| Project/Area Number |
25670169
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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) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | リソソーム / ミトコンドリア / タンパク質分解 / オートファジー / 活性酸素種 / 酸化ストレス / 酸化タンパク質 / 品質管理機構 / ミトコンドリア品質管理 / Mieap / 品質管理 / p53 |
|---|
| Outline of Final Research Achievements |
In the present study, by performing electron microscopic and immune-electron microscopic analyses and protenase K protection assay, we confirmed that at least four lysosomal proteins (Cathepsin-B, Cathepsin-D, LAMP1 and LAMP2) are accumulated within mitochondria without destroying the mitochondrial structure in response to hypoxia in mouse embryonic fibroblasts and human normal mammary epithelial cells. Therefore, the Mieap-induced accumulation of lysosome-like organelles within mitochondria is a hypoxic-responsive physiological function in the cell, which is conserved at least from mouse to human.
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