin mitophagy and the ubiquitin code that drives not only Parkin recruitment and activation by PINK1 but also the downstream signaling events of mitophagy.
科研通智能强力驱动
Strongly Powered by AbleSci AI