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

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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(o/o)). 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-γ 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-κB 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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Yang, Y. L., Reis, L. F. L., Paylovic, J., Aguzzi, S., Schäfer, R., Kumar, A., … Weissmann, C. (1995). Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinase. EMBO Journal, 14(24), 6095–6106. https://doi.org/10.1002/j.1460-2075.1995.tb00300.x

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