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ATM Modulates the Loading of Recombination Proteins onto a Chromosomal Translocation Breakpoint Hotspot

https://hiroshima.repo.nii.ac.jp/records/2007934
https://hiroshima.repo.nii.ac.jp/records/2007934
ba507199-79c0-4be9-9d43-cda3cae08dc2
名前 / ファイル ライセンス アクション
PLoS-One_5_e13554.pdf PLoS-One_5_e13554.pdf (2.5 MB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル ATM Modulates the Loading of Recombination Proteins onto a Chromosomal Translocation Breakpoint Hotspot
言語 en
作成者 Sun, Jiying

× Sun, Jiying

en Sun, Jiying

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Oma, Yukako

× Oma, Yukako

en Oma, Yukako

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Harata, Masahiko

× Harata, Masahiko

en Harata, Masahiko

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Kono, Kazuteru

× Kono, Kazuteru

en Kono, Kazuteru

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Shima, Hiroki

× Shima, Hiroki

en Shima, Hiroki

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Kinomura, Aiko

× Kinomura, Aiko

en Kinomura, Aiko

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Ikura, Tsuyoshi

× Ikura, Tsuyoshi

en Ikura, Tsuyoshi

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Suzuki, Hidekazu

× Suzuki, Hidekazu

en Suzuki, Hidekazu

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Mizutani, Shuki

× Mizutani, Shuki

en Mizutani, Shuki

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Kanaar, Roland

× Kanaar, Roland

en Kanaar, Roland

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Tashiro, Satoshi

× Tashiro, Satoshi

en Tashiro, Satoshi

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 Copyright (c) 2010 Sun et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
主題
主題Scheme NDC
主題 460
内容記述
内容記述 Chromosome translocations induced by DNA damaging agents, such as ionizing radiation and certain chemotherapies, alter genetic information resulting in malignant transformation. Abrogation or loss of the ataxia-telangiectasia mutated (ATM) protein, a DNA damage signaling regulator, increases the incidence of chromosome translocations. However, how ATM protects cells from chromosome translocations is still unclear. Chromosome translocations involving the MLL gene on 11q23 are the most frequent chromosome abnormalities in secondary leukemias associated with chemotherapy employing etoposide, a topoisomerase II poison. Here we show that ATM deficiency results in the excessive binding of the DNA recombination protein RAD51 at the translocation breakpoint hotspot of 11q23 chromosome translocation after etoposide exposure. Binding of Replication protein A (RPA) and the chromatin remodeler INO80, which facilitate RAD51 loading on damaged DNA, to the hotspot were also increased by ATM deficiency. Thus, in addition to activating DNA damage signaling, ATM may avert chromosome translocations by preventing excessive loading of recombinational repair proteins onto translocation breakpoint hotspots.
言語 en
出版者
出版者 Public Library Science
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
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
関連情報
識別子タイプ DOI
関連識別子 10.1371/journal.pone.0013554
関連情報
識別子タイプ DOI
関連識別子 http://dx.doi.org/10.1371/journal.pone.0013554
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1932-6203
開始ページ
開始ページ e13554-1
書誌情報 PLoS ONE
PLoS ONE

巻 5, 号 10, p. e13554-1-e13554-10, 発行日 2010-10-27
旧ID 30778
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