Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
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A MAPK docking site is critical for downregulation of Capicua by Torso and EGFR RTK signalingAltered subcellular distribution of MSK1 induced by glucocorticoids contributes to NF-kappaB inhibition.Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promoter.Dexamethasone causes sustained expression of mitogen-activated protein kinase (MAPK) phosphatase 1 and phosphatase-mediated inhibition of MAPK p38.A nuclear isoform of the focal adhesion LIM-domain protein Trip6 integrates activating and repressing signals at AP-1- and NF-kappaB-regulated promotersPathogen recognition and inflammatory signaling in innate immune defensesBOL-303242-X, a novel selective glucocorticoid receptor agonist, with full anti-inflammatory properties in human ocular cellsGlucocorticoid receptor inhibits transforming growth factor-beta signaling by directly targeting the transcriptional activation function of Smad3Selective alteration of gene expression in response to natural and synthetic retinoidsA phosphorylation defective retinoic acid receptor mutant mimics the effects of retinoic acid on EGFR mediated AP-1 expression and cancer cell proliferation.Glucocorticoids synergize with IL-1beta to induce TLR2 expression via MAP Kinase Phosphatase-1-dependent dual Inhibition of MAPK JNK and p38 in epithelial cellsGlucocorticoids: do we know how they work?Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells.Regulation of the nongenomic actions of retinoid X receptor-α by targeting the coregulator-binding sitesIdentification of glucocorticoid receptor domains involved in transrepression of transforming growth factor-beta actionRegulation of retinoic acid-induced inhibition of AP-1 activity by orphan receptor chicken ovalbumin upstream promoter-transcription factorGrb4/Nckbeta acts as a nuclear repressor of v-Abl-induced transcription from c-jun/c-fos promoter elementsSteroid receptor coactivator-1 coactivates activating protein-1-mediated transactivations through interaction with the c-Jun and c-Fos subunitsBcl3, an IkappaB protein, as a novel transcription coactivator of the retinoid X receptorGlucocorticoids act within minutes to inhibit recruitment of signalling factors to activated EGF receptors through a receptor-dependent, transcription-independent mechanismGlucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP-1Characterization of retinoic acid receptor-deficient keratinocytesFarnesol stimulates differentiation in epidermal keratinocytes via PPARalphaChromium(VI) inhibits the transcriptional activity of nuclear factor-kappaB by decreasing the interaction of p65 with cAMP-responsive element-binding protein-binding proteinGlucocorticoids antagonize AP-1 by inhibiting the Activation/phosphorylation of JNK without affecting its subcellular distribution.Distinct p300-responsive mechanisms promote caspase-dependent apoptosis by human T-cell lymphotropic virus type 1 Tax protein.Crosstalk in inflammation: the interplay of glucocorticoid receptor-based mechanisms and kinases and phosphatasesSer484 and Ser494 in REL are the major sites of IKK phosphorylation in vitro: evidence that IKK does not directly enhance GAL4-REL transactivation.Minireview: latest perspectives on antiinflammatory actions of glucocorticoids.Endocrine perturbation increases susceptibility of mice to anthrax lethal toxin.Cofactor competition between the ligand-bound oestrogen receptor and an intron 1 enhancer leads to oestrogen repression of ERBB2 expression in breast cancer.Glucocorticoid receptor recruitment of histone deacetylase 2 inhibits interleukin-1beta-induced histone H4 acetylation on lysines 8 and 12.Peroxisome proliferator-activated receptor gamma-dependent repression of the inducible nitric oxide synthase gene.Nuclear receptors and inflammation control: molecular mechanisms and pathophysiological relevance.Presentation at the National Asthma Campaign International Congress, June 1999. Controlling the inflammatory response through transcriptional mechanisms.Different glucocorticoids vary in their genomic and non-genomic mechanism of action in A549 cells.Inhibition of p38 MAPK by glucocorticoids via induction of MAPK phosphatase-1 enhances nontypeable Haemophilus influenzae-induced expression of toll-like receptor 2.Cross-talk between glucocorticoid receptor and AP-1.Metabolic conversion as a pre-receptor control mechanism for lipophilic hormones.MAP kinases and the regulation of nuclear receptors.
P2860
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P2860
Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年学术文章
@wuu
1997年学术文章
@zh-cn
1997年学术文章
@zh-hans
1997年学术文章
@zh-my
1997年学术文章
@zh-sg
1997年學術文章
@yue
1997年學術文章
@zh
1997年學術文章
@zh-hant
name
Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
@en
type
label
Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
@en
prefLabel
Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
@en
P2093
P2860
P356
P1433
P1476
Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
@en
P2093
J M González-Sancho
P2860
P304
P356
10.1101/GAD.11.24.3351
P577
1997-12-01T00:00:00Z