Journal
CURRENT OPINION IN CELL BIOLOGY
Volume 33, Issue -, Pages 95-101Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2015.01.002
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Funding
- Japan Society for the Promotion of Science (JSPS) [25650067, 25291045]
- Ministry of Education, Culture, Sports, Science, and Technology [26111513]
- JSPS
- Grants-in-Aid for Scientific Research [15H01536, 26111513, 25650067] Funding Source: KAKEN
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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.
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