期刊
AUTOPHAGY
卷 18, 期 1, 页码 231-232出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2021.1998872
关键词
Mitophagy; mitochondrial turnover; PINK1; PARKIN; Parkinson's disease
类别
资金
- Joan and David Traitel Family Trust
- Betty Brown's Family
- NIH [RO1NS091902, RO1AG065428]
- Hillblom Fellowship
- Berkelhammer Award for Excellence in Neuroscience
This study summarizes recent findings enabled by a new platform for tracking individual mitochondria in neurons, outlining the steps of PINK1- and PRKN-dependent mitochondrial turnover, including the unexplored fates of mitochondria after fusion with lysosomes. These studies reveal unexpected mechanisms of mitochondrial quality control, which may contribute to the reliance of neurons on PINK1 under stress conditions.
Parkinson disease remains a debilitating neurodegenerative disorder, despite the discovery of multiple causative genes that account for familial forms. Prominent among these are PRKN/Parkin and PINK1, whose protein products participate in mitochondrial turnover, or mitophagy. But our poor understanding of the basic biological mechanisms driven by those genes in neurons limits our ability to target them therapeutically. Here, we summarize our recent findings enabled by a new platform to track individual mitochondria in neurons. Our analysis delineates the steps of PINK1- and PRKN-dependent mitochondrial turnover, including the unexplored fates of mitochondria after fusion with lysosomes. These studies reveal unexpected mechanisms of mitochondrial quality control, which may contribute to the reliance of neurons on PINK1 under conditions of stress.
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