Suppression of INK4a/ARF expression by EBV protein EBNA3C
Project/Area Number |
20590464
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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 |
Virology
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Research Institution | Hokkaido University |
Principal Investigator |
MARUO Seiji Hokkaido University, 遺伝子病制御研究所, 准教授 (70292018)
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Project Period (FY) |
2008 – 2010
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Project Status |
Completed (Fiscal Year 2010)
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Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | EBウイルス / 形質転換 / 不死化 / がん抑制遺伝子 / エピジェネティクス / INK4a/ARF / EBNA3C / EBNA3A / RBP-Jκ / 癌抑制遺伝子 / INK4a / ARF / ヒストン修飾 |
Research Abstract |
In this study, the mechanism underlying EBNA3C suppression of the INK4a/ARF expression was analyzed. We clarified that (1) EBNA3C does not influence the DNA methylation status of the INK4a/ARF promoters. (2) EBNA3C changes histone modifications of the p16 (INK4a) locus from active state to silent state. (3) EBNA3C association with RBP-Jkappa is essential for EBNA3C to function. These results suggest that EBNA3C regulates epigenetic histone modifications of the INK4a/ARF locus.
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Report
(4 results)
Research Products
(25 results)
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[Journal Article] Epstein-Barr virus nuclear antigen 3C regulated genes in lymphoblastoid cell lines.2011
Author(s)
Zhao B, Mar JC, Maruo S, Lee S, Gewurz BE, Johannsen E, Holton K, Rubio R, Takada K, Quackenbush J, Kieff E.
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Journal Title
Proc Natl Acad Sci USA. 108
Pages: 337-342
Related Report
Peer Reviewed
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