Yang, Y. L.Reis, L. F.Pavlovic, J.Aguzzi, A.Schafer, R.Kumar, A.Williams, B. R.Aguet, M.Weissmann, C.2007-12-122007-12-122007-12-12199510.1002/j.1460-2075.1995.tb00300.xhttps://infoscience.epfl.ch/handle/20.500.14299/15470Double-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.text::journal::journal article::research article