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    Proc Natl Acad Sci U S A. 2004 May 25;101(21):7994-8. Epub 2004 May 17.

    Inhibitor of kappaB kinase is required to activate a subset of interferon gamma-stimulated genes.

    Sizemore N, Agarwal A, Das K, Lerner N, Sulak M, Rani S, Ransohoff R, Shultz D, Stark GR.

    Source

    Departments of Cancer Biology, Neurosciences, and Molecular Biology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

    Abstract

    IkappaB kinase (IKK), discovered as the major activator of NF-kappaB, plays additional roles in signaling. By using mouse embryo fibroblasts (MEFs) lacking both the alpha and beta subunits of IKK, we find that these proteins are required for induction of a major subset of IFNgamma-stimulated genes and that this requirement is independent of NF-kappaB activation. Furthermore, there is no defect in IFNgamma-stimulated signal transducer and activator of transcription 1 (Stat1) activation or function in the IKKalpha/beta-null MEFs. Therefore, although activated Stat1 dimers are necessary for the activation of these genes in response to IFNgamma, they are not sufficient. These results reveal an important additional pathway for IFNgamma-stimulated gene expression in which an NF-kappaB-independent function of IKK is required.

    PMID:
    15148408
    [PubMed - indexed for MEDLINE]
    PMCID: PMC419545
    Free PMC Article

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