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• W2049671131 startingPage "752" @default.
• W2049671131 abstract "Glucocorticoids, which are widely used as antiinflammatory agents, downregulate the expression of the interleukin 6 gene and of additional cytokine genes involved in inflammatory responses. Conversely, the transcription factor NF-kappa B, a member of the Rel family of transcription factors, has been implicated in the induction of multiple genes involved in the early processes of immune and inflammatory responses. This prompted us to investigate whether one of the mechanisms by which glucocorticoids exert their antiinflammatory activities is through inhibition of gene activation mediated by NF-kappa B. We report that, in intact cells, activation of the interleukin 6 promoter by a combination of the factor NF-IL6 and the p65 subunit of NF-kappa B is inhibited by dexamethasone (ligand)-activated glucocorticoid receptor. Conversely, activation of the mouse mammary tumor virus promoter by a combination of dexamethasone and glucocorticoid receptor is inhibited by overexpression of p65. Furthermore, we provide evidence for physical association between glucocorticoid receptor and p65 in protein crosslinking and coimmunoprecipitation experiments, using either in vitro translated proteins or those present in cell extracts. These studies suggest that direct interactions between NF-kappa B and glucocorticoid receptor may partly account for the antiinflammatory properties of glucocorticoids in vivo." @default.
• W2049671131 created "2016-06-24" @default.
• W2049671131 creator A5040784287 @default.
• W2049671131 creator A5071185951 @default.
• W2049671131 date "1994-01-18" @default.
• W2049671131 modified "2023-10-10" @default.
• W2049671131 title "Physical association and functional antagonism between the p65 subunit of transcription factor NF-kappa B and the glucocorticoid receptor." @default.
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• W2049671131 doi "https://doi.org/10.1073/pnas.91.2.752" @default.
• W2049671131 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/43027" @default.
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