Autocrine Amplification of Type I Interferon Gene Expression Mediated by Interferon Stimulated Gene Factor 3 (ISGF3).
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概要
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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.
- 社団法人 日本生化学会の論文
著者
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SATO Mayumi
Department of Astronomy, Graduate School of Science, The University of Tokyo
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Ozato Keiko
Department Of Health And Human Services National Institute Of Child Health And Human Development
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Fukuhara Yukiko
Department Of Tumor Cell Biology The Tokyo Metropolitan Institute Of Medical Science
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Suhara Wakako
Department Of Tumor Cell Biology The Tokyo Metropolitan Institute Of Medical Science
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Yoneyama Mitsutoshi
Department Of Tumor Cell Biology The Tokyo Metropolitan Institute Of Medical Science
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Fujita Takashi
Department Of Anesthesiology Suwa Red Cross Hospital
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