粒体自噬
帕金
品脱1
泛素连接酶
泛素
线粒体
细胞生物学
生物
脱氮酶
遗传学
帕金森病
自噬
医学
疾病
基因
细胞凋亡
病理
作者
Baris Bingol,Morgan Sheng
标识
DOI:10.1016/j.freeradbiomed.2016.04.015
摘要
Mitochondrial quality control is central for maintaining a healthy population of mitochondria. Two Parkinson's disease genes, mitochondrial kinase PINK1 and ubiquitin ligase Parkin, degrade damaged mitochondria though mitophagy. In this pathway, PINK1 senses mitochondrial damage and activates Parkin by phosphorylating Parkin and ubiquitin. Activated Parkin then builds ubiquitin chains on damaged mitochondria to tag them for degradation in lysosomes. USP30 deubiquitinase acts as a brake on mitophagy by opposing Parkin-mediated ubiquitination. Human genetic data point to a role for mitophagy defects in neurodegenerative diseases. This review highlights the molecular mechanisms of the mitophagy pathway and the recent advances in the understanding of mitophagy in vivo.
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