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Novel Function of HATs and HDACs in Homologous Recombination through Acetylation of Human RAD52 at Double-Strand Break Sites
https://repo.qst.go.jp/records/49047
https://repo.qst.go.jp/records/49047f00d4175-cbb2-4bac-b07b-4d9189d23d26
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2018-05-18 | |||||
| タイトル | ||||||
| タイトル | Novel Function of HATs and HDACs in Homologous Recombination through Acetylation of Human RAD52 at Double-Strand Break Sites | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Yasuda, Takeshi
× Yasuda, Takeshi× Kagawa, Wataru× Ogi, Tomoo× A., Kato Takamitsu× Suzuki, Takehiro× Dohmae, Naoshi× Takizawa, Kazuya× Nakazawa, Yuka× D., Genet Matthew× Saotome, Mika× Hama, Michio× Konishi, Teruaki× Izumi, Nakajima Nakako× Hazawa, Masaharu× Tomita, Masanori× Koike, Manabu× Noshiro, Katsuko× Tomiyama, Kenichi× Obara, Chizuka× Gotoh, Takaya× Ui, Ayako× Fujimori, Akira× Nakayama, Fumiaki× Hanaoka, Fumio× Sugasawa, Kaoru× Okayasu, Ryuichi× A., Jeggo Penny× Tajima, Katsushi× 安田 武嗣× 滝澤 和也× 濱 三知夫× 小西 輝昭× 中島 菜花子× 小池 学× 野代 勝子× 富山 健一× 小原 千寿香× 後藤 孝也× 藤森 亮× 中山 文明× 岡安 隆一× 田嶋 克史 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | 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. | |||||
| 書誌情報 |
PLOS Genetics 巻 14, 号 3, 発行日 2018-03 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | e1007277 | |||||
| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 29590107 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1371/journal.pgen.1007277 | |||||
| 関連サイト | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1371/journal.pgen.1007277 | |||||
| 関連名称 | https://doi.org/10.1371/journal.pgen.1007277 | |||||
