| Project/Area Number |
17K11617
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
MATSUO Yuki 長崎大学, 医歯薬学総合研究科(歯学系), 技術職員 (40792601)
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| Co-Investigator(Kenkyū-buntansha) |
小守 壽文 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (00252677)
宮崎 敏博 長崎大学, 医歯薬学総合研究科(歯学系), 准教授 (10174161)
森石 武史 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (20380983)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | Supt3 / Runx2 / 造血 / 骨形成 / 胎生致死 / 間葉系幹細胞 / 間葉系細胞 / 発生・分化 / 転写活性 / 細胞・組織 / 基礎歯学 |
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| Outline of Final Research Achievements |
Supt3 is a component of the SPT-TAF9-GCN5 acetyltransferase complex having histone acetyltransferase activity. Runx2 is the transcription for osteoblast differentiation and latter term of chondrocyte differentiation, and expression is controlled in two promoters of distal (P1) and proximal (P2). Promoter of Supt3 and Exon 1, 2 are located between P1 and P2 promoter of Runx2 and are reported when Supt3 and Runx2 interact and regulate expression of Runx2. The Supt3 knockout (KO) mice became embryonic lethal at 10.5days and were extremely dwarfed. Furthermore, in the Supt3 KO mice, cell proliferation was decreased and apoptosis was enhanced.
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| Academic Significance and Societal Importance of the Research Achievements |
Supt3の生理的機能を明らかにすることは、転写制御機構の解明に大きく貢献する。また、骨形成に必須の転写因子であるRunx2およびSupt3プロモーターの相互作用が、Runx2の発現及び骨格形成にどのような作用を発揮するか明らかにできれば、骨粗鬆症および変形性関節症の治療薬開発に大きく寄与する。
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