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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4433-4439. Prepublished online as a Blood First Edition Paper on January 26, 2006; DOI 10.1182/blood-2005-09-3815. This Article Full Text (PDF) All Versions of this Article: 2005-09-3815v1 107/11/4433    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mohan, J. Articles by Tolnay, M. Search for Related Content PubMed PubMed Citation Articles by Mohan, J. Articles by Tolnay, M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 23, 2005 Accepted January 19, 2006 Epstein-Barr virus nuclear antigen 2 induces FcRH5 expression through CBF1 Joanne Mohan, Jessica Dement-Brown, Sabine Maier, Tomoko Ise, Bettina Kempkes, and Mate Tolnay* Division of Monoclonal Antibodies, Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, MD, USA Institute of Clinical Molecular Biology, GSF National Research Center for Environment and Health, Munich, Germany Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA * Corresponding author; email: mate.tolnay{at}fda.hhs.gov. Fc-receptor homolog 5 (FcRH5) is a recently identified B cell membrane protein of unknown function. In Burkitt's lymphoma cell lines with chromosome 1q21 abnormalities FcRH5 expression is deregulated, implicating FcRH5 in lymphomagenesis. Epstein-Barr virus infects and immortalizes B cells, and is implicated in the etiology of several tumors of B cell origin. Overexpression of genes located on 1q21-25 has been proposed as a surrogate for Epstein-Barr virus in Burkitt's lymphoma. We now report that Epstein-Barr virus nuclear antigen 2 (EBNA2) markedly induces the expression of the FcRH5 gene, encoded on chromosome 1q21. Induction occurred in the absence of other viral proteins and did not require de novo protein synthesis. EBNA2 lacks a DNA binding domain and can target responsive genes through the host DNA binding protein CBF1. We show that induction of FcRH5 by EBNA2 is strictly CBF1 dependent, as it was abolished in CBF1 deficient cells. Accordingly, EBNA2 targeted CBF1 binding sites present in the FcRH5 promoter in vivo, as detected by chromatin immunoprecipitation. These results identify FcRH5 as a novel, direct target of EBNA2 that may contribute to the development of Epstein-Barr virus associated tumors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. L. Haga, G. R. A. Ehrhardt, R. J. Boohaker, R. S. Davis, and M. D. Cooper Fc receptor-like 5 inhibits B cell activation via SHP-1 tyrosine phosphatase recruitment PNAS, June 5, 2007; 104(23): 9770 - 9775. [Abstract] [Full Text] [PDF] S. Maier, G. Staffler, A. Hartmann, J. Hock, K. Henning, K. Grabusic, R. Mailhammer, R. Hoffmann, M. Wilmanns, R. Lang, et al. Cellular Target Genes of Epstein-Barr Virus Nuclear Antigen 2 J. Virol., October 1, 2006; 80(19): 9761 - 9771. [Abstract] [Full Text] [PDF]

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