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

HANDLE オープンアクセス

書誌事項

タイトル別名
  • Interactions between STAT1 and KAP1

この論文をさがす

抄録

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 corepressor 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.

収録刊行物

詳細情報 詳細情報について

  • CRID
    1050001338996362624
  • NII論文ID
    120000952715
  • NII書誌ID
    AA00564395
  • ISSN
    10902104
    0006291X
  • HANDLE
    2115/33893
  • 本文言語コード
    en
  • 資料種別
    journal article
  • データソース種別
    • IRDB
    • CiNii Articles

問題の指摘

ページトップへ