Contractility-dependent regulation of homeostasis in the sarcomere
| Project/Area Number |
26460371
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | University of Miyazaki |
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Principal Investigator |
Takeya Ryu 宮崎大学, 医学部, 教授 (50335981)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | アクチン / 細胞骨格 / 心臓 / サルコメア / 心筋症 / フォルミン / ミオシン / 心筋 |
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| Outline of Final Research Achievements |
Fhod3 is a cardiac member of the formin family proteins that play pivotal roles in the regulation of the actin dynamics. In the present study, we have generated conditional knock-out mice where Fhod3 is deleted at different stages, and found that Fhod3 is required for cardiac development and the maintenance of the normal cardiac function of the heart. In addition, we discovered a direct molecular link between Fhod3 and cMyBP-C, a thick myosin filament-associated protein that modulates myocardial contraction via cross-bridge arrangement. Since Fhod3 adversely affected cardiac function in the absence of cMyBP-C, the interaction appears to serve to control the Fhod3-mediated actin turnover at the cross-bridge region.
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Report
(5 results)
Research Products
(31 results)
