Complex roles of Stat1 in regulating gene expression

被引:264
作者
Ramana, CV [1 ]
Chatterjee-Kishore, M [1 ]
Nguyen, H [1 ]
Stark, GR [1 ]
机构
[1] Cleveland Clin Fdn, Lerner Res Inst, Dept Mol Biol, Cleveland, OH 44195 USA
关键词
constitutive transcription; negative regulation; interferons; growth factors; crosstalk;
D O I
10.1038/sj.onc.1203525
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
Stat1 is a fascinating and complex protein with multiple, yet contrasting transcriptional functions. Upon activation, it drives the expression of many genes but also suppresses the transcription of others, These opposing characteristics also apply to its role in facilitating crosstalk between signal transduction pathways, as it participates in both synergistic activation and inhibition of gene expression, Stat1 is a functional transcription factor even in the absence of inducer-mediated activation, participating in the constitutive expression of some genes. This review summarizes the well studied involvement of Stat1 in IFN-dependent and growth factor-dependent signaling and then describes the roles of Stat1 in positive, negative and constitutive regulation of gene expression as well as its participation in crosstalk between signal transduction pathways.
引用
收藏
页码:2619 / 2627
页数:9
相关论文
共 126 条
[1]   Unresponsiveness to interferon associated with STAT1 protein deficiency in a gastric adenocarcinoma cell line [J].
Abril, E ;
Real, LM ;
Serrano, A ;
Jimenez, P ;
García, A ;
Canton, J ;
Trigo, I ;
Garrido, F ;
Ruiz-Cabello, F .
CANCER IMMUNOLOGY IMMUNOTHERAPY, 1998, 47 (02) :113-120
[2]   Inhibition of collagenase-3 (MMP-13) expression in transformed human keratinocytes by interferon-γ is associated with activation of extracellular signal-regulated kinase-1,2 and STAT1 [J].
Ala-aho, R ;
Johansson, N ;
Grénman, R ;
Fusenig, NE ;
López-Otín, C ;
Kähäri, VM .
ONCOGENE, 2000, 19 (02) :248-257
[3]   INTERFERON-GAMMA INHIBITS THYROTROPIN-INDUCED THYROIDAL PEROXIDASE GENE-EXPRESSION IN CULTURED HUMAN THYROCYTES [J].
ASHIZAWA, K ;
YAMASHITA, S ;
NAGAYAMA, Y ;
KIMURA, H ;
HIRAYU, H ;
IZUMI, M ;
NAGATAKI, S .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1989, 69 (02) :475-477
[4]  
Bach EA, 1996, MOL CELL BIOL, V16, P3214
[5]   Three-dimensional structure of the Stat3β homodimer bound to DNA [J].
Becker, S ;
Groner, B ;
Müller, CW .
NATURE, 1998, 394 (6689) :145-151
[6]   DEREGULATED EXPRESSION OF THE C-MYC ONCOGENE ABOLISHES INHIBITION OF PROLIFERATION OF RAT VASCULAR SMOOTH-MUSCLE CELLS BY SERUM REDUCTION, INTERFERON-GAMMA, HEPARIN, AND CYCLIC-NUCLEOTIDE ANALOGS AND INDUCES APOPTOSIS [J].
BENNETT, MR ;
EVAN, GI ;
NEWBY, AC .
CIRCULATION RESEARCH, 1994, 74 (03) :525-536
[7]   Cooperation of Stat2 and p300/CBP in signalling induced by interferon-alpha [J].
Bhattacharya, S ;
Eckner, R ;
Grossman, S ;
Oldread, E ;
Arany, Z ;
DAndrea, A ;
Livingston, DM .
NATURE, 1996, 383 (6598) :344-347
[8]   COMBINATORIAL ASSOCIATION AND ABUNDANCE OF COMPONENTS OF INTERFERON-STIMULATED GENE FACTOR-3 DICTATE THE SELECTIVITY OF INTERFERON RESPONSES [J].
BLUYSSEN, HAR ;
MUZAFFAR, R ;
VLIESTSTRA, RJ ;
VANDERMADE, ACJ ;
LEUNG, S ;
STARK, GR ;
KERR, IM ;
TRAPMAN, J ;
LEVY, DE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (12) :5645-5649
[9]   Stat2 is a transcriptional activator that requires sequence-specific contacts provided by Stat1 and p48 for stable interaction with DNA [J].
Bluyssen, HAR ;
Levy, DE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (07) :4600-4605
[10]  
Boehm U, 1998, J IMMUNOL, V161, P6715