KAP1 regulates type I interferon/STAT1-mediated IRF-1 gene expression

Shinya Kamitani, Norihiko Ohbayashi, Osamu Ikeda, Sumihito Togi, Ryuta Muromoto, Yuichi Sekine, Kazuhide Ohta, Hironobu Ishiyama, Tadashi Matsuda

    Research output: Contribution to journalArticlepeer-review

    24 Citations (Scopus)


    Signal transducers and activators of transcription (STATs) mediate cell proliferation, differentiation, and survival in immune responses, hematopoiesis, neurogenesis, and other biological processes. Recently, we showed that KAP1 is a novel STAT-binding partner that regulates STAT3-mediated transactivation. KAP1 is a universal co-repressor protein for the KRAB zinc finger protein superfamily of transcriptional repressors. In this study, we found KAP1-dependent repression of interferon (IFN)/STAT1-mediated signaling. We also demonstrated that endogenous KAP1 associates with endogenous STAT1 in vivo. Importantly, a small-interfering RNA-mediated reduction in KAP1 expression enhanced IFN-induced STAT1-dependent IRF-1 gene expression. These results indicate that KAP1 may act as an endogenous regulator of the IFN/STAT1 signaling pathway.

    Original languageEnglish
    Pages (from-to)366-370
    Number of pages5
    JournalBiochemical and biophysical research communications
    Issue number2
    Publication statusPublished - 2008 May 30


    • IFN
    • IRF-1
    • KAP1
    • STAT1
    • Transcriptional regulation

    ASJC Scopus subject areas

    • Biophysics
    • Biochemistry
    • Molecular Biology
    • Cell Biology


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