2012 Fiscal Year Final Research Report
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 |
Section | 一般 |
Research Field |
Cell biology
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Research Institution | Nara Institute of Science and Technology |
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)
|
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)
|
Project Period (FY) |
2010 – 2012
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Keywords | 細胞増殖、オートファジー |
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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