JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JVI.01816-06v1
81/3/1511    most recent
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 Muñoz-Fontela, C.
Right arrow Articles by Rivas, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Muñoz-Fontela, C.
Right arrow Articles by Rivas, C.

 Previous Article  |  Next Article 

Journal of Virology, February 2007, p. 1511-1516, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01816-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Latent Protein LANA2 from Kaposi's Sarcoma-Associated Herpesvirus Interacts with 14-3-3 Proteins and Inhibits FOXO3a Transcription Factor{triangledown}

Cesar Muñoz-Fontela,1 Laura Marcos-Villar,1 Pedro Gallego,1 Javier Arroyo,1 Marco Da Costa,2 Karen M. Pomeranz,2 Eric W.-F. Lam,2 and Carmen Rivas1*

Microbiología II, Fac Farmacia, UCM, Madrid, Spain,1 Cancer Research-UK Laboratories and Department of Oncology, Imperial College London, London, United Kingdom2

Received 21 August 2006/ Accepted 5 November 2006

The Kaposi's sarcoma-associated herpesvirus latent protein LANA2 has been suggested to have an important role in the transforming activity of the virus based on its capacity to inhibit p53 and PKR-dependent apoptosis as well as the interferon-dependent response. Here, we describe a novel interaction between LANA2 and both the phosphoserine/phosphothreonine-binding 14-3-3 proteins and the transcription factor FOXO3a. In addition, our results indicate that LANA2 inhibits the transcriptional activity of FOXO3a and blocks the G2/M arrest induced by 14-3-3 protein overexpression. These results suggest a novel mechanism by which LANA2 may promote tumorigenesis.


* Corresponding author. Mailing address: Microbiologia II, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain. Phone: 34 91 3941746. Fax: 34 91 3941745. E-mail: mdcrivas{at}farm.ucm.es.

{triangledown} Published ahead of print on 15 November 2006.


Journal of Virology, February 2007, p. 1511-1516, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01816-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2007 by the American Society for Microbiology. All rights reserved.