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Sci. STKE, 3 July 2001
Vol. 2001, Issue 89, p. re1
[DOI: 10.1126/stke.2001.89.re1]

REVIEWS

PACT and PKR: Turning on NF-{kappa}B in the Absence of Virus

Fulvio D'Acquisto and Sankar Ghosh

The authors are in the Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA. E-mail: sankar.ghosh{at}yale.edu

Gloss: Viral infections are one of the major causes of morbidity and mortality in humans. Insufficient knowledge of host-virus interrelationships has in general prevented the development of effective antiviral therapies. Therefore, greater understanding of the responses evoked by viruses will be necessary for developing effective strategies to block viral infections. A cellular enzyme, double-stranded RNA (dsRNA)-dependent protein kinase (PKR), plays an important role as a sensor of viral infection by responding to double-stranded RNA: a specific intermediate in the life cycle of many viruses. However, recent studies have revealed that PKR might also function in normal cellular physiology and that a protein named PACT (PKR-activating protein) may play a key role in regulating the virus-independent activation of PKR. We discuss the roles of PACT and PKR in cellular function.

Citation: F. D'Acquisto, S. Ghosh, PACT and PKR: Turning on NF-{kappa}B in the Absence of Virus. Sci. STKE 2001, re1 (2001).

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Suppression of PACT-Induced Type I Interferon Production by Herpes Simplex Virus 1 Us11 Protein.
C. Kew, P.-Y. Lui, C.-P. Chan, X. Liu, S. W. N. Au, I. Mohr, D.-Y. Jin, and K.-H. Kok (2013)
J. Virol. 87, 13141-13149
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