Mechanisms of mitophagy: PINK1, Parkin, USP30 and beyond

被引：247

作者：

Bingol, Baris ^{[1
]}

Sheng, Morgan ^{[1
]}

机构：

[1] Genentech Inc, Dept Neurosci, San Francisco, CA 94080 USA

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2016年 / 100卷

关键词：

Parkin; PINK1; USP30; Mitophagy; Parkinson's Disease; FRONTOTEMPORAL LOBAR DEGENERATION; UNFOLDED PROTEIN RESPONSE; E3 LIGASE PARKIN; MITOCHONDRIAL-DNA; CATALYTIC-ACTIVITY; EARLY-ONSET; PHOSPHORYLATED UBIQUITIN; DAMAGED MITOCHONDRIA; MISFOLDED PROTEINS; AUTOPHAGY RECEPTOR;

D O I：

10.1016/j.freeradbiomed.2016.04.015

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：210 / 222

页数：13

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