ArticleThe Biochemical journal2001
Phosphorylation and desensitization of alpha1d-adrenergic receptors.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 44 citations in OpenAlex.
- The Differential Involvement of α1-Adrenoceptor Subtypes in the Molecular Effects of Antidepressant Drugs.International journal of molecular sciences · 2025Article
- Targeting Lysophosphatidic Acid in Cancer: The Issues in Moving from Bench to Bedside.Cancers · 2019Review
- Updates in the function and regulation of αBritish journal of pharmacology · 2019Review
- Long-Term High-Altitude Hypoxia and Alpha Adrenoceptor-Dependent Pulmonary Arterial Contractions in Fetal and Adult Sheep.Frontiers in physiology · 2019Article
- Novel Structural Approaches to Study GPCR Regulation.International journal of molecular sciences · 2016Review
- Carboxyl terminus-truncated α1D-adrenoceptors inhibit the ERK pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Roles of the α1A-adrenergic receptor carboxyl tail in protein kinase C-induced phosphorylation and desensitization.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Signaling properties of human alpha(1D)-adrenoceptors lacking the carboxyl terminus: intrinsic activity, agonist-mediated activation, and desensitization.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Influence of combined hypertension and renal failure on functional alpha(1)-adrenoceptor subtypes in the rat kidney.British journal of pharmacology · 2008Article
- Neuron specific alpha-adrenergic receptor expression in human cerebellum: implications for emerging cerebellar roles in neurologic disease.Neuroscience · 2005Article
- Vascular alpha-1D-adrenoceptors are overexpressed in aorta of the aryl hydrocarbon receptor null mouse: role of increased angiotensin II.Autonomic & autacoid pharmacologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In rat-1 fibroblasts stably expressing rat alpha(1d)-adrenoceptors, noradrenaline and PMA markedly decreased alpha(1d)-adrenoceptor function (noradrenaline-elicited increases in calcium in whole cells and [(35)S]guanosine 5'-[gamma-thio]triphosphate binding in membranes), suggesting homologous and heterologous desensitizations. Photoaffinity labelling, Western blotting and immunoprecipitation identified alpha(1d)-adrenoceptors as a broad band of 70-80 kDa. alpha(1d)-Adrenoceptors were phosphorylated in the basal state and noradrenaline and PMA increased it. The effect of noradrenaline was concentration-dependent (EC(50) 75 nM), rapid (maximum at 1 min) and transient. Phorbol ester-induced phosphorylation was concentration-dependent (EC(50) 25 nM), slightly slower (maximum at 5 min) and stable for at least 60 min. Inhibitors of protein kinase C decreased the effect of phorbol esters but not that of noradrenaline. Evidence of cross-talk of alpha(1d)-adrenoceptors with receptors endogenously expressed in rat-1 fibroblasts was given by the ability of endothelin, lysophosphatidic acid and bradykinin to induce alpha(1d)-adrenoceptor phosphorylation. In summary, it is shown for the first time here that alpha(1d)-adrenoceptors are phosphoproteins and that receptor phosphorylation is increased by the natural ligand, noradrenaline, by direct activation of protein kinase C and via cross-talk with other receptors endogenously expressed in rat-1 fibroblasts. Receptor phosphorylation has functional repercussions.
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