Integration of G-protein coupled receptor signaling pathways for activation of a transcription factor (EGR-3) / 基因组蛋白质组与生物信息学报·英文版
Genomics, Proteomics & Bioinformatics
;
(4): 173-179, 2003.
Artículo
en Inglés
| WPRIM
| ID: wpr-339509
ABSTRACT
We recently reported the use of a gene-trapping approach to isolate cell clones in which a reporter gene had integrated into genes modulated by T-cell activation. We have now tested a panel of clones from that report and identified the one that responds to a variety of G-protein coupled receptors (GPCR). The beta-lactamase tagged EGR-3 Jurkat cell was used to dissect specific GPCR signaling in vivo. Three GPCRs were studied, including the chemokine receptor CXCR4 (Gi-coupled) that was endogenously expressed, the platelet activation factor (PAF) receptor (Gq-coupled), and beta2 adrenergic receptor (Gs-coupled) that was both stably transfected. Agonists for each receptor activated transcription of the beta-lactamase tagged EGR-3 gene. Induction of EGR-3 through CXCR4 was blocked by pertussis toxin and PD58059, a specific inhibitor of MEK (MAPK/ERK kinase). Neither of these inhibitors blocked isoproterenol or PAF-mediated activation of EGR-3. Conversely, beta2- and PAF-mediated EGR-3 activation was blocked by the p38, specific inhibitor SB580. In addition, both beta2- and PAF-mediated EGR-3 activation could be synergistically activated by CXCR4 activation. This combined result indicates that EGR-3 can be activated through distinct signal transduction pathways by different GPCRs and that signals can be integrated and amplified to efficiently tune the level of activation.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Factores de Transcripción
/
Beta-Lactamasas
/
Transducción de Señal
/
Regulación de la Expresión Génica
/
Genes Reporteros
/
Células Jurkat
/
Receptores CXCR4
/
Sistema de Señalización de MAP Quinasas
/
Medios de Cultivo
/
Receptores Acoplados a Proteínas G
Tipo de estudio:
Estudio pronóstico
Límite:
Humanos
Idioma:
Inglés
Revista:
Genomics, Proteomics & Bioinformatics
Año:
2003
Tipo del documento:
Artículo
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