A novel role of Jmjd5, a candidate cancer-related gene, during mouse embryogenesis
| Project/Area Number |
25460266
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 遺伝子 / 発生・分化 / 細胞増殖 / がん / 発現制御 / 癌 |
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| Outline of Final Research Achievements |
We previously identified Jmjd5 as a candidate cancer-related gene by retroviral mutagenesis. Jmjd5 belongs to Jumonji C (JmjC) family, some of which encode histone demethylase. Our genetic studies using Jmjd5 deficient mice showed that Jmjd5 was a regulator for Cdkn1a expression during mouse embryogenesis. In this study, we found that a subset of p53-regulated genes highly expressed in Jmjd5 knockout embryos. We also showed that Jmjd5 protein could directly associate with p53 protein, one of the most famous tumor suppressor genes, and inhibited the recruitment of endogenous p53 protein at several p53 target loci such as Cdkn1a. Pmaip1 and Mdm2. In general, aberrant activation of p53 signaling leads to embryonic lethality, suggesting that maintaining a fine balance of p53 translational level is important for normal development. Thus, Jmjd5 may keep basal level of p53 signaling in embryonic cells through the control of p53 recruitment at its target genes.
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Report
(4 results)
Research Products
(13 results)
