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Genes & Dev. 24 (23): 2583-2586

Copyright © 2010 by Cold Spring Harbor Laboratory Press.


PERSPECTIVE

Herpes Simplex Virus is Akt-ing in translational control

Kara L. Norman, and Peter Sarnow1

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA

Abstract: All viruses depend on the cellular protein synthesis machinery for the production of viral proteins. Thus, viruses have evolved a variety of strategies to avoid innate host responses that inhibit protein synthesis. In this issue of Genes & Development, Chuluunbaatar and colleagues (pp. 2627–2639) demonstrate that Herpes Simplex Virus-1 counteracts this response through viral kinase Us3, which mimics cellular kinase Akt to phosphorylate and repress tuberous sclerosis complex 2 (TSC2), resulting in the activation of mammalian target of rapamycin complex 1 (mTORC1) and enhancement of mRNA translation.

Key Words: Translational control • herpesvirus replication • viral kinase • mTOR activation • Akt signaling


1 Corresponding author.

E-MAIL psarnow{at}stanford.edu; FAX (650) 498-7147.

Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.2004510.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Varicella-Zoster Virus ORF12 Protein Activates the Phosphatidylinositol 3-Kinase/Akt Pathway To Regulate Cell Cycle Progression.
X. Liu and J. I. Cohen (2013)
J. Virol. 87, 1842-1848
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Role for the Phosphatidylinositol 3-Kinase-Akt-TOR Pathway during Sindbis Virus Replication in Arthropods.
R. K. Patel and R. W. Hardy (2012)
J. Virol. 86, 3595-3604
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