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论文名称：
Oxidative stress impairs cell death by repressing the nuclease activity of mitochondrial endonuclease G
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发表刊物：
Cell reports
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摘要：
Endonuclease G (EndoG) is a mitochondrial protein that is released from mitochondria and relocated into the nucleus to promote chromosomal DNA fragmentation during apoptosis. Here, we show that oxidative stress causes cell-death defects in C. elegans through an EndoG-mediated cell-death pathway. In response to high reactive oxygen species (ROS) levels, homodimeric CPS-6-the C. elegans homolog of EndoG-is dissociated into monomers with diminished nuclease activity. Conversely, the nuclease activity of CPS-6 is enhanced, and its dimeric structure is stabilized by its interaction with the worm AIF homolog, WAH-1, which shifts to disulfide cross-linked dimers under high ROS levels. CPS-6 thus acts as a ROS sensor to regulate the life and death of cells. Modulation of the EndoG dimer conformation could present an avenue for prevention and treatment of diseases resulting from oxidative stress.
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第一作者：
Akihisa Nakagawa#,Jason LJ Lin#
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通讯作者：
Ding Xue*,Hanna S Yuan*
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全部作者：
Riley Skeen-Gaar,Wei-Zen Yang,Pei Zhao,张哲,Xiao Ge,Shohei Mitani
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论文类型：
期刊论文
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论文编号：
8
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影响因子：
8.12
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DOI码：
10.1016/j.celrep.2016.05.090.
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是否译文：
否
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发表时间：
2016-07
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收录刊物：
SCI
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发布时间：
2016-07-01
En
