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タイトル: 低線量放射線と細胞内シグナリング
その他のタイトル: Low-dose Radiation Effects and Intracellular Signaling Pathways
著者: 鈴木, 啓司 / 児玉, 靖司 / 渡邉, 正己
著者(別表記) : Suzuki, Kenji / Kodama, Seiji / Watanabe, Masami
発行日: 2006年10月
出版者: 日本薬学会
引用: YAKUGAKU ZASSHI v.126(10) p.859-867, 2006
抄録: Accumulated evidence has shown that exposure to low-dose radiation, especially doses less than 0.1 Gy, induces observable effects on mammalian cells. However, the underlying molecular mechanisms have not yet been clarified. Recently, it has been shown that low-dose radiation stimulates growth factor receptor, which results in a sequential activation of the mitogen-activated protein kinase pathway. In addition to the activation of the membrane-bound pathways, it is becoming evident that nuclear pathways are also activated by low-dose radiation. Ionizing radiation has detrimental effects on chromatin structure, since radiation-induced DNA double-strand breaks result in discontinuity of nucleosomes. Recently, it has been shown that ATM protein, the product of the ATM gene mutated in ataxia-telangiectasia, recognizes alteration in the chromatin structure, and it is activated through intermolecular autophosphorylation at serine 1981. Using antibodies against phosphorylated ATM, we found that the activated and phosphorylated ATM protein is detected as discrete foci in the nucleus between doses of 10 mGy and 1 Gy. Interestingly, the size of the foci induced by low-dose radiation was equivalent to the foci induced by high-dose radiation. These results indicate that the initial signal is amplified through foci growth, and cells evolve a system by which they can respond to a small number of DNA double-strand breaks. From these results, it can be concluded that low-dose radiation is sensed both in the membrane and in the nucleus, and activation of multiple signal transduction pathways could be involved in manifestations of low-dose effects.
キーワード: radiation / signal transduction / DNA damage / phosphorylation / ATM
URI: http://hdl.handle.net/10069/8414
ISSN: 00316903
DOI: 10.1248/yakushi.126.859
PubMed ID: 17016017
関連リンク : http://dx.doi.org/10.1248/yakushi.126.859
資料タイプ: Journal Article
原稿種類: publisher
出現コレクション:050 学術雑誌論文

引用URI : http://hdl.handle.net/10069/8414



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