Abstract
Sustained 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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenylyl Cyclases / metabolism
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Adrenergic beta-2 Receptor Antagonists
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Alprenolol / analogs & derivatives
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Alprenolol / pharmacology
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Down-Regulation
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GTP-Binding Proteins / metabolism*
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Gene Expression
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Glioma / metabolism
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Humans
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Hybrid Cells / drug effects
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Hybrid Cells / metabolism
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Isoproterenol / pharmacology
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Neuroblastoma / metabolism
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Receptors, Adrenergic, beta-2 / genetics
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Receptors, Adrenergic, beta-2 / metabolism*
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Tumor Cells, Cultured / drug effects
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Tumor Cells, Cultured / metabolism
Substances
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Adrenergic beta-2 Receptor Antagonists
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Receptors, Adrenergic, beta-2
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bromoacetylalprenololmenthane
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Alprenolol
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GTP-Binding Proteins
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Adenylyl Cyclases
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Isoproterenol