| Project/Area Number |
23659178
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | National Cancer Center Japan |
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Principal Investigator |
ARAKAWA Hirofumi 独立行政法人国立がん研究センター, 研究所, 分野長 (70313088)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | ミトコンドリア / 品質管理 / 酸化ストレス / 活性酸素種 / リソソーム / 発がん / p53 / がん抑制 / タンパク質分解 / 酸化タンパク質 |
|---|
| Research Abstract |
In this study, we obtained several important findings on the mechanism for induction of the intramitochondrial lysosome. First, BNIP3 and NIX, two mitochondrial outer membrane proteins, play a pivotal role in induction of the intramitochondrial lysosome. The interaction of Mieap, BNIP3 and NIX at mitochondrial outer membrane induces the opening of a pore in the mitochondrial double membrane. Surprisingly, this is completely unrelated to cell death. Second, 14-3-3gamma interacts with Mieap and is translocated into mitochondria. Intramitochondrial 14-3-3gamma plays a critical role in the elimination of oxidized mitochondrial proteins. These results suggest that the opening of a pore in the mitochondrial double membrane and an adaptor protein are very substantial in the mechanism for the intramitochondrial lysosome.
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