Control of IRF-3 activation by phosphorylation

被引：142

作者：

Yoneyama, M ^{[1
]}

Suhara, W ^{[1
]}

Fujita, T ^{[1
]}

机构：

[1] Tokyo Metropolitan Inst Med Sci, Dept Tumor Cell Biol, Bunkyo Ku, Tokyo 1138613, Japan

来源：

JOURNAL OF INTERFERON AND CYTOKINE RESEARCH | 2002年 / 22卷 / 01期

关键词：

D O I：

10.1089/107999002753452674

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：

Interferon (IFN) regulatory factor-3 (IRF-3) is a unique member of the IRF family. Its transcriptional activity is regulated solely by posttranslational modifications. We review current knowledge of the mechanism of IRF-3 activation: signalling triggered by infections including viruses and bacteria, phosphorylation of IRF-3 on certain serine residues, homodimer formation, and active holocomplex formation with coactivator CBP/p300.

引用

页码：73 / 76

页数：4

共 22 条

[21] Downregulation of IRF-3 levels by ribozyme modulates the profile of IFNA subtypes expressed in infected human cells [J].

Yeow, WS ;

Au, WC ;

Lowther, WJ ;

Pitha, PM .

JOURNAL OF VIROLOGY, 2001, 75 (06) :3021-3027

[22] Direct triggering of the type I interferon system by virus infection: activation of a transcription factor complex containing IRF-3 and CBP/p300 [J].

Yoneyama, M ;

Suhara, W ;

Fukuhara, Y ;

Fukuda, M ;

Nishida, E ;

Fujita, T .

EMBO JOURNAL, 1998, 17 (04) :1087-1095

← 1 2 3 →