| Project/Area Number |
22590802
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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 | University of Tsukuba |
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Principal Investigator |
HOMMA Satoshi 筑波大学, 医学医療系, 教授 (00302422)
|
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Satoshi 筑波大学, 医学医療系, 講師 (30282362)
ISHII Tetsuro 筑波大学, 医学医療系, 教授 (20111370)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 心肥大 / 心不全 / RNAポリメラーゼII / 脱リン酸化酵素FCP1 / ＲＮＡポリメラーゼ / 脱リン酸化酵素 / アポトーシス / RNAポリメラーゼ / 遺伝子発現制御 |
|---|
| Research Abstract |
In the development of cardiac hypertrophy, the transcriptional activity of RNA polymerase II (RNAPII), which activity is increased by phosphorylation and is reduced by dephosphorylation, is augmented. It is unknown the role of phosphatase FCP1 on RNAPII in the development of heart failure. We generated the FCP1 transgenic mouse specifically overexpressing in the heart. The mice developed heart failure accompanied with the severe chamber dilatation and cardiac dysfunction, age-dependently. It implies that the impaired activity of RNAPII, especially the reduced phosphorylation of RNAPII, induces cardiac failure.
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