Autocrine Amplification of Type I Interferon Gene Expression Mediated by Interferon Stimulated Gene Factor 3 (ISGF3)

Web Site 被引用文献3件 参考文献52件
  • YONEYAMA Mitsutoshi
    Department of Tumor Cell Biology, The Tokyo Metropolitan Institute of Medical Science
  • SUHARA Wakako
    Department of Tumor Cell Biology, The Tokyo Metropolitan Institute of Medical Science
  • FUKUHARA Yukiko
    Department of Tumor Cell Biology, The Tokyo Metropolitan Institute of Medical Science
  • SATO Mayumi
    Department of Tumor Cell Biology, The Tokyo Metropolitan Institute of Medical Science
  • OZATO Keiko
    Department of Health and Human Services, National Institute of Child Health and Human Development
  • FUJITA Takashi
    Department of Tumor Cell Biology, The Tokyo Metropolitan Institute of Medical Science

この論文をさがす

抄録

Interferon regulatory factor (IRF)-1 and IRF-2 have been implicated for the virus-induced expression of the interferon-α and β (type I IFN) genes. However, recent gene disruption studies in mice suggested the presence of other factor(s) interacting with overlapping promoter elements. In the present paper, we describe the characterization of a DNA binding factor which is strongly induced after virus infection and recognizes these promoter elements. After extensive purification, the factor was revealed to be identical to IFN-stimulated gene factor 3 (ISGF3), a transcription factor complex activated by IFN treatment. ISGF3 binds to the promoter element of IFN-β, positive regulatory domain I (PRDI), with significantly higher affinity than IRF-1, 2, and mutational analysis of PRDI showed that the gene expression and binding of ISGF3, but not of IRF-1, 2, are highly correlated. Furthermore, our functional analysis involving a dominant negative inhibitor for ISGF3 activation and an anti-IFN neutralizing antibody clearly demonstrated the presence of a positive feedback pathway for type I IFN genes mediated by ISGF3.

収録刊行物

被引用文献 (3)*注記

もっと見る

参考文献 (52)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ