| Project/Area Number |
26460378
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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 | Kumamoto Health Science University |
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Principal Investigator |
Masato Yano 熊本保健科学大学, 保健科学部, 教授 (60315299)
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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 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ミトコンドリア / ストレス / ABCB10 / TMEM65 / ストレス応答 / 酸化ストレス / トランスポーター / 膜タンパク質 / シグナル伝達 |
|---|
| Outline of Final Research Achievements |
When abnormal proteins accumulate in mitochondria, the mitochondrial stress signaling pathway is activated, and the signal is transmitted from the mitochondria to the nucleus. Then, the mitochondrial unfolded protein response (UPR), which induces the expression of nuclear-encoded mitochondrial molecular chaperones and proteases, is activated. In this study, to elucidate the mitochondrial stress signaling pathway in mammals, the function of candidate factors, such as ABCB10, in this pathway was analyzed. As a result, depletion of ABCB10 reduced the mitochondrial UPR, suggesting that ABCB10 is involved in the mitochondrial stress signaling pathway.
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