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http://hdl.handle.net/2445/25210
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DC Field | Value | Language |
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dc.contributor.author | González, María Victoria | cat |
dc.contributor.author | Jiménez, Benilde | cat |
dc.contributor.author | Berciano, María T. | cat |
dc.contributor.author | González Sancho, José Manuel | cat |
dc.contributor.author | Caelles Franch, Carme | cat |
dc.contributor.author | Lafarga, Miguel | cat |
dc.contributor.author | Muñoz, Alberto | cat |
dc.date.accessioned | 2012-05-09T09:47:39Z | - |
dc.date.available | 2012-05-09T09:47:39Z | - |
dc.date.issued | 2000-09-04 | - |
dc.identifier.issn | 0021-9525 | - |
dc.identifier.uri | http://hdl.handle.net/2445/25210 | - |
dc.description.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. | - |
dc.format.extent | 9 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | eng |
dc.publisher | Rockefeller University Press | - |
dc.relation.isformatof | Reproducció digital del document publicat a: http://dx.doi.org/10.1083/jcb.150.5.1199 | - |
dc.relation.ispartof | Journal of Cell Biology, 2000, vol. 150, núm. 5, p. 1199-1208 | - |
dc.relation.uri | http://dx.doi.org/10.1083/jcb.150.5.1199 | - |
dc.rights | (c) Rockefeller University Press, 2000 | - |
dc.source | Articles publicats en revistes (Bioquímica i Biomedicina Molecular) | - |
dc.subject.classification | Glucocorticoides | cat |
dc.subject.classification | Interacció cel·lular | cat |
dc.subject.other | Glucocorticoides | eng |
dc.subject.other | Cell interaction | eng |
dc.title | Glucocorticoids antagonize AP-1 inhibiting the activation/phosphorylation of JNK without affecting its subcellular distribution | eng |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 168021 | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 10974006 | - |
Appears in Collections: | Articles publicats en revistes (Bioquímica i Biomedicina Molecular) |
Files in This Item:
File | Description | Size | Format | |
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168021.pdf | 466.19 kB | Adobe PDF | View/Open |
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