| Project/Area Number |
26462392
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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 |
Urology
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
篠原 信雄 北海道大学, 医学研究科, 教授 (90250422)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | ユビキチン / 前立腺癌 |
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| Outline of Final Research Achievements |
We previously found that the putative E3 ubiquitin ligase TRIM68, which is preferentially expressed in prostate cancer cells, interacts with the AR (androgen receptor) and enhances transcriptional activity of the AR in the presence of androgen. We also found that TRIM68 functionally interacts with TIP60 and p300, which act as coactivators of the AR, and synergizes in transactivation of the AR.
To reveal how the ubiquitination contribute to the AR function, we used molecular biology approaches such as immunoprecipitation assay, western blotting and Ubiquitination assay.Using several AR co-repressors and TRIM68 specific antibody, we performed immunoprecipitation and ubiquitination assay to identify the substrate of TRIM68 ubiquitin ligase. Unfortunately, we could not identify it, but these results indicate that TRIM68 functions as a cofactor for AR-mediated transcription and is likely to be a novel diagnostic tool and a potentially therapeutic target for prostate cancer.
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