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. 1995 Dec 15;14(24):6095-106.
doi: 10.1002/j.1460-2075.1995.tb00300.x.

Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinase

Y L Yang  1 , L F Reis, J Pavlovic, A Aguzzi, R Schäfer, A Kumar, B R Williams, M Aguet, C Weissmann
Affiliations

Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinase

Y L Yang et al. EMBO J. .

Abstract

Double-stranded RNA-dependent protein kinase (PKR) has been implicated in interferon (IFN) induction, antiviral response and tumor suppression. We have generated mice devoid of functional PKR (Pkr%). Although the mice are physically normal and the induction of type I IFN genes by poly(I).poly(C) (pIC) and virus is unimpaired, the antiviral response induced by IFN-gamma and pIC was diminished. However, in embryo fibroblasts from Pkr knockout mice, the induction of type I IFN as well as the activation of NF-kappa B by pIC, were strongly impaired but restored by priming with IFN. Thus, PKR is not directly essential for responses to pIC, and a pIC-responsive system independent of PKR is induced by IFN. No evidence of the tumor suppressor activity of PKR was demonstrated.

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