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

来源：

BIOLOGICAL CHEMISTRY | 1999年 / 380卷 / 06期

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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