| Project/Area Number |
23790341
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
OGURA Masato 福島県立医科大学, 医学部, 助教 (10548978)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | シグナル伝達 / プロテオーム / チロシンキナーゼ / ミトコンドリア / エネルギー代謝 / 活性酸素種 / 電子伝達系 / 複合体 |
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| Research Abstract |
Non-receptor-type tyrosine kinase c-Src is implicated in fundamental cellular functions including proliferation, differentiation and survival. Recent studies have suggested that c-Src is also present in mitochondria and involved in the regulatory mechanisms of mitochondrial energy production. Here we have identified novel interaction proteins with c-Src in mitochondria, and investigated their function in the regulation of c-Src kinase activity. Serum starvation exhibits significant reductions of respiration and mitochondrial c-Src activity, and an enhancement of reactive oxygen species production in human T98G cells. Proteome analysis reveals mitochondrial c-Srcinteraction proteins including ATP5A1 of respiratory complex V. Overexpression of ATP5A1 in cells exhibits a significant increase in c-Src kinase activity and respiration in mitochondria. These results suggest that ATP5A1 regulates c-Src kinase activity by its interaction with c-Src complex in mitochondria, and that their interaction is essential for cellular respiration.
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