IRF-3-dependent and augmented target genes during viral infection

被引：92

作者：

Andersen, J. ^{[2
]}

VanScoy, S. ^{[1
]}

Cheng, T-F ^{[1
]}

Gomez, D. ^{[1
]}

Reich, N. C. ^{[1
]}

机构：

[1] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA

[2] SUNY Stony Brook, Dept Biochem & Cell Biol, Stony Brook, NY 11794 USA

来源：

GENES AND IMMUNITY | 2008年 / 9卷 / 02期

关键词：

transcription factor; host defense; innate immunity; global profiling; gene expression; signal transduction;

D O I：

10.1038/sj.gene.6364449

中图分类号：

Q3 [遗传学];

学科分类号：

071007 [遗传学]; 090102 [作物遗传育种];

摘要：

Activation of the transcription factor interferon regulatory factor-3 (IRF-3) is an essential event in the innate immune response to viral infection. To understand the contribution of IRF-3 to host defense, we used a systems biology approach to analyze global gene expression dependent on IRF-3. Comparison of expression profiles in cells from IRF-3 knockout animals or wild-type siblings following viral infection revealed three sets of induced genes, those that are strictly dependent on IRF-3, augmented with IRF-3, or not responsive to IRF-3. Products of identified IRF-3 target genes are involved in innate or acquired immunity, or in the regulation of cell cycle, apoptosis and proliferation. These results reveal the global effects of one transcription factor in the immune response and provide information to evaluate the integrated response to viral infection.

引用

页码：168 / 175

页数：8

共 51 条

[1]

Ordered recruitment of chromatin modifying and general transcription factors to the IFN-β promoter [J].

Agalioti, T ;

Lomvardas, S ;

Parekh, B ;

Yie, JM ;

Maniatis, T ;

Thanos, D .

CELL, 2000, 103 (04) :667-678

[2]

HIV blocked by chemokine antagonist [J].

ArenzanaSeisdedos, F ;

Virelizier, JL ;

Rousset, D ;

ClarkLewis, I ;

Loetscher, P ;

Moser, B ;

Baggiolini, M .

NATURE, 1996, 383 (6599) :400-400

[3]

STRUCTURE, CHROMOSOME LOCALIZATION, AND REGULATION OF EXPRESSION OF THE INTERFERON-REGULATED MOUSE IFI54/IFI56 GENE FAMILY [J].

BLUYSSEN, HAR ;

VLIETSTRA, RJ ;

FABER, PW ;

SMIT, EME ;

HAGEMEIJER, A ;

TRAPMAN, J .

GENOMICS, 1994, 24 (01) :137-148

[4]

IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA [J].

Calfon, M ;

Zeng, HQ ;

Urano, F ;

Till, JH ;

Hubbard, SR ;

Harding, HP ;

Clark, SG ;

Ron, D .

NATURE, 2002, 415 (6867) :92-96

[5]

Recognition by gamma/delta T cells [J].

Chien, YH ;

Jores, R ;

Crowley, MP .

ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :511-532

[6]

Viperin (cig5), an IFN-inducible antiviral protein directly induced by human cytomegalovirus [J].

Chin, KC ;

Cresswell, P .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (26) :15125-15130

[7]

DOUBLE-STRANDED-RNA ACTIVATES NOVEL FACTORS THAT BIND TO THE INTERFERON-STIMULATED RESPONSE ELEMENT [J].

DALY, C ;

REICH, NC .

MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (06) :3756-3764

[8]

CHARACTERIZATION OF SPECIFIC DNA-BINDING FACTORS ACTIVATED BY DOUBLE-STRANDED-RNA AS POSITIVE REGULATORS OF INTERFERON ALPHA/BETA-STIMULATED GENES [J].

DALY, C ;

REICH, NC .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (40) :23739-23746

[9]

Analysis of genes induced by Sendai virus infection of mutant cell lines reveals essential roles of interferon regulatory factor 3, NF-κB, and interferon but not Toll-like receptor 3 [J].

Elco, CP ;

Guenther, JM ;

Williams, BRG ;

Sen, GC .

JOURNAL OF VIROLOGY, 2005, 79 (07) :3920-3929

[10]

Interferon-induced exonuclease ISG20 exhibits an antiviral activity against human immunodeficiency virus type 1 [J].

Espert, L ;

Degols, G ;

Lin, YL ;

Vincent, T ;

Benkirane, M ;

Mechti, N .

JOURNAL OF GENERAL VIROLOGY, 2005, 86 :2221-2229

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