期刊
EMBO REPORTS
卷 16, 期 1, 页码 97-106出版社
WILEY
DOI: 10.15252/embr.201438976
关键词
AAA protease; mitochondrial proteostasis; oxidative stress; YME1L
资金
- Ellison Medical Foundation
- NIH [R21NS079882]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS079882] Funding Source: NIH RePORTER
Mitochondrial proteostasis is maintained by a network of ATP-dependent quality control proteases including the inner membrane protease YME1L. Here, we show that YME1L is a stress-sensitive mitochondrial protease that is rapidly degraded in response to acute oxidative stress. This degradation requires reductions in cellular ATP and involves the activity of the ATP-independent protease OMA1. Oxidative stress-dependent reductions in YME1L inhibit protective YME1L-dependent functions and increase cellular sensitivity to oxidative insult. Collectively, our results identify stress-induced YME1L degradation as a biologic process that attenuates protective regulation of mitochondrial proteostasis and promotes cellular death in response to oxidative stress.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据