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  1. 原著論文

Signatures of DNA double strand breaks produced in irradiated G1 and G2 cells persist into mitosis.

https://repo.qst.go.jp/records/45509
https://repo.qst.go.jp/records/45509
b189ed3b-5f62-4936-a0ee-3c94963a1ab2
Item type 学術雑誌論文 / Journal Article(1)
公開日 2009-05-14
タイトル
タイトル Signatures of DNA double strand breaks produced in irradiated G1 and G2 cells persist into mitosis.
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 Kato, Takamitsu

× Kato, Takamitsu

WEKO 452189

Kato, Takamitsu

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Okayasu, Ryuichi

× Okayasu, Ryuichi

WEKO 452190

Okayasu, Ryuichi

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S., Bedford Joel

× S., Bedford Joel

WEKO 452191

S., Bedford Joel

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加藤 宝光

× 加藤 宝光

WEKO 452192

en 加藤 宝光

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岡安 隆一

× 岡安 隆一

WEKO 452193

en 岡安 隆一

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抄録
内容記述タイプ Abstract
内容記述 We have observed that some of the DNA damage or damage product caused by irradiation of interphase cells persisted throughout the cell cycle, and resulted in the expression of gamma-H2AX foci on the mitotic chromosomes. These mitotic expressions of damage after gamma-irradiation of G1 or G2 phase cells were compared in wild-type CHO and their DNA repair deficient XR-1 and UV-1 cells. gamma-H2AX foci were located on one of the chromatids or on both chromatids as isolocus paired foci. DNA double strand break (DSB) repair deficient XR-1 cells exhibited greater persistence of gamma-H2AX foci than wild-type cells when irradiated at G1 phase. Delayed subculture after irradiation significantly reduced the persistence of damage in mitotic cells and the radiosensitivity in wild-type cells, but this was not the case for XR-1 cells. Interestingly, UV and crosslinking agents sensitive UV-1 cells which show similar sensitivity to gamma-irradiation as wild-type cells by gamma-irradiation, exhibited significantly higher gamma-H2AX persistence at mitosis when they were irradiated in G1-phase but not in G2-phase. One interpretation of this is that it is due to DNA damage accumulating at stalled replication forks. As in wild type cells, in delayed subculture after gamma-ray exposure of UV-1 cells, a reduced number of foci was also seen. Our results suggest that the persistence of gamma-H2AX foci does not always correspond with the radiosensitivities of cells, but rather depends on cells' ability to repair the different kinds of DNA damages. J. Cell. Physiol. (c) 2009 Wiley-Liss, Inc.
書誌情報 Journal of Cellular Physiology

巻 219, 号 3, p. 760-765, 発行日 2009-02
ISSN
収録物識別子タイプ ISSN
収録物識別子 0021-9541
DOI
識別子タイプ DOI
関連識別子 10.1002/jcp.21726
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