Please use this identifier to cite or link to this item:
http://hdl.handle.net/10261/5362
Share/Export:
![]() ![]() |
|
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE | |
Title: | Glucocorticoids antagonize Ap-1 by inhibiting the activation/phosphorylation of Jnk without affecting its subcellular distribution |
Authors: | González, María Victoria; Jiménez, Benilde CSIC; Berciano, María T.; González-Sancho, José Manuel CSIC ORCID; Caelles, Carme; Lafarga, Miguel; Muñoz Terol, Alberto CSIC ORCID | Keywords: | Dexamethasone Activating protein-1 Tumor necrosis factor α c-Jun NH2-terminal kinase Nuclear translocation |
Issue Date: | 4-Sep-2000 | Publisher: | Rockefeller University Press | Citation: | Journal of Cell Biology 150(5): 1199–1208 (2000) | Abstract: | The immunosuppressive and antiinflammatory actions of glucocorticoid hormones are mediated by their transrepression of activating protein-1 (AP-1) and nuclear factor-kappa B (NFκB) transcription factors. Inhibition of the c-Jun NH2-terminal kinase (JNK) signaling pathway, the main mediator of AP-1 activation, has been described in extracts of hormone-treated cells. Here, we show by confocal laser microscopy, enzymatic assays, and immunoblotting that the synthetic glucocorticoid dexamethasone inhibited tumor necrosis factor α (TNF-α)–induced phosphorylation and activation of JNK in the cytoplasm and nucleus of intact HeLa cells. As a result, c-Jun NH2-terminal domain phosphorylation and induction were impaired. Dexamethasone did not block the TNF-α–induced JNK nuclear translocation, but rather induced, per se, nuclear accumulation of the enzyme. Consistently with previous findings, a glucocorticoid receptor mutant (GRdim), which is deficient in dimerization, DNA binding, and transactivation, but retains AP-1 transrepressing activity, was as efficient as wild-type GR in mediating the same effects of dexamethasone on JNK in transfected Cos-7 cells. Our results show that glucocorticoids antagonize the TNF-α–induced activation of AP-1 by causing the accumulation of inactive JNK without affecting its subcellular distribution. | Publisher version (URL): | http://dx.doi.org/10.1083/jcb.150.5.1199 | URI: | http://hdl.handle.net/10261/5362 | DOI: | 10.1083/jcb.150.5.1199 | ISSN: | 0021-9525 |
Appears in Collections: | (IIBM) Artículos |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
Glucocorticoids.pdf | 462,12 kB | Adobe PDF | ![]() View/Open |
Review this work
PubMed Central
Citations
19
checked on May 21, 2022
SCOPUSTM
Citations
90
checked on May 23, 2022
WEB OF SCIENCETM
Citations
89
checked on May 20, 2022
Page view(s)
351
checked on May 24, 2022
Download(s)
246
checked on May 24, 2022
Google ScholarTM
Check
Altmetric
Dimensions
Related articles:
WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.