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.
Original language | English |
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Pages (from-to) | 6095-6106 |
Number of pages | 12 |
Journal | The EMBO Journal |
Volume | 14 |
Issue number | 24 |
Publication status | Published - 1 Dec 1995 |
Externally published | Yes |
Keywords
- Antiviral response
- Double-stranded RNA-dependent protein kinase
- Interferon induction
- Tumor suppression