Chromosome tethering mechanism of latently infected Epstein-Barr virus genome
| Project/Area Number |
24590567
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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 |
Virology
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| Research Institution | Aichi Cancer Center Research Institute |
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Principal Investigator |
KANDA Teru 愛知県がんセンター(研究所), 感染腫瘍学部, 室長 (50333472)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | EBウイルス / 染色体 / 潜伏感染 / 蛍光蛋白質 / マイクロRNA / EBNA1 / ヌクレオソーム |
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| Outline of Final Research Achievements |
Epstein-Barr virus (EBV) genome is stably maintained in EBV-infected cells. EBV genomes are maintained as circular double-stranded DNA molecules without being integrated into cellular chromosomes. Our study revealed a molecular mechanism by which viral protein EBNA1, a key molecule required for the chromosome tethering of viral genomes, localizes onto host chromosomes. Furthermore, out study demonstrated that EBV-encoded microRNAs strongly suppress the expression of a cellular gene NDRG1, which is specifically expressed in epithelial cells. These results should contribute to further understand the mechanisms of EBV latent infection and viral carcinogenesis.
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Report
(4 results)
Research Products
(16 results)
