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c-ABL tyrosine kinase stabilizes RAD51 chromatin association
http://hdl.handle.net/2297/17331
http://hdl.handle.net/2297/17331055ddb4f-bfc2-4317-8536-c40693795fc1
名前 / ファイル | ライセンス | アクション |
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CA-PR-YAMAMOTO-K-286.pdf (737.2 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | c-ABL tyrosine kinase stabilizes RAD51 chromatin association | |||||
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 | |||||
著者 |
Shimizu, Hiroko
× Shimizu, Hiroko× Popova, Milena× Fleury, Fabrice× Kobayashi, Masahiko× Hayashi, Naoyuki× Sakane, Isao× Kurumisaka, Hitoshi× Venkitaraman, Ashok R.× Takahashi, Masayuki× Yamamoto, Ken-ichi |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学がん研究所がん分子細胞制御 | |||||
書誌情報 |
Biochemical and Biophysical Research Communications 巻 382, 号 2, p. 286-291, 発行日 2009-05-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0006-291X | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00564395 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.bbrc.2009.03.020 | |||||
出版者 | ||||||
出版者 | Elsevier | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The assembly of RAD51 recombinase on DNA substrates at sites of breakage is essential for their repair by homologous recombination repair (HRR). The signaling pathway that triggers RAD51 assembly at damage sites to form subnuclear foci is unclear. Here, we provide evidence that c-ABL, a tyrosine kinase activated by DNA damage which phosphorylates RAD51 on Tyr-315, works at a previously unrecognized, proximal step to initiate RAD51 assembly. We first show that c-ABL associates with chromatin after DNA damage in a manner dependent on its kinase activity. Using RAD51 mutants that are unable to oligomerize to form a nucleoprotein filament, we separate RAD51 assembly on DNA to form foci into two steps: stable chromatin association followed by oligomerization. We show that phosphorylation on Tyr-315 by c-ABL is required for chromatin association of oligomerization-defective RAD51 mutants, but is insufficient to restore oligomerization. Our findings suggest a new model for the regulation of early steps of HRR. © 2009 Elsevier Inc. All rights reserved. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.elsevier.com/locate/issn/00006291X |