| Project/Area Number |
20790683
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
SUZUKI Mitsuhiro University of Occupational and Environmental Health, Japan, 医学部, 講師 (00321662)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 血球細胞 / 発生・分化 / 転写調節 / タンパク質修飾 / 再生医学 / 遺伝子発現調節 |
|---|
| Research Abstract |
Transcription factor PU.1 is a hematopoietic master regulator and essential for the development of myeloid and B-cell lineages. PU.1 functions in concert with other transcription factors and cofactors. As we shown previously represented, PU.1 interact with both p300/cbp, which function as a coactivator and HDAC, which function as a corepressor. In this study, to determine whether modification of PU.1 is responsible for switching its association between coactivaor and corepressor, we examined whether acetylation regulates the physical and fnctional activities of PU.1. We found that PU.1 was acetylated in vivo and its repressor activity was reduced when the putative acetylation motif in ETS domain were mutated. Our data suggest that acetylation might regulate the biological functions in eryhroid cells.
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