This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cludts, I.
Right arrow Articles by Farrell, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cludts, I.
Right arrow Articles by Farrell, P. J.

 Previous Article  |  Next Article 

J Virol, March 1998, p. 1862-1869, Vol. 72, No. 3
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Multiple Functions within the Epstein-Barr Virus EBNA-3A Protein

Isabelle Cludts1 and Paul J. Farrell1,2,*

Ludwig Institute for Cancer Research1 and Virology and Cell Biology,2 Imperial College School of Medicine at St. Mary's, London W2 1PG, United Kingdom

Received 5 September 1997/Accepted 4 December 1997

Two regions of the EBNA-3A protein of Epstein-Barr virus were shown to be capable of binding to the cell protein RBP-Jk (also known as CBF-1), a component of the Notch signaling pathway. Consistent with this binding, EBNA-3A inhibited reporter gene expression from plasmids containing RBP-Jk DNA binding sites within their promoters, including the Cp promoter. When EBNA-3A was linked to a GAL4 DNA binding domain, it repressed the activity of a promoter containing GAL4 binding sites at all plasmid concentrations tested. However, a deletion mutant of EBNA-3A lacking amino acids 100 to 364 showed a biphasic response in the GAL4 assay: it inhibited transcription at low DNA concentrations but activated it at high DNA concentrations. There appears to be a gene activation function within EBNA-3A that is masked in the full-length protein in this assay. Current models for EBNA-3 function have stressed transcription repression through binding to RBP-Jk, but we consider an alternative scheme in which the role of the binding of EBNA-3A, -3B, and -3C to RBP-Jk is to buffer the levels of active EBNA-3 protein. We have also found that the behavior of EBNA-3A in a cell fractionation procedure that distinguishes insoluble matrix from soluble cell fractions is modified by EBNA-LP, indicating a further novel level of interplay between the EBNA proteins.

* Corresponding author. Mailing address: Ludwig Institute for Cancer Research, Imperial College School of Medicine at St. Mary's, Norfolk Place, London W2 1PG, United Kingdom. Phone: 44-171-724-5522. Fax: 44-171-724-8586. E-mail: p.farrell{at}ic.ac.uk.




This article has been cited by other articles:

  • Lee, S., Sakakibara, S., Maruo, S., Zhao, B., Calderwood, M. A., Holthaus, A. M., Lai, C.-Y., Takada, K., Kieff, E., Johannsen, E. (2009). Epstein-Barr Virus Nuclear Protein 3C Domains Necessary for Lymphoblastoid Cell Growth: Interaction with RBP-J{kappa} Regulates TCL1. J. Virol. 83: 12368-12377 [Abstract] [Full Text]  
  • Young, P., Anderton, E., Paschos, K., White, R., Allday, M. J. (2008). Epstein-Barr virus nuclear antigen (EBNA) 3A induces the expression of and interacts with a subset of chaperones and co-chaperones. J. Gen. Virol. 89: 866-877 [Abstract] [Full Text]  
  • Buck, M., Burgess, A., Stirzaker, R., Krauer, K., Sculley, T. (2006). Epstein-Barr virus nuclear antigen 3A contains six nuclear-localization signals.. J. Gen. Virol. 87: 2879-2884 [Abstract] [Full Text]  
  • Maruo, S., Johannsen, E., Illanes, D., Cooper, A., Zhao, B., Kieff, E. (2005). Epstein-Barr Virus Nuclear Protein 3A Domains Essential for Growth of Lymphoblasts: Transcriptional Regulation through RBP-J{kappa}/CBF1 Is Critical. J. Virol. 79: 10171-10179 [Abstract] [Full Text]  
  • Touitou, R., O'Nions, J., Heaney, J., Allday, M. J. (2005). Epstein-Barr virus EBNA3 proteins bind to the C8/{alpha}7 subunit of the 20S proteasome and are degraded by 20S proteasomes in vitro, but are very stable in latently infected B cells. J. Gen. Virol. 86: 1269-1277 [Abstract] [Full Text]  
  • Maruo, S., Johannsen, E., Illanes, D., Cooper, A., Kieff, E. (2003). Epstein-Barr Virus Nuclear Protein EBNA3A Is Critical for Maintaining Lymphoblastoid Cell Line Growth. J. Virol. 77: 10437-10447 [Abstract] [Full Text]  
  • Cooper, A., Johannsen, E., Maruo, S., Cahir-McFarland, E., Illanes, D., Davidson, D., Kieff, E. (2002). EBNA3A Association with RBP-J{kappa} Down-Regulates c-myc and Epstein-Barr Virus-Transformed Lymphoblast Growth. J. Virol. 77: 999-1010 [Abstract] [Full Text]  
  • Hickabottom, M., Parker, G. A., Freemont, P., Crook, T., Allday, M. J. (2002). Two Nonconsensus Sites in the Epstein-Barr Virus Oncoprotein EBNA3A Cooperate to Bind the Co-repressor Carboxyl-terminal-binding Protein (CtBP). J. Biol. Chem. 277: 47197-47204 [Abstract] [Full Text]  
  • Pajic, A., Polack, A., Staege, M. S., Spitkovsky, D., Baier, B., Bornkamm, G. W., Laux, G. (2001). Elevated expression of c-myc in lymphoblastoid cells does not support an Epstein-Barr virus latency III-to-I switch. J. Gen. Virol. 82: 3051-3055 [Abstract] [Full Text]  
  • Dufva, M., Olsson, M., Rymo, L. (2001). Epstein-Barr virus nuclear antigen 5 interacts with HAX-1, a possible component of the B-cell receptor signalling pathway. J. Gen. Virol. 82: 1581-1587 [Abstract] [Full Text]  
  • Pokrovskaja, K., Mattsson, K., Kashuba, E., Klein, G., Szekely, L. (2001). Proteasome inhibitor induces nucleolar translocation of Epstein-Barr virus-encoded EBNA-5. J. Gen. Virol. 82: 345-358 [Abstract] [Full Text]  
  • Dalbiès-Tran, R., Stigger-Rosser, E., Dotson, T., Sample, C. E. (2001). Amino Acids of Epstein-Barr Virus Nuclear Antigen 3A Essential for Repression of J{kappa}-Mediated Transcription and Their Evolutionary Conservation. J. Virol. 75: 90-99 [Abstract] [Full Text]  
  • Jiang, H., Cho, Y.-g., Wang, F. (2000). Structural, Functional, and Genetic Comparisons of Epstein-Barr Virus Nuclear Antigen 3A, 3B, and 3C Homologues Encoded by the Rhesus Lymphocryptovirus. J. Virol. 74: 5921-5932 [Abstract] [Full Text]  
  • Spender, L. C., Cannell, E. J., Hollyoake, M., Wensing, B., Gawn, J. M., Brimmell, M., Packham, G., Farrell, P. J. (1999). Control of Cell Cycle Entry and Apoptosis in B Lymphocytes Infected by Epstein-Barr Virus. J. Virol. 73: 4678-4688 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»