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新規放射線応答遺伝子ASPMの生物学的研究

https://repo.qst.go.jp/records/64488
https://repo.qst.go.jp/records/64488
797bb511-4ef5-4093-81fa-1abb2c13197e
Item type 会議発表用資料 / Presentation(1)
公開日 2012-01-31
タイトル
タイトル 新規放射線応答遺伝子ASPMの生物学的研究
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_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 藤森, 亮

× 藤森, 亮

WEKO 635700

藤森, 亮

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その他

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WEKO 635701

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藤森 亮

× 藤森 亮

WEKO 635702

en 藤森 亮

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内容記述タイプ Abstract
内容記述 We previously found that ionizing radiation (IR) commonly suppresses expression of ASPM gene, which are found mutated in a majority of human patients of familiar microcephaly (MCPH5). In pregnant mice, sub-lethal doses of IR drastically reduced the protein level of Aspm in their developing embryos, particularly in the neural stem cells that express nestins. To further investigating a cause of microcephaly, we developed a knock-out system where disruption of the Aspm gene can be controlled through Cre-loxP recombination systems. Aspm null homozygotes are obtained by mating Aspm +/- parental mice following Mendellian rule. They grew apparently healthy but had significantly small brains (85% in weight) and testes (20% in weight) compared to +/+ and +/- animals. HE staining has detected no pathological abnormality in the affected brains but loss of spermatogenesis in most seminiferous tubule. Next we destroyed the floxed Aspm genes selectively in CNS by introducing Cre expression under the murine Nestin gene promotors. A similar defect in the brain size was obtained in the homozygote animals of the floxed alleles only when Nes-Cre transgenes were inherited, while no testes were affected. Our results suggested that any synthetic suppression of Aspm can cause microcephaly phenotypes only if nestin expressing tissues are targeted during the CNS development.
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 第34回日本分子生物学会年会
発表年月日
日付 2011-12-16
日付タイプ Issued
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