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ATM activation by a sulfhydryl-reactive inflammatory cyclopentenone prostaglandin
https://doi.org/10.24517/00027353
https://doi.org/10.24517/0002735356097c9e-c38a-42bc-ba6a-9de672df0fdb
名前 / ファイル | ライセンス | アクション |
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CA-PR-KOBAYASHI-M-779.pdf (2.2 MB)
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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 | ATM activation by a sulfhydryl-reactive inflammatory cyclopentenone prostaglandin | |||||
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 | |||||
ID登録 | ||||||
ID登録 | 10.24517/00027353 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Kobayashi, Masahiko
× Kobayashi, Masahiko× Ono, Hirohito× Mihara, Keiko× Tauchi, Hiroshi× Komatsu, Kenshi× Shibata, Takashi× Shimizu, Hiroko× Uchida, Koji× Yamamoto, Ken-ichi |
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著者別表示 |
小林, 昌彦
× 小林, 昌彦× 清水, 弘子× 山本, 健一 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | がん研究所がん分子細胞制御 | |||||
書誌情報 |
Genes to Cells 巻 11, 号 7, p. 779-789, 発行日 2006-07-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1356-9597 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1111/j.1365-2443.2006.00976.x | |||||
出版者 | ||||||
出版者 | Blackwell Publishing | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | ATM (ataxia-telangiectasia mutated) is activated by a variety of noxious agent, including oxidative stress, and ATM deficiency results in an anomalous cellular response to oxidative stress. However, the mechanisms for ATM activation by oxidative stress remain to be established. Furthermore, it is not clear whether ATM responds to oxidative DNA damage or to a change in the intracellular redox state, independent of DNA damage. We found that ATM is activated by N-methyl-N′-nitro-nitrosoguanidine (MNNG) and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), in NBS1- or MSH6-deficient cells. We further found that ATM is activated by treating chromatin-free immunoprecipitated ATM with MNNG or 15d-PGJ2, which modifies free sulfhydryl (SH) groups, and that 15d-PGJ2 binds covalently to ATM. Interestingly, 15d-PGJ2-induced ATM activation leads to p53 activation and apoptosis, but not to Chk2 or H2AX phosphorylation. These results indicate that ATM is activated through the direct modification of its SH groups, independent of DNA damage, and this activation leads, downstream, to apoptosis. © 2006 The Authors Journal compilation © 2006 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd. | |||||
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 |