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Deficient signaling in mice devoid of double‐stranded RNA‐dependent protein kinase.
Author(s) -
Yang Y. L.,
Reis L. F.,
Pavlovic J.,
Aguzzi A.,
Schäfer R.,
Kumar A.,
Williams B. R.,
Aguet M.,
Weissmann C.
Publication year - 1995
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1995.tb00300.x
Subject(s) - combinatorics , biology , physics , humanities , philosophy , mathematics
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.