pubmed-article:8092990 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C0017710 | lld:lifeskim |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C1335671 | lld:lifeskim |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:8092990 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:8092990 | pubmed:dateCreated | 1994-10-14 | lld:pubmed |
pubmed-article:8092990 | pubmed:abstractText | The expression of beta 2-adrenergic receptors is up-regulated by glucocorticoids. In contrast, beta 1-adrenergic receptors display glucocorticoid-induced down-regulation. In rat C6 glioma cells, which express both of these subtypes of beta-adrenergic receptors, the synthetic glucocorticoid dexamethasone stimulates no change in the total beta-adrenergic receptor content, but rather shifts the beta 1:beta 2 ratio from 80:20 to 50:50. Radioligand binding and immunoblotting demonstrate a sharp decline in beta 1-adrenergic receptor expression. Metabolic labelling of cells with [35S]-methionine in tandem with immunoprecipitation by beta 1-adrenergic-receptor-specific antibodies reveals a sharp decline in the synthesis of the receptor within 48 h for cells challenged with glucocorticoid. Steady-state levels of beta 1-adrenergic-receptor mRNA declined from 0.47 to 0.26 amol/microgram of total cellular RNA within 2 h of dexamethasone challenge, as measured by DNA-excess solution hybridization. The stability of receptor mRNA was not influenced by glucocorticoid; the half-lives of the beta 1- and beta 2-subtype mRNAs were 1.7 and 1.5 h respectively. Nuclear run-on assays revealed the basis for the down-regulation of receptor expression, i.e. a sharp decline in the relative rate of transcription for the beta 1-adrenergic-receptor gene in nuclei from dexamethasone-treated as compared with vehicle-treated cells. These data demonstrate transcriptional suppression as a molecular explanation for glucocorticoid-induced down-regulation of beta 1-adrenergic receptors. | lld:pubmed |
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pubmed-article:8092990 | pubmed:language | eng | lld:pubmed |
pubmed-article:8092990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8092990 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8092990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8092990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8092990 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8092990 | pubmed:month | Sep | lld:pubmed |
pubmed-article:8092990 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:8092990 | pubmed:author | pubmed-author:MalbonC CCC | lld:pubmed |
pubmed-article:8092990 | pubmed:author | pubmed-author:HadcockJ RJR | lld:pubmed |
pubmed-article:8092990 | pubmed:author | pubmed-author:BahouthS WSW | lld:pubmed |
pubmed-article:8092990 | pubmed:author | pubmed-author:KielyJJ | lld:pubmed |
pubmed-article:8092990 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8092990 | pubmed:day | 1 | lld:pubmed |
pubmed-article:8092990 | pubmed:volume | 302 ( Pt 2) | lld:pubmed |
pubmed-article:8092990 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8092990 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8092990 | pubmed:pagination | 397-403 | lld:pubmed |
pubmed-article:8092990 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8092990 | pubmed:meshHeading | pubmed-meshheading:8092990-... | lld:pubmed |
pubmed-article:8092990 | pubmed:year | 1994 | lld:pubmed |
pubmed-article:8092990 | pubmed:articleTitle | Glucocorticoids down-regulate beta 1-adrenergic-receptor expression by suppressing transcription of the receptor gene. | lld:pubmed |
pubmed-article:8092990 | pubmed:affiliation | Department of Molecular Pharmacology, School of Medicine, University at Stony Brook, NY 11794-8651. | lld:pubmed |
pubmed-article:8092990 | pubmed:publicationType | Journal Article | lld:pubmed |