Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinase

被引：566
作者：
Yang, YL
Reis, LFL
Pavlovic, J
Aguzzi, A
Schafer, R
Kumar, A
Williams, BRG
Aguet, M
Weissmann, C
机构：
[1] UNIV ZURICH, INST MOLEK BIOL 1, CH-8093 ZURICH, SWITZERLAND
[2] UNIV ZURICH, INST MED VIROL, CH-8028 ZURICH, SWITZERLAND
[3] UNIV SPITAL ZURICH, INST NEUROPATHOL, CH-8091 ZURICH, SWITZERLAND
[4] UNIV SPITAL ZURICH, DEPT PATHOL, KREBSFORSCH ABT, CH-8091 ZURICH, SWITZERLAND
[5] CLEVELAND CLIN FDN, DEPT CANC BIOL, CLEVELAND, OH 44195 USA
来源：
EMBO JOURNAL | 1995年 / 14卷 / 24期
关键词：
antiviral response; double-stranded; RNA-dependent protein kinase; interferon induction; tumor suppression;
D O I：
10.1002/j.1460-2075.1995.tb00300.x
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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-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.
引用
收藏
页码：6095 / 6106
页数：12
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