Format

Send to

Choose Destination
Curr Opin Cell Biol. 2015 Apr;33:95-101. doi: 10.1016/j.ceb.2015.01.002. Epub 2015 Feb 17.

PINK1/Parkin-mediated mitophagy in mammalian cells.

Author information

1
Graduate School of Frontier Biosciences, Osaka University, Suita 565-0871, Japan.
2
Graduate School of Frontier Biosciences, Osaka University, Suita 565-0871, Japan. Electronic address: kokamoto@fbs.osaka-u.ac.jp.

Abstract

Mitochondria-specific autophagy (mitophagy) is a fundamental process critical for maintaining mitochondrial fitness in a myriad of cell types. Particularly, mitophagy contributes to mitochondrial quality control by selectively eliminating dysfunctional mitochondria. In mammalian cells, the Ser/Thr kinase PINK1 and the E3 ubiquitin ligase Parkin act cooperatively in sensing mitochondrial functional state and marking damaged mitochondria for disposal via the autophagy pathway. Notably, ubiquitin and deubiquitinases play vital roles in modulating Parkin activity and mitophagy efficiency. In this review, we highlight recent breakthroughs addressing the key issues of how PINK1 activates Parkin in response to mitochondrial malfunction, how Parkin localizes specifically to impaired mitochondria, and how ubiquitination and deubiquitination regulate PINK1/Parkin-mediated mitophagy.

PMID:
25697963
DOI:
10.1016/j.ceb.2015.01.002
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center