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
[61]   Regulation of STAT-dependent pathways by growth factors and cytokines [J].
Leaman, DW ;
Leung, S ;
Li, XX ;
Stark, GR .
FASEB JOURNAL, 1996, 10 (14) :1578-1588
[62]   Differential regulation of constitutive major histocompatibility complex class I expression in T and B lymphocytes [J].
Lee, CK ;
Gimeno, R ;
Levy, DE .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 190 (10) :1451-1463
[63]   STAT1 affects lymphocyte survival and proliferation partially independent of its role downstream of IFN-γ [J].
Lee, CK ;
Smith, E ;
Gimeno, R ;
Gertner, R ;
Levy, DE .
JOURNAL OF IMMUNOLOGY, 2000, 164 (03) :1286-1292
[64]  
Lewis M, 1999, J CELL BIOCHEM, V72, P373, DOI 10.1002/(SICI)1097-4644(19990301)72:3<373::AID-JCB7>3.0.CO
[65]  
2-N
[66]   Formation of STAT1-STAT2 heterodimers and their role in the activation of IRF-1 gene transcription by interferon-alpha [J].
Li, XX ;
Leung, S ;
Qureshi, S ;
Darnell, JE ;
Stark, GR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (10) :5790-5794
[67]   Cooperative binding of Stat1-2 heterodimers and ISGF3 to tandem DNA elements [J].
Li, XX ;
Leung, S ;
Burns, C ;
Stark, GR .
BIOCHIMIE, 1998, 80 (8-9) :703-710
[68]   Stat1 depends on transcriptional synergy with Sp1 [J].
Look, DC ;
Pelletier, MR ;
Tidwell, RM ;
Roswit, WT ;
Holtzman, MJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (51) :30264-30267
[69]   INTERFERONS AND INTERLEUKIN-6 SUPPRESS THE DNA-BINDING ACTIVITY OF E2F IN GROWTH-SENSITIVE HEMATOPOIETIC-CELLS [J].
MELAMED, D ;
TIEFENBRUN, N ;
YARDEN, A ;
KIMCHI, A .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (09) :5255-5265
[70]   Targeted disruption of the STAT1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway [J].
Meraz, MA ;
White, JM ;
Sheehan, KCF ;
Bach, EA ;
Rodig, SJ ;
Dighe, AS ;
Kaplan, DH ;
Riley, JK ;
Greenlund, AC ;
Campbell, D ;
CarverMoore, K ;
DuBois, RN ;
Clark, R ;
Aguet, M ;
Schreiber, RD .
CELL, 1996, 84 (03) :431-442