Mitochondria at the crossroads of ATM-mediated stress signaling and regulation of reactive oxygen species

被引：56

作者：

Lee, Ji-Hoon ^{[1
]}

Paull, Tanya T. ^{[1
]}

机构：

[1] Univ Texas Austin, Dept Mol Biosci, Austin, TX 78712 USA

来源：

REDOX BIOLOGY | 2020年 / 32卷

关键词：

Ataxia; Mitochondria; Reactive oxygen species; DNA repair; TELANGIECTASIA GENE-PRODUCT; DOUBLE-STRAND BREAKS; ATAXIA-TELANGIECTASIA; OXIDATIVE STRESS; PROTEIN-KINASE; DNA-DAMAGE; FIBROBLAST-CULTURES; CELLULAR-RESPONSE; PROTECTIVE ROLES; REDOX REGULATION;

D O I：

10.1016/j.redox.2020.101511

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：

The Ataxia-telangiectasia mutated (ATM) kinase responds to DNA double-strand breaks and other forms of cellular stress, including reactive oxygen species (ROS). Recent work in the field has uncovered links between mitochondrial ROS and ATM activation, suggesting that ATM acts as a sensor for mitochondrial derived ROS and regulates ROS accumulation in cells through this pathway. In addition, characterization of cells from Ataxia-telangiectasia patients as well as ATM-deficient mice and cell models suggest a role for ATM in modulating mitochondrial gene expression and function. Here we review ROS responses related to ATM function, recent evidence for ATM roles in mitochondrial maintenance and turnover, and the relationship between ATM and regulation of protein homeostasis.

引用

页数：8

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