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J-GLOBAL ID：201702273352980340   整理番号：17A1387825

ACLYによる核アセチルCoA産生相同組換を促進する【Powered by NICT】

Nuclear Acetyl-CoA Production by ACLY Promotes Homologous Recombination

著者 (30件)： Sivanand Sharanya (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Sivanand Sharanya (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Rhoades Seth (Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Jiang Qinqin (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Jiang Qinqin (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Lee Joyce V. (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Lee Joyce V. (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Benci Joseph (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Benci Joseph (Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Benci Joseph (Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Zhang Jingwen (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Zhang Jingwen (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Yuan Salina (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Yuan Salina (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Viney Isabella (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Viney Isabella (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Zhao Steven (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Zhao Steven (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Carrer Alessandro (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Carrer Alessandro (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Bennett Michael J. (Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Bennett Michael J. (Children’s Hospital of Philadelphia, Philadelphia, PA 19104, USA) ,  Minn Andy J. (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Minn Andy J. (Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Minn Andy J. (Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Weljie Aalim M. (Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Greenberg Roger A. (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Greenberg Roger A. (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Wellen Kathryn E. (Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA) ,  Wellen Kathryn E. (Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA)
資料名： Molecular Cell  (Molecular Cell)
巻： 67  号： 2  ページ： 252-265.e6  発行年： 2017年 
JST資料番号： W1167A  ISSN： 1097-2765  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： オランダ (NLD)  言語： 英語 (EN)

抄録/ポイント： ゲノムの完全性を維持し,生物エネルギーを維持する細胞の基本的な機能の両方がが,代謝とDNA修復経路間の潜在的クロストークはあまり理解されていない。ヒストンアセチル化はDNA修復において重要な役割を果たし,アセチル補酵素A(アセチルCoA)の利用可能性に敏感であるので,著者らはDNA損傷応答におけるヒストンアセチル化の代謝調節の役割を検討した。本研究では,著者らは核ATP-くえん酸リアーゼ(ACLY)はDNA損傷後の毛細血管拡張性運動失調症変異(ATM)およびAKTのS455下流でりん酸化されることを報告した。ACLYは二本鎖切断(DSB)部位でのヒストンアセチル化を促進し,53BP1局在化を損ない,相同組換によるBRCA1の動員とDNA修復を可能にした。ACLYりん酸化と核局在化はBRCA1の動員の促進におけるその役割に必要である。PARP阻害により,ACLYサイレンシングはゲノム不安定性と細胞死を促進する。ACLYによるアセチルCoA産生の空間的および時間的制御はDNA修復経路選択の機構に関与する。Copyright 2017 Elsevier B.V., Amsterdam. All rights reserved. Translated from English into Japanese by JST.【Powered by NICT】

シソーラス用語： リン酸化 ,  DNA損傷 ,  細胞死 ,  二本鎖DNA切断 ,  *相同組換 ,  血管拡張性失調症 ,  DNA修復 ,  代謝調節 ,  ゲノム ,  遺伝子サイレンシング
準シソーラス用語： ゲノム不安定性 ,  BRCA1蛋白質 ,  53BP1 ,  DNA損傷応答 ,  ヒストンアセチル化 , 【Automatic Indexing@JST】

著者キーワード (9件)： アセチルCoA ,  ATP-くえん酸リアーゼ ,  DNA修復 ,  DNA損傷 ,  nucleus ,  ヒストンアセチル化 ,  metabolism ,  相同組換 ,  非相同末端は接合

分類 (3件)： 分子遺伝学一般  (EC02010J) ,  細胞分裂・増殖  (EF02020D) ,  細胞生理一般  (EF02010S)

タイトルに関連する用語 (4件)： 核 ,  アセチルCoA ,  相同組換 ,  促進