A Role for NF- Bi n the Induction of -R1 by Interferon-*

Previous experiments have suggested that inductionof the -R1 gene by interferon (IFN)- required tran-scription factor ISGF-3 (IFN-stimulated gene factor-3)and an additional component. We now provide evidencethat nuclear factor- B (NF- B) can serve as this compo-nent. Site-directed mutagenesis of an NF- B binding sitein the -R1 promoter or over-expression of an I Bsuper-repressor abrogated IFN- -mediated inductionof a -R1 promoter-reporter. IFN- treatment did notaugment abundance of NF- B but did lead to phospho-rylation of the p65 NF- B subunit. It is proposed thatIFN- -mediated enhancement of the transactivationcompetence of NF- B components is required for induc-ible transcription of the -R1 promoter. These resultsprovide a novel insight into the role of NF- Binthetranscriptional response to IFN- .