期刊
NUCLEIC ACIDS RESEARCH
卷 48, 期 12, 页码 6611-6623出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkaa393
关键词
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资金
- Intramural Research Program, National Institute on Aging
- National Institute on Aging, Intramural Research
- NATIONAL INSTITUTE ON AGING [ZIAAG000733] Funding Source: NIH RePORTER
Mitochondria are vital for cellular energy supply and intracellular signaling after stress. Here, we aimed to investigate how mitochondria respond to acute DNA damage with respect to mitophagy, which is an important mitochondrial quality control process. Our results show thatmitophagy increases after DNA damage in primary fibroblasts, murine neurons and Caenorhabditis elegans neurons. Our results indicate that modulation of mitophagy after DNA damage is independent of the type of DNA damage stimuli used and that the protein Spata18 is an important player in this process. Knockdown of Spata18 suppresses mitophagy, disturbs mitochondrial Ca2+ homeostasis, affects ATP production, and attenuates DNA repair. Importantly, mitophagy after DNA damage is a vital cellular response to maintain mitochondrial functions and DNA repair.
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