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KAKEN_25461560seika.pdf
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Title |
Title |
ヒストンメチル化機構の異常が神経幹細胞の細胞分裂動態に与える影響に関する研究
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Kana |
ヒストン メチルカ キコウ ノ イジョウ ガ シンケイ カンサイボウ ノ サイボウ ブンレツ ドウタイ ニ アタエル エイキョウ ニ カンスル ケンキュウ
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Hisuton mechiruka kiko no ijo ga shinkei kansaibo no saibo bunretsu dotai ni ataeru eikyo ni kansuru kenkyu
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Effects of abnormal histone methylation on cell cycle kinetics of neuronal progenitor cells
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三橋, 隆行
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ミツハシ, タカユキ
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Mitsuhashi, Takayuki
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慶應義塾大学・医学部・講師
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Research team head
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科研費研究者番号 : 80338110
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小崎, 健次郎
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コサキ, ケンジロウ
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Kosaki, Kenjiro
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慶應義塾大学・医学部・教授
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Research team member
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科研費研究者番号 : 30234743
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高橋, 孝雄
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タカハシ, タカオ
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Takahashi, Takao
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慶應義塾大学・医学部・教授
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Research team member
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科研費研究者番号 : 80171495
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2016
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科学研究費補助金研究成果報告書
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2015
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本研究では過成長をきたす先天奇形症候群の原因について, 大脳皮質を形成する神経幹細胞の細胞分裂動態を中心に解析しようと試みた。具体的には, Sotos症候群の原因遺伝子NSD1蛋白の発現量を神経幹細胞でのみ減少可能な遺伝子改変マウスを作成しようとしたが, 実施期間中に完成させることができなかった。今後, ゲノム編集技術など別の方法を用いて遺伝子改変マウスを作成する計画を進めている。
A purpose of this research is to elucidate potential roles of histone methylation on cell cycle kinetics of neuronal progenitor cells. In detail, we have attempted to generate transgenic mice that would be capable of decreasing expression level of NSD1 protein, a causative protein for overgrowth syndrome Sotos syndrome, by applying RNA interference (RNAi) strategy in vivo. However, we were unable to obtain functional transgenic mouse lines during the research period, suggesting that RNAi might not be the appropriate method to generate the mice. We are planning to generate transgenic mouse lines using genome editing technique.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2013~2015
課題番号 : 25461560
研究分野 : 医歯薬学
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