| Project/Area Number |
25860221
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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 |
General medical chemistry
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| Research Institution | Takasaki University of Health and Welfare |
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Principal Investigator |
OHMORI Shin'ya 高崎健康福祉大学, 薬学部, 助手 (10509194)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 転写因子 / Gata2 / Cebpa / 細胞分化 / マスト細胞 / 脱分化 / 分化転換 / 生体分子医学 / GATA2 / BMMC / 形質転換 |
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| Outline of Final Research Achievements |
To clarify roles GATA2 plays in the BMMCs, the DNA binding C-finger domain of GATA2 was genetically disrupted by Cre-LoxP system in BMMCs (G2ΔCF-BMMCs). We found that deletion of GATA2 CF results in a loss of mast cell identity of BMMCs, whereas the expression of Mac1- and/or Ly-6C/G-positive cells was significantly increased in G2ΔCF-BMMCs. Furthermore, GATA2 ablation led to a significant upregulation of C/EBPα, a key player of myeloid cell differentiation, and forced expression of C/EBPα in wild-type BMMCs phenocopied the GATA2ΔCF cells. Our findings suggest that the repression of Cebpa by GATA2 is essential for maintaining mast cell identity in BMMCs.
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