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A Novel ATM/TP53/p21-Mediated Checkpoint Only Activated by Chronic γ-Irradiation
http://hdl.handle.net/10069/34752
http://hdl.handle.net/10069/34752e69094b7-0411-4d43-a0d4-e34451943df3
名前 / ファイル | ライセンス | アクション |
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PLoS9_104279.pdf (2.5 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2014-10-06 | |||||
タイトル | ||||||
タイトル | A Novel ATM/TP53/p21-Mediated Checkpoint Only Activated by Chronic γ-Irradiation | |||||
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 |
Cao, Lili
× Cao, Lili× Kawai, Hidehiko× Sasatani, Megumi× Iizuka, Daisuke× Masuda, Yuji× Inaba, Toshiya× Suzuki, Keiji× Ootsuyama, Akira× Umata, Toshiyuki× Kamiya, Kenji× Suzuki, Fumio |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Different levels or types of DNA damage activate distinct signaling pathways that elicit various cellular responses, including cell-cycle arrest, DNA repair, senescence, and apoptosis. Whereas a range of DNA-damage responses have been characterized, mechanisms underlying subsequent cell-fate decision remain elusive. Here we exposed cultured cells and mice to different doses and dose rates of γ-irradiation, which revealed cell-type-specific sensitivities to chronic, but not acute, γ-irradiation. Among tested cell types, human fibroblasts were associated with the highest levels of growth inhibition in response to chronic γ-irradiation. In this context, fibroblasts exhibited a reversible G1 cell-cycle arrest or an irreversible senescence-like growth arrest, depending on the irradiation dose rate or the rate of DNA damage. Remarkably, when the same dose of γ-irradiation was delivered chronically or acutely, chronic delivery induced considerably more cellular senescence. A similar effect was observed with primary cells isolated from irradiated mice. We demonstrate a critical role for the ataxia telangiectasia mutated (ATM)/tumor protein p53 (TP53)/p21 pathway in regulating DNA-damage-associated cell fate. Indeed, blocking the ATM/TP53/p21 pathway deregulated DNA damage responses, leading to micronucleus formation in chronically irradiated cells. Together these results provide insights into the mechanisms governing cell-fate determination in response to different rates of DNA damage. | |||||
書誌情報 |
PLoS ONE 巻 9, 号 8, p. e104279, 発行日 2014-08-05 |
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出版者 | ||||||
出版者 | Public Library of Science | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 19326203 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1371/journal.pone.0104279 | |||||
権利 | ||||||
権利情報 | c 2014 Cao 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. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | PLoS ONE, 9(8), e104279; 2014 |