| Project/Area Number |
25461342
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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 |
Metabolomics
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
今村 武史 滋賀医科大学, 医学部, 准教授 (00552093)
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| Co-Investigator(Renkei-kenkyūsha) |
IMAMURA TAKESHI 滋賀医科大学, 医学部, 准教授 (00552093)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ミトコンドリア / 糖尿病 / 骨格筋 / microRNA / 加齢 / iPS細胞 / 発現調節 / 脂肪細胞 |
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| Outline of Final Research Achievements |
Skeletal muscle fibers have metabolic and mechanical differences that allow them to be classified into different types. Each fiber contains different amount of mitochondria and different type of myosin heavy chain. It has not been well understood how muscle fiber type is regulated. Thus, the aim of this study was to explore the role of microRNA in the regulation of mitochondria. We have found that miR-494 regulates mitochondria biogenesis via TFAM and Foxj3. miR-494 expression was acutely increased and gradually reduced after induction of muscle differentiation in iPS cells. Overexpression of miR-494 decreased type 2A fiber, mitochondria rich fiber, and also attenuate oxygen consumption.
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