期刊
NUCLEIC ACIDS RESEARCH
卷 48, 期 12, 页码 6530-6546出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkaa392
关键词
-
资金
- NORDEA Foundation, Denmark [02-2013-0220]
- EU Joint Programme-Neurodegenerative Disease Research (JPND)
- Innovation Fund Denmark [5188-00001]
- Olav Thon Foundation Norway [531811-710131]
- Novo Nordisk Foundation Denmark [NNF17OC0027812]
- Intramural Research Program of the NIH, National Institute on Aging [AG000733]
- The Company of Biologists [JCSTF190394]
- ICMM, University of Copenhagen
- NATIONAL INSTITUTE ON AGING [ZIAAG000727, ZIAAG000726] Funding Source: NIH RePORTER
OGG1 initiated base excision repair (BER) is the major pathway for repair of oxidative DNA base damage 8-oxoguanine (8-oxoG). Here, we report that RECQL4 DNA helicase, deficient in the cancer-prone and premature aging Rothmund-Thomson syndrome, physically and functionally interacts with OGG1. RECQL4 promotes catalytic activity of OGG1 and RECQL4 deficiency results in defective 8-oxoG repair and increased genomic 8-oxoG. Furthermore, we show that acute oxidative stress leads to increased RECQL4 acetylation and its interaction with OGG1. The NAD(+)-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state. Collectively, we find that RECQL4 is involved in 8-oxoG repair through interaction with OGG1, and that SIRT1 indirectly modulates BER of 8-oxoG by controlling RECQL4-OGG1 interaction.
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