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B by IFN-
in a STAT1-Independent Pathway1
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
. It also acts as a signal transducer for transcription
factors NF-
B, IFN regulatory factor-1, and activating transcription
factor-2. IFN-
, a pleiotropic cytokine, elicits gene
expression by activating the Janus kinase-STAT signaling pathway.
IFN- can synergize with TNF- to activate NF-B in a number of
cell lines. Here we show that IFN- alone can activate NF-B, by a
Janus kinase-1-mediated, but Stat1-independent, mechanism. NF-B
activation by IFN- is associated with degradation of IB 
. The
IFN- response can be blocked by 2',5'-oligoadenylate-linked
antisense chimeras against PKR mRNA. There was no activation of NF-B
by IFN in PKR-null cells, indicating that PKR is required for IFN-
signaling to NF-B.
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