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Functional analysis of EBNA1 protein by using a recombinant EBV with gene replacement

Research Project

Project/Area Number14570258
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Virology
Research InstitutionHOKKAIDO UNIVERSITY

Principal Investigator

KANDA Teru  Hokkaido Univ., Inst. for Genetic Med., Lec., 遺伝子病制御研究所, 助手 (50333472)

Project Period (FY) 2002 – 2003
Project Status Completed(Fiscal Year 2003)
Budget Amount *help
¥4,000,000 (Direct Cost : ¥4,000,000)
Fiscal Year 2003 : ¥1,900,000 (Direct Cost : ¥1,900,000)
Fiscal Year 2002 : ¥2,100,000 (Direct Cost : ¥2,100,000)
KeywordsEB virus / latent infection / EBNA1 / gene replacement / transcriptional regulation / bacterial artificial chromosome / EBウィルス / ターゲッティング / 大腸菌 / 人工染色体 / Bリンパ球
Research Abstract

EBNA1 protein, a viral protein encoded by Epstein-Barr virus (EBY), is a multi-functional protein. It is well known to be essential for the replication and segregation of EBV episomes in latently-infected cells, and it also regulates viral gene expression as a transcriptional activator. We generated a recombinant EBV, designated HMG1-EBNA1 knock-in EBV, in which the EBNA1 gene is replaced with a HMGI-EBNA1 chimeilc gene. The HMG1-EBNA1 chimeric gene encodes an EBNA1 mutant with greatly-impaired transcriptional activity, while keeping the ability of EBNA1 to episomally riiaintain EBV based plasmids. Akata cells harboring wild-type EBV and HMG1-EBNA1 knock-in virus were established. The mixture of wild-type EBV and HMGI-EBNA1 knock-in EBV Was used to infect: EBV-negative Akata cells and cord blood lymphocytes. We found that HMG1-EBNA1 knock-in virus was maintained as episomes in Akata cells. By contrast, the analyses of BACmids that had been rescued from the established lymphoblastoid cell lines revealed that the HMG1-EBNA1. chimeric gene was frequently replaced with the wild-type EBNA1 gene, presumably due to the recombination between HMGI-EBNA1 knock-in EBY and wild-type EBV. These results strongly suggest that the regulation of viral gene expression by EBNA1 as a transactivator is critical, for EBV-induced B cell growth transformation.

Report

(3results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report

Research Products

(5results)

All Other

All Publications

  • [Publications] Teru Kanda: "Production of high-titer Epstein-Barr virus recombinants derived from Akata cells by using a bacterial artificial chromosome system"Journal of Virology. 78. 7004-7015 (2004)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] 神田 輝: "EBウイルス(基礎・第4章)"診断と治療社. 8 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Yajima, M., Ahsan, N., Tanaka, M., Takada, K.: "Production of high-titer Epstein-Barr virus recombinants derived from Akata cells by using a bacterial artificial chromosome system"J.Virol.. 78(13). 7004-7015 (2004)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Teru Kanda: "Production of high-titer EBV recombinants derived from Akata cells using a bacterial artificial chromosome system"J.Virol.. (in press). (2004)

    • Related Report
      2003 Annual Research Report
  • [Publications] 神田 輝: "EBウイルス(基礎・第4章)"診断と治療社. 8 (2003)

    • Related Report
      2003 Annual Research Report

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Published : 2002-04-01   Modified : 2016-04-21  

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