The molecular mechanism focused on calcium in pathogenesis of heart failure and its clinical application.
| Project/Area Number |
21790723
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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 |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
TAKEDA Toshihiro Osaka University, 医学部附属病院, 医員 (70506493)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 分子心臓病態学 / カルシウム / 興奮収縮連関 / ノックアウトマウス / 循環器・高血圧 / 蛋白質 / 動物 / 心筋細胞 |
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| Research Abstract |
In the heart, calcium plays important roles in excitation-contraction (E-C) coupling. SERCA2a and ryanodine receptor (RyR2) are two major Ca^<2+> signaling proteins involving in E-C coupling. The activity of these proteins is regulated by their accessory proteins, which may play an important role in the pathogenesis of heart failure. Sorcin is the one of the protein that is associated with RyR2
The expression level of sorcin was altered in remodeling hearts. In order to elucidate a role of sorcin in the heart, we generated sorcin knockout mice. The mice showed no abnormal E-C coupling.
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Report
(3 results)
Research Products
(11 results)
