| Project/Area Number |
15K10579
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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 |
Urology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
YOSHIDA Soichiro 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (80383280)
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| Co-Investigator(Kenkyū-buntansha) |
小野 竜一 国立医薬品食品衛生研究所, 毒性部, 室長 (10401358)
齋藤 一隆 東京医科歯科大学, 医歯(薬)学総合研究科, 助教 (10422495)
藤井 靖久 東京医科歯科大学, 医歯(薬)学総合研究科, 准教授 (70282754)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 分子シャペロン / ミトコンドリア / 尿路上皮癌 / TRAP1 |
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| Outline of Final Research Achievements |
TRAP1 (TNF receptor-associated protein), a homologue of HSP90, is mitochondrial molecular chaperone which regulates a metabolic switch between mitochondrial respiration and aerobic glycolysis. We explored the possibility that TRAP1 phosphorylation regulates its chaperone activity. We identified Y498 as a possible tyrosine phosphorylated residue, and found attenuation of c-Src mediated phosphorylation in TRAP1 with non-phosphomimetic mutation of this residue, while there was no significant difference in the ATP binding activity between the wild type, and phospho- or non-phosphomimetic mutation TRAP1.
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