| Project/Area Number |
22590803
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
|
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| Research Institution | The University of Tokyo |
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Principal Investigator |
HIROI Yukio 東京大学, 医学部附属病院, 講師 (30311624)
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| Co-Investigator(Kenkyū-buntansha) |
KOIBUCHI Nobutaka 熊本大学, 医学系大学院, 助教 (30456131)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 分子心臓病学 / Tbx5 / リン酸化 / DNA-PKcs / Ku70 / Ku80 / ANP / 転写因子 / 心筋 / 翻訳後修飾 |
|---|
| Research Abstract |
Tbx5 associates with DNA-PK complex (Ku70, KU80, and DNA-PKcs) and it is phosphorylated at Ser289 and Ser301. A DNA-PK inhibitor suppresses the activation of ANP promoter-luciferase and overexpression of either Ku70, Ku80,or DNA-PKcs increases . The mutation of S289A, S301A, and S289A/S301A decreases its ability to activate ANP promoter and synergistic effect with Nkx2-5.
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