Activation of the transcription factor ISGF3 by interferon-γ

被引:94
作者
Matsumoto, M
Tanaka, N
Harada, H
Kimura, T
Yokochi, T
Kitagawa, M
Schindler, C
Taniguchi, T
机构
[1] Univ Tokyo, Fac Med, Bunkyo Ku, Tokyo 1130033, Japan
[2] Tokyo Med & Dent Univ, Sch Med, Dept Microbiol, Bunkyo Ku, Tokyo 1138519, Japan
[3] Tokyo Med & Dent Univ, Sch Med, Dept Mol Virol, Bunkyo Ku, Tokyo 1138519, Japan
[4] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA
[5] Univ Tokyo, Grad Sch Med, Fac Med, Dept Immunol,Bunkyo Ku, Tokyo 1130033, Japan
基金
日本学术振兴会;
关键词
IFN-gamma; ISGF3; ISRE; Stat2;
D O I
10.1515/BC.1999.087
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The interferon-stimulated gene factor 3 (ISGF3) transcription factor has been extensively studied in the context of the type I interferon (IFN-alpha/beta)-mediated antiviral response; it consists of the major DNA-binding component p48, and the signal transducers and activators of transcription (Stat)1 and Stat2. We show here that type II IFN (IFN-gamma) can also invoke the activation of ISGF3 in mouse primary embryonic fibroblasts. In fact, the two Stat proteins were tyrosine phosphorylated in IFN-gamma stimulated cells. Our present findings reveal an additional mechanism by which these two distinct types of cytokines, IFN-alpha/beta and -gamma, can commonly elicit antiviral activities.
引用
收藏
页码:699 / 703
页数:5
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