2014 Fiscal Year Final Research Report
Molecular mechanisms for p53 inactivation by EHF in colorectal cancer.
| Project/Area Number |
25830073
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TANIUE Kenzui 東京大学, 分子細胞生物学研究所, 助教 (90648627)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Keywords | EHF / p53 / MDM2 / ユビキチン化 / FOSL1 / KMT2D |
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| Outline of Final Research Achievements |
We revealed that FOSL1 and KMT2D, a histone H3K4 methyltransferase, regulated the expressionof EHF in colorectal cancer cells. Moreover, we found that FOSL1 and KMT2D were required for the proliferation of colon cancer cells. Furthermore, we show that EHF knockdown stabilizes p53 protein. In addition, EHF interacts with and stabilizes the MDM2, a ubiquitin ligase, by interfering with its ubiquitination, which in turn destabilizes p53 protein. Finally, we identified RAD18 as a novel ubiquitinase for MDM2.
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| Free Research Field |
分子生物学
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