English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/79575
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

Title

Hormone-activated nuclear receptors inhibit the stimulation of the JNK and ERK signalling pathways in endothelial cells

AuthorsGonzález, María Victoria; González-Sancho, José Manuel ; Caelles, Carme; Muñoz Terol, Alberto ; Jiménez, Benilde
Issue Date1999
PublisherElsevier
CitationFEBS Letters 459(2): 272-276 (1999)
AbstractGlucocorticoid hormones, retinoids, and vitamin D3 display anti- angiogenic activity in tumor-bearing animals. However, despite their in vivo effect on the tumor vasculature little is known about their mechanism of action. Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) signalling pathways by the pro-angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. In contrast, Dex and RA failed to inhibit the activation of the p38 mitogen-activated protein kinase cascade. As a number of pro-angiogenic factors activate AP-1 transcription factor via the JNK and ERK pathways, our results suggest that the antagonism with AP-1 may underlie at least partially the anti-angiogenic effect of glucocorticoids and retinoids.
URIhttp://hdl.handle.net/10261/79575
DOI10.1016/S0014-5793(99)01257-0
Identifiersdoi: 10.1016/S0014-5793(99)01257-0
issn: 0014-5793
e-issn: 1873-3468
Appears in Collections:(IIBM) Artículos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.