Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 16 May 2006
Vol. 2006, Issue 335, p. re4
[DOI: 10.1126/stke.3352006re4]

REVIEWS

Notch and Wnt Signaling: Mimicry and Manipulation by Gamma Herpesviruses

S. Diane Hayward1*, Jianyong Liu1, and Masahiro Fujimuro2

1Viral Oncology Program, Sidney Kimmel Cancer Center, Johns Hopkins School of Medicine, 1650 Orleans Street, Baltimore, MD 21231, USA.
2Department of Biochemistry, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.

Gloss: A small number of cell signaling pathways regulate the proliferation and differentiation of cells during normal development. Two of these pathways, the Notch and Wnt pathways, are targets for virus interaction and manipulation. In general, viral gene expression and replication are intimately linked to the differentiation state of the infected cell and, in the case of the gamma herpesviruses, establishment of a lifelong persistent infection in the host depends on proliferation of an infected population of B cells. This review examines the ways in which the gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi’s sarcoma–associated herpesvirus (KSHV) have exploited the Notch and Wnt pathways to advance their own life cycles. The ways in which EBV and KSHV interact with the Notch and Wnt pathways are compared with each other and with the mechanisms and outcome of cellular Notch and Wnt signaling.

*Corresponding author. Telephone, (410) 614-0592; fax, (410) 502-6802; e-mail, dhayward{at}jhmi.edu

Citation: S. D. Hayward, J. Liu, M. Fujimuro, Notch and Wnt Signaling: Mimicry and Manipulation by Gamma Herpesviruses. Sci. STKE 2006, re4 (2006).

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Remodeling of Endothelial Adherens Junctions by Kaposi's Sarcoma-Associated Herpesvirus.
M. Mansouri, P. P. Rose, A. V. Moses, and K. Fruh (2008)
J. Virol. 82, 9615-9628
   Abstract »    Full Text »    PDF »
{beta}C1, the pathogenicity factor of TYLCCNV, interacts with AS1 to alter leaf development and suppress selective jasmonic acid responses.
J.-Y. Yang, M. Iwasaki, C. Machida, Y. Machida, X. Zhou, and N.-H. Chua (2008)
Genes & Dev. 22, 2564-2577
   Abstract »    Full Text »    PDF »
Suppression of Viral Gene Expression in Bovine Leukemia Virus-Associated B-Cell Malignancy: Interplay of Epigenetic Modifications Leading to Chromatin with a Repressive Histone Code.
M. Merimi, P. Klener, M. Szynal, Y. Cleuter, P. Kerkhofs, A. Burny, P. Martiat, and A. Van den Broeke (2007)
J. Virol. 81, 5929-5939
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882