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ATM protein is indispensable to repair complex-type DNA double strand breaks induced by high LET heavy ion irradiation.

https://repo.qst.go.jp/records/62652
https://repo.qst.go.jp/records/62652
b8c0d5b1-c365-498b-afce-4bd6936149c3
Item type 会議発表用資料 / Presentation(1)
公開日 2008-07-30
タイトル
タイトル ATM protein is indispensable to repair complex-type DNA double strand breaks induced by high LET heavy ion 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_c94f
資源タイプ conference object
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 Sekine, Emiko

× Sekine, Emiko

WEKO 618965

Sekine, Emiko

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Yu, Dong

× Yu, Dong

WEKO 618966

Yu, Dong

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Ninomiya, Yasuharu

× Ninomiya, Yasuharu

WEKO 618967

Ninomiya, Yasuharu

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Fujimori, Akira

× Fujimori, Akira

WEKO 618968

Fujimori, Akira

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Anzai, Kazunori

× Anzai, Kazunori

WEKO 618969

Anzai, Kazunori

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Okayasu, Ryuichi

× Okayasu, Ryuichi

WEKO 618970

Okayasu, Ryuichi

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関根 絵美子

× 関根 絵美子

WEKO 618971

en 関根 絵美子

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于 冬

× 于 冬

WEKO 618972

en 于 冬

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二宮 康晴

× 二宮 康晴

WEKO 618973

en 二宮 康晴

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藤森 亮

× 藤森 亮

WEKO 618974

en 藤森 亮

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安西 和紀

× 安西 和紀

WEKO 618975

en 安西 和紀

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岡安 隆一

× 岡安 隆一

WEKO 618976

en 岡安 隆一

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抄録
内容記述タイプ Abstract
内容記述 ATM (ataxia telangiectasia-mutated) protein responsible for a rare genetic disease with hyper-radiosensitivity, is the one of the earliest repair proteins sensing DNA double-strand breaks (DSB). ATM is known to phosphorylate DNA repair proteins such as MRN complex (Mre11, Rad50 and NBS1), 53BP1, Artemis, Brca1, gamma-H2AX, and MDC. We studied the interactions between ATM and DNA-PKcs, a crucial NHEJ repair protein, after cells exposure to high and low LET irradiation.
Normal human (HFL III, MRC5VA) and AT homozygote (AT2KY, AT5BIVA, AT3BIVA) cells were irradiated with X-rays and high LET radiation (carbon ions: 290MeV/n initial energy at 70 keV/um, and iron ions: 500MeV/n initial energy at 200KeV/um), and several critical end points were examined. AT cells with high LET irradiation showed a significantly higher radiosensitivity when compared with normal cells. The behavior of DNA DSB repair was monitored by immuno-fluorescence techniques using DNA-PKcs (pThr2609, pSer2056) and ATM (pSer1981) antibodies. In normal cells, the phosphorylation of DNA-PKcs was clearly detected after high LET irradiation, though the peak of phosphorylation was delayed when compared to X-irradiation. In contrast, almost no DNA-PKcs phosphorylation foci were detected in AT cells irradiated with high LET radiation. A similar result was also observed in normal cells treated with 10 uM ATM kinase specific inhibitor (KU55933) one hour before irradiation. These data suggest that the phosphorylation of DNA-PKcs with low LET X-rays is mostly ATM-independent, and the phosphorylation of DNA-PKcs with high LET radiation seems to require ATM probably due to its complex nature of DSB induced. Our study indicates that high LET heavy ion irradiation which we can observe in the space environment would provide a useful tool to study the fundamental mechanism associated with DNA DSB repair.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 37th COSPAR Scientific Assembly
発表年月日
日付 2008-07-20
日付タイプ Issued
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