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The Journal of Immunology, 2001, 166: 6170-6180.
Copyright © 2001 by The American Association of Immunologists

RNA-Dependent Protein Kinase PKR Is Required for Activation of NF-{kappa}B by IFN-{gamma} in a STAT1-Independent Pathway1

Amitabha Deb, S. Jaharul Haque, Trine Mogensen2, Robert H. Silverman and Bryan R. G. Williams3

Department of Cancer Biology, The Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195

The IFN-inducible dsRNA-activated protein kinase PKR regulates protein synthesis through phosphorylation of eukaryotic initiation factor-2{alpha}. It also acts as a signal transducer for transcription factors NF-{kappa}B, IFN regulatory factor-1, and activating transcription factor-2. IFN-{gamma}, a pleiotropic cytokine, elicits gene expression by activating the Janus kinase-STAT signaling pathway. IFN-{gamma} can synergize with TNF-{alpha} to activate NF-{kappa}B in a number of cell lines. Here we show that IFN-{gamma} alone can activate NF-{kappa}B, by a Janus kinase-1-mediated, but Stat1-independent, mechanism. NF-{kappa}B activation by IFN-{gamma} is associated with degradation of I{kappa}B {beta}. The IFN-{gamma} response can be blocked by 2',5'-oligoadenylate-linked antisense chimeras against PKR mRNA. There was no activation of NF-{kappa}B by IFN in PKR-null cells, indicating that PKR is required for IFN-{gamma} signaling to NF-{kappa}B.




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