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.
|Number of pages||12|
|Journal||The EMBO Journal|
|Publication status||Published - 1 Dec 1995|
- Antiviral response
- Double-stranded RNA-dependent protein kinase
- Interferon induction
- Tumor suppression