| Project/Area Number |
26860860
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Osama Woman's and Children's Hospital |
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Principal Investigator |
Tsume Mami 地方独立行政法人大阪府立病院機構大阪母子医療センター(研究所), 病因病態部門, 研究技術員 (70711026)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | ヒストンアセチル化 / BETファミリータンパク質 / 幹細胞 / マウス / 転写 / ヒストンアセチル化修飾 / 転写制御 / RNAポリメラーゼII / 胚盤胞 / Nanog / Oct3/4 / ブロモドメイン / 神経細胞 / 細胞分化制御 |
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| Outline of Final Research Achievements |
During mammalian early neurogenesis, neural stem/progenitor cells proliferate by self-renewal and differentiate into neurons in a developmental-stage dependent manner, but the roles of histone acetylation in maintenance of stemness and neurogenesis remain unclear. In this study, I analyzed roles of BET family proteins (BET), which specifically bind to lysine residues of acetylated histone H4 through their bromodomains and regulate transcription. I found that BET binding acetylated histones such as H4K5ac and H4K12ac were up-regulated in S-phase of neural progenitor cells specifically. By exploiting a BET inhibitor that blocks the binding to acetylated histones, I also identified that BET is required for the transcription of genes involved in maintenance of stem cells.
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