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pubmed-article:7982493pubmed:abstractTextSustained exposure of neuroblastoma x glioma hybrid, NG108-15, cells transfected to express the human beta 2-adrenoceptor (clone beta N22) to isoprenaline or iloprost (an agonist at the endogenously expressed IP prostanoid receptor) resulted in a substantial and selective down-regulation of the alpha subunit of the G-protein Gs. Treatment of these cells with the irreversible beta-adrenoceptor antagonist bromoacetyl alprenolol menthane diminished both the potency and the maximal ability of isoprenaline but not of iloprost to cause Gs alpha down-regulation. These results demonstrate that the extent of agonist-mediated Gs alpha down-regulation is dependent upon the availability of receptor to agonist.lld:pubmed
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pubmed-article:7982493pubmed:articleTitleReceptor availability defines the extent of agonist-mediated G-protein down-regulation in neuroblastoma x glioma hybrid cells transfected to express the beta 2-adrenoceptor.lld:pubmed
pubmed-article:7982493pubmed:affiliationDivision of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Scotland, UK.lld:pubmed
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