2011 Fiscal Year Final Research Report
Mechanism of host chromosome binding of latently infected Epstein-Barr virus episomes
| Project/Area Number |
21590523
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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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), 腫瘍ウイルス学部, 室長 (50333472)
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| Project Period (FY) |
2008 – 2011
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| Keywords | EBウイルス / 潜伏感染 / EBNA1 / リンパ芽球様細胞株 / 免疫沈降 / 質量分析 |
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| Research Abstract |
Latently-infected Epstein-Barr virus(EBV) genomes are stably maintained by attaching to host chromosomes via virally-encoded EBNA1(Epstein-Barr virus Nuclear Antigen 1) protein. We examined whether cellular p32(TAP, gC1q-R) protein, a major binding partner of EBNA1, plays any role in the chromosome binding of EBNA1.Suppression of p32 expression in EBV infected cells did not affect the chromosomal localization of EBNA1.The result argues against the possibility that p32 protein has any role in the chromosome binding of EBNA1.
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