Analyses of cross talk between cell proliferation and autophagyregulated by the MLF1-CSN-COP1-p53 pathway
| Project/Area Number |
22570186
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
KATO Noriko 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (10252785)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Jun-ya 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (00273839)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 細胞増殖、オートファジー / 細胞増殖 / オートファジー |
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| Research Abstract |
We analyzed cross talk between cell cycle inhibition and autophagy through a leukemia-associated MLF1-CSN-COP1-p53 pathway, in which the center regulator is the E3 ubiquitin ligase COP1. We found that COP1 markedly inhibits DNA damage-induced (UV irradiation) autophagy leading to tumorigenesis and interacts with FIP200, an autophagy-promoting factor. These data suggest that the MLF1-CSN-COP1-p53 pathway contributes to tumorigenesis by controlling the regulation between cell cycle and autophagy.
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Report
(4 results)
Research Products
(24 results)
