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- W3026407776 abstract "Abstract 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." @default.
- W3026407776 created "2020-05-29" @default.
- W3026407776 creator A5017796398 @default.
- W3026407776 creator A5032953882 @default.
- W3026407776 creator A5071049713 @default.
- W3026407776 creator A5075856075 @default.
- W3026407776 creator A5081521414 @default.
- W3026407776 creator A5089917586 @default.
- W3026407776 date "2020-05-20" @default.
- W3026407776 modified "2023-10-15" @default.
- W3026407776 title "Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase" @default.
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