Epstein-Barr Virus EBNA-3C Is Targeted to and Regulates Expression from the Bidirectional LMP-1/2B Promoter

Jiménez-Ramírez, Carmilia, Brooks, Andrew J., Forshell, Linus Plym, Yakimchuk, Konstantin, Zhao, Bo, Fulgham, Tacha Zi and Sample, Clare E. (2006) Epstein-Barr Virus EBNA-3C Is Targeted to and Regulates Expression from the Bidirectional LMP-1/2B Promoter. Journal of Virology, 80 22: 11200-11208. doi:10.1128/JVI.00897-06

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Author Jiménez-Ramírez, Carmilia
Brooks, Andrew J.
Forshell, Linus Plym
Yakimchuk, Konstantin
Zhao, Bo
Fulgham, Tacha Zi
Sample, Clare E.
Title Epstein-Barr Virus EBNA-3C Is Targeted to and Regulates Expression from the Bidirectional LMP-1/2B Promoter
Journal name Journal of Virology   Check publisher's open access policy
ISSN 0022-538X
Publication date 2006-11-01
Year available 2006
Sub-type Article (original research)
DOI 10.1128/JVI.00897-06
Open Access Status File (Publisher version)
Volume 80
Issue 22
Start page 11200
End page 11208
Total pages 9
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Subject 111201 Cancer Cell Biology
110804 Medical Virology
060111 Signal Transduction
060506 Virology
Abstract pstein-Barr virus (EBV) nuclear antigen 3C (EBNA-3C) is essential for EBV-mediated immortalization of human B lymphocytes and regulates both the cell cycle and transcription. Transient reporter gene assays have implicated a pivotal role for EBNA-3C in the regulation of transcription of the majority of latency-associated genes expressed during the EBV growth program, including the viral oncoprotein LMP-1. To examine the regulation of latency gene expression by EBNA-3C, we generated an EBV-positive cell line that inducibly expresses EBNA-3C. This cell line allowed us to examine expression from the endogenous latency gene promoters in the context of an actual latent infection and the presence of other EBNA proteins, in particular EBNA-2, which is presumed to coregulate transcription with EBNA-3C. EBNA-3C induced the expression of both LMP-1 and LMP-2B mRNAs from the bidirectional LMP-1/LMP-2B promoter. In contrast, no effect was seen on expression from the common EBNA promoter Cp, which is responsive to EBNA-3C in reporter assays. Activation of LMP expression was not the consequence of increases in EBNA-2, PU.1 or Spi-B transcription factors, all of which are believed to be critical for activation of LMP-1. Chromatin immunoprecipitation assays furthermore indicated that EBNA-3C is present at the bidirectional LMP-1/LMP-2B promoter. These results indicate that EBNA-3C directly activates the expression of LMP-1 and LMP-2B but is unlikely to significantly regulate EBNA expression via Cp under normal growth conditions.
Keyword Virology
Q-Index Code C1
Grant ID CA21765
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
Institute for Molecular Bioscience - Publications
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Citation counts: TR Web of Science Citation Count  Cited 17 times in Thomson Reuters Web of Science Article | Citations
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Created: Fri, 30 Jan 2009, 21:41:50 EST by Marianne Steentsma on behalf of Institute for Molecular Bioscience