WEKO3
アイテム
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酸化的DNA損傷誘発突然変異を回避する分子機構 ─DNA修復欠損マウスにおける突然変異と発がんの解析─
https://repo.qst.go.jp/records/57190
https://repo.qst.go.jp/records/5719051e5cd37-d937-42ba-9a11-117a8b47c14e
Item type | 一般雑誌記事 / Article(1) | |||||
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公開日 | 2006-09-29 | |||||
タイトル | ||||||
タイトル | 酸化的DNA損傷誘発突然変異を回避する分子機構 ─DNA修復欠損マウスにおける突然変異と発がんの解析─ | |||||
言語 | ||||||
言語 | jpn | |||||
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 | 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 |
續, 輝久
× 續, 輝久× 山内, 一己× 磯田, 拓郎× 江頭, 明典× 藏, 忍× 中津, 可道× 山内 一己 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Oxygen radicals are produced through normal cellular metabolism, and formation of such radicals is further enhanced by ionizing radiation and by various chemicals. Among various classes of oxidative DNA damage, 8-oxo-7,8-dihydroguanine (8-oxoG) is the most abundant, and appears to play important roles in mutagenesis and carcinogenesis. Enzymatic activities that may be responsible for preventing 8-oxoG-evoked mutations were identified in mammalian cells. We have focused on following the two enzymes. MTH1 (Mth1) protein is the mammalian counterpart of E. coli MutT protein, which hydrolyzes 8-oxo-dGTP to its monophosphate form in the nucleotide pool, thereby preventing the incorporation of the mutagenic substrate into DNA. On the other hand, MUTYH (Mutyh) protein, a counterpart of E. coli MutY protein, having adenine/2-hydroxyadenine DNA glycosylase activity, is expected to prevent G:C to T:A transversions, by excising adenine from G:A mismatches induced by 8-oxoG and 2-OH-A. To analyze the function of the mammalian Mth1 and Mutyh proteins in vivo, we established gene-knockout mice for these two enzymes by gene targeting, and investigated spontaneous tumorigenesis as well as mutagenesis. Here we discuss our recent progress on spontaneous and oxidative stress-induced mutagenesis with these mutant mouse lines. |
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書誌情報 |
環境変異原研究 巻 27, 号 2, p. 101-110, 発行日 2005-10 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0910-0865 |