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タイトル: | A novel interplay between the Fanconi anemia core complex and ATR-ATRIP kinase during DNA cross-link repair. |
著者: | Tomida, Junya Itaya, Akiko Shigechi, Tomoko Unno, Junya Uchida, Emi Ikura, Masae https://orcid.org/0000-0002-0426-8923 (unconfirmed) Masuda, Yuji Matsuda, Shun Adachi, Jun Kobayashi, Masahiko Meetei, Amom Ruhikanta Maehara, Yoshihiko Yamamoto, Ken-Ichi Kamiya, Kenji Matsuura, Akira Matsuda, Tomonari https://orcid.org/0000-0002-6177-1066 (unconfirmed) Ikura, Tsuyoshi Ishiai, Masamichi Takata, Minoru https://orcid.org/0000-0002-4926-3675 (unconfirmed) |
著者名の別形: | 髙田, 穣 |
発行日: | 1-Aug-2013 |
出版者: | Oxford University Press |
誌名: | Nucleic acids research |
巻: | 41 |
号: | 14 |
開始ページ: | 6930 |
終了ページ: | 6941 |
抄録: | When DNA replication is stalled at sites of DNA damage, a cascade of responses is activated in the cell to halt cell cycle progression and promote DNA repair. A pathway initiated by the kinase Ataxia teleangiectasia and Rad3 related (ATR) and its partner ATR interacting protein (ATRIP) plays an important role in this response. The Fanconi anemia (FA) pathway is also activated following genomic stress, and defects in this pathway cause a cancer-prone hematologic disorder in humans. Little is known about how these two pathways are coordinated. We report here that following cellular exposure to DNA cross-linking damage, the FA core complex enhances binding and localization of ATRIP within damaged chromatin. In cells lacking the core complex, ATR-mediated phosphorylation of two functional response targets, ATRIP and FANCI, is defective. We also provide evidence that the canonical ATR activation pathway involving RAD17 and TOPBP1 is largely dispensable for the FA pathway activation. Indeed DT40 mutant cells lacking both RAD17 and FANCD2 were synergistically more sensitive to cisplatin compared with either single mutant. Collectively, these data reveal new aspects of the interplay between regulation of ATR-ATRIP kinase and activation of the FA pathway. |
著作権等: | © The Author(s) 2013. Published by Oxford University Press. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
URI: | http://hdl.handle.net/2433/178688 |
DOI(出版社版): | 10.1093/nar/gkt467 |
PubMed ID: | 23723247 |
出現コレクション: | 学術雑誌掲載論文等 |
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