@article{oai:repo.qst.go.jp:00049047,
 author = {Yasuda, Takeshi and Kagawa, Wataru and Ogi, Tomoo and A., Kato Takamitsu and Suzuki, Takehiro and Dohmae, Naoshi and Takizawa, Kazuya and Nakazawa, Yuka and D., Genet Matthew and Saotome, Mika and Hama, Michio and Konishi, Teruaki and Izumi, Nakajima Nakako and Hazawa, Masaharu and Tomita, Masanori and Koike, Manabu and Noshiro, Katsuko and Tomiyama, Kenichi and Obara, Chizuka and Gotoh, Takaya and Ui, Ayako and Fujimori, Akira and Nakayama, Fumiaki and Hanaoka, Fumio and Sugasawa, Kaoru and Okayasu, Ryuichi and A., Jeggo Penny and Tajima, Katsushi and 安田 武嗣 and 滝澤 和也 and 濱 三知夫 and 小西 輝昭 and 中島 菜花子 and 小池 学 and 野代 勝子 and 富山 健一 and 小原 千寿香 and 後藤 孝也 and 藤森 亮 and 中山 文明 and 岡安 隆一 and 田嶋 克史},
 issue = {3},
 journal = {PLOS Genetics},
 month = {Mar},
 note = {The p300 and CBP histone acetyltransferases are recruited to DNA double-strand break (DSB) sites where they induce histone acetylation, thereby influencing the chromatin structure and DNA repair process. Whether p300/CBP at DSB sites also acetylate non-histone proteins, and how their acetylation affects DSB repair, remain unknown. Here we show that p300/CBP acetylate RAD52, a human homologous recombination (HR) DNA repair protein, at DSB sites. Using in vitro acetylated RAD52, we identified 13 potential acetylation sites in RAD52 by a mass spectrometry analysis. An immunofluorescence microscopy analysis revealed that RAD52 acetylation at DSBs sites is counteracted by SIRT2- and SIRT3-mediated deacetylation, and that non-acetylated RAD52 initially accumulates at DSB sites, but dissociates prematurely from them. In the absence of RAD52 acetylation, RAD51, which plays a central role in HR, also dissociates prematurely from DSB sites, and hence HR is impaired. Furthermore, inhibition of ataxia telangiectasia mutated (ATM) protein by siRNA or inhibitor treatment demonstrated that the acetylation of RAD52 at DSB sites is dependent on the ATM protein kinase activity, through the formation of RAD52, p300/CBP, SIRT2, and SIRT3 foci at DSB sites. Our findings clarify the importance of RAD52 acetylation in HR and its underlying mechanism.},
 title = {Novel Function of HATs and HDACs in Homologous Recombination through Acetylation of Human RAD52 at Double-Strand Break Sites},
 volume = {14},
 year = {2018}
}