ArticleThe Journal of biological chemistry2008
Blood pressure is regulated by an alpha1D-adrenergic receptor/dystrophin signalosome.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
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- N-glycosylation of αScientific reports · 2020Article
- Scribble co-operatively binds multiple αScientific reports · 2019Article
- Updates in the function and regulation of αBritish journal of pharmacology · 2019Review
- Syntrophins entangled in cytoskeletal meshwork: Helping to hold it all together.Cell proliferation · 2019Review
- Central Arterial Function Measured by Non-invasive Pulse Wave Analysis is Abnormal in Patients with Duchenne Muscular Dystrophy.Pediatric cardiology · 2017Article
- Label-Free Dynamic Mass Redistribution Reveals Low-Density, ProsurvivalThe Journal of pharmacology and experimental therapeutics · 2017Article
- Novel Structural Approaches to Study GPCR Regulation.International journal of molecular sciences · 2016Review
- Endogenous N-terminal Domain Cleavage Modulates α1D-Adrenergic Receptor Pharmacodynamics.The Journal of biological chemistry · 2016Article
- Carboxyl terminus-truncated α1D-adrenoceptors inhibit the ERK pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Dynamic mass redistribution reveals diverging importance of PDZ-ligands for G protein-coupled receptor pharmacodynamics.Pharmacological research · 2016Article
- Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Physiological reviews · 2016Review
- LXR Agonism Upregulates the Macrophage ABCA1/Syntrophin Protein Complex That Can Bind ApoA-I and Stabilized ABCA1 Protein, but Complex Loss Does Not Inhibit Lipid Efflux.Biochemistry · 2015Article
- Evaluation of the specificity of four commercially available antibodies to alpha-syntrophin.Analytical biochemistry · 2015Article
- Epistasis analysis for quantitative traits by functional regression model.Genome research · 2014Article
- α1D-Adrenoceptors are responsible for the high sensitivity and the slow time-course of noradrenaline-mediated contraction in conductance arteries.Pharmacology research & perspectives · 2013Article
- Adiponectin receptor 1 C-terminus interacts with PDZ-domain proteins such as syntrophins.Experimental and molecular pathology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Hypertension is a cardiovascular disease associated with increased plasma catecholamines, overactivation of the sympathetic nervous system, and increased vascular tone and total peripheral resistance. A key regulator of sympathetic nervous system function is the alpha(1D)-adrenergic receptor (AR), which belongs to the adrenergic family of G-protein-coupled receptors (GPCRs). Endogenous catecholamines norepinephrine and epinephrine activate alpha(1D)-ARs on vascular smooth muscle to stimulate vasoconstriction, which increases total peripheral resistance and mean arterial pressure. Indeed, alpha(1D)-AR KO mice display a hypotensive phenotype and are resistant to salt-induced hypertension. Unfortunately, little information exists about how this important GPCR functions because of an inability to obtain functional expression in vitro. Here, we identified the dystrophin proteins, syntrophin, dystrobrevin, and utrophin as essential GPCR-interacting proteins for alpha(1D)-ARs. We found that dystrophins complex with alpha(1D)-AR both in vitro and in vivo to ensure proper functional expression. More importantly, we demonstrate that knock-out of multiple syntrophin isoforms results in the complete loss of alpha(1D)-AR function in mouse aortic smooth muscle cells and abrogation of alpha(1D)-AR-mediated increases in blood pressure. Our findings demonstrate that syntrophin and utrophin associate with alpha(1D)-ARs to create a functional signalosome, which is essential for alpha(1D)-AR regulation of vascular tone and blood pressure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.