Article: article from journal or magazin.
Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinase.
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.
Animals, Base Sequence, Cell Transformation, Neoplastic, Cells, Cultured, DNA Primers/genetics, Encephalomyocarditis virus/pathogenicity, Gene Expression Regulation/drug effects, Interferon Type I/genetics, Interferons/pharmacology, Mice, Mice, Knockout, Molecular Sequence Data, NF-kappa B/metabolism, Poly I-C/pharmacology, Protein-Serine-Threonine Kinases/genetics, Protein-Serine-Threonine Kinases/physiology, Signal Transduction, eIF-2 Kinase
Web of science
Last modification date