Actin filament assembly during myofibrillogenesis
| Project/Area Number |
23590337
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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 (2013)
Kyushu University (2011-2012) |
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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) |
2011 – 2014
|
| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | サルコメア / アクチン / 心筋 / 筋原線維 / 発生・分化 / 細胞・組織 / 循環器 / 循環器・高血圧 |
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| Outline of Final Research Achievements |
Fhod3 is a cardiac member of the formin family proteins that play pivotal roles in actin filament assembly. In the present study, we show that Fhod3 KO mice appear normal up to embryonic day (E) 8.5, but fail to develop further and died by E11.5 with aborted development of myofibrils. These findings indicate that actin dynamics, regulated by Fhod3, participate in sarcomere organization during myofibrillogenesis and thus play a crucial role in heart development.
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Report
(4 results)
Research Products
(14 results)
