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SIRT1 promotes DNA repair activity and deacetylation of Ku70

Cited 211 time in Web of Science Cited 230 time in Scopus
Authors
Jeong, Jaemin; Juhn, Kyungmi; Lee, Hansoo; Kim, Sang-Hoon; Min, Bon-Hong; Lee, Kyung-Mi; Cho, Myung-Haeng; Park, Gil-Hong; Lee, Kee-Ho
Issue Date
2007-02
Citation
Experimental and Molecular Medicine, Vol.39 No.1, pp.8-13
Keywords
DNA damageDNA repairKu auto-antigenradiation, ionizingSIRT1 proteinhuman
Abstract
Human SIRT1 controls various physiological responses including cell fate, stress, and aging, through deacetylation of its specific substrate protein. In processing DNA damage signaling, SIRT1 attenuates a cellular apoptotic response by deacetylation of p53 tumor suppressor. The present study shows that, upon exposure to radiation, SIRT1 could enhance DNA repair capacity and deacetylation of repair protein Ku70. Ectopically over-expressed SIRT1 resulted in the increase of repair of DNA strand breakages produced by radiation. On the other hand, repression of endogenous SIRT1 expression by SIRT1 siRNA led to the decrease of this repair activity, indicating that SIRT1 can regulate DNA repair capacity of cells with DNA strand breaks. In addition, we found that SIRT1 physically complexed with repair protein Ku70, leading to subsequent deacetylation. The dominant-negative SIRT1, a catalytically inactive form, did not induce deacetylation of Ku70 protein as well as increase of DNA repair capacity. These observations suggest that SIRT1 modulates DNA repair activity, which could be regulated by the acetylation status of repair protein Ku70 following DNA damage.
ISSN
1226-3613
URI
https://hdl.handle.net/10371/172376
DOI
https://doi.org/10.1038/emm.2007.2
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College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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