| Project/Area Number |
17K19889
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Health science and related fields
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2017-06-30 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2018: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2017: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 代謝産物 / センサー / エピゲノム / インスリン / 膵β細胞 / 代謝 / 発現制御 / 内科 / 糖尿病 / 脂質 / ゲノム |
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| Outline of Final Research Achievements |
We investigated the role of CtBP2 in epigenomic transcriptional regulation mainly by focusing on pancreatic beta cells, where activation of CtBP2 opened the chromatin archtecture by changing histone modifications represented by H3K4me2, H3K4me3, H3K9, H3H27ac and H3K27me.
We further generated pancreatic beta-cell specific CtBP2 knockout mice that showed impaired insulin secretion consistent with these findings.
We are currently analyzing mice lacking the metabolite-sensing pocket in CtBP2.
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| Academic Significance and Societal Importance of the Research Achievements |
CtBP2の代謝産物センシング機構、およびそのポケット構造は代謝疾患治療薬として標的に出来ることが申請者らの研究でわかってきており、今回の研究もそれをさらに裏付けるものとなっている。
新しい機序の治療薬開発に向けた準備の意義が大きい。
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