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  1. 原著論文

Pre-exposure to ionizing radiation stimulates DNA double strand break end resection, promoting the use of homologous recombination repair.

https://repo.qst.go.jp/records/47449
https://repo.qst.go.jp/records/47449
04dc65ec-3fdc-4109-8f79-dc1deb066497
Item type 学術雑誌論文 / Journal Article(1)
公開日 2016-08-10
タイトル
タイトル Pre-exposure to ionizing radiation stimulates DNA double strand break end resection, promoting the use of homologous recombination repair.
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 Izumi, Nakajima Nakako

× Izumi, Nakajima Nakako

WEKO 475320

Izumi, Nakajima Nakako

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Hagiwara, Yoshihiko

× Hagiwara, Yoshihiko

WEKO 475321

Hagiwara, Yoshihiko

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Oike, Takahiro

× Oike, Takahiro

WEKO 475322

Oike, Takahiro

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Okayasu, Ryuichi

× Okayasu, Ryuichi

WEKO 475323

Okayasu, Ryuichi

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Murakami, Takeshi

× Murakami, Takeshi

WEKO 475324

Murakami, Takeshi

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Nakano, Takashi

× Nakano, Takashi

WEKO 475325

Nakano, Takashi

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Shibata, Atsushi

× Shibata, Atsushi

WEKO 475326

Shibata, Atsushi

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中島 菜花子

× 中島 菜花子

WEKO 475327

en 中島 菜花子

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岡安 隆一

× 岡安 隆一

WEKO 475328

en 岡安 隆一

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村上 健

× 村上 健

WEKO 475329

en 村上 健

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抄録
内容記述タイプ Abstract
内容記述 The choice of DNA double strand break (DSB) repair pathway is determined at the stage of DSB end resection. Resection was proposed to control the balance between the two major DSB repair pathways, homologous recombination (HR) and non-homologous end joining (NHEJ). Here, we examined the regulation of DSB repair pathway choice at two-ended DSBs following ionizing radiation (IR) in G2 phase of the cell cycle. We found that cells pre-exposed to low-dose IR preferred to undergo HR following challenge IR in G2, whereas NHEJ repair kinetics in G1 were not affected by pre-IR treatment. Consistent with the increase in HR usage, the challenge IR induced Replication protein A (RPA) foci formation and RPA phosphorylation, a marker of resection, were enhanced by pre-IR. However, neither major DNA damage signals nor the status of core NHEJ proteins, which influence the choice of repair pathway, was significantly altered in pre-IR treated cells. Moreover, the increase in usage of HR due to pre-IR exposure was prevented by treatment with ATM inhibitor during the incubation period between pre-IR and challenge IR. Taken together, the results of our study suggest that the ATM-dependent damage response after pre-IR changes the cellular environment, possibly by regulating gene expression or post-transcriptional modifications in a manner that promotes resection.
書誌情報 PloS one

巻 10, 号 3, p. e0122582-1-e0122582-15, 発行日 2016-01
出版者
出版者 PLOS ONE
ISSN
収録物識別子タイプ ISSN
収録物識別子 1932-6203
PubMed番号
識別子タイプ PMID
関連識別子 25826455
DOI
識別子タイプ DOI
関連識別子 10.1371/journal.pone.0122582
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