ArticleProceedings of the National Academy of Sciences of the United States of America1996
Monoclonal antibodies reveal receptor specificity among G-protein-coupled receptor kinases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 97 citations in OpenAlex.
- GRK5 functions as an oncogenic factor in non-small-cell lung cancer.Cell death & disease · 2018Article
- G-protein-coupled receptor kinase-5 promotes glioblastoma progression by targeting the nuclear factor kappa B pathway.American journal of translational research · 2018Article
- Dual role of GRK5 in cancer development and progression.Translational medicine @ UniSa · 2016Article
- International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli [corrected].Pharmacological reviews · 2015Review
- Dopamine and renal function and blood pressure regulation.Comprehensive Physiology · 2011Review
- Dopamine and G protein-coupled receptor kinase 4 in the kidney: role in blood pressure regulation.Biochimica et biophysica acta · 2010Review
- Reciprocal regulation of the platelet-derived growth factor receptor-beta and G protein-coupled receptor kinase 5 by cross-phosphorylation: effects on catalysis.Molecular pharmacology · 2009Article
- Effects of decreased renal cortical expression of G protein-coupled receptor kinase 4 and angiotensin type 1 receptors in rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2008Article
- An RNA molecule that specifically inhibits G-protein-coupled receptor kinase 2 in vitro.RNA (New York, N.Y.) · 2008Article
- G-protein-coupled receptor phosphorylation: where, when and by whom.British journal of pharmacology · 2008Review
- Type 1 angiotensin receptor pharmacology: signaling beyond G proteins.Pharmacology & therapeutics · 2007Review
- Functional antagonism of different G protein-coupled receptor kinases for beta-arrestin-mediated angiotensin II receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Chronic morphine induces the concomitant phosphorylation and altered association of multiple signaling proteins: a novel mechanism for modulating cell signaling.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Desensitization of the neurokinin-1 receptor (NK1-R) in neurons: effects of substance P on the distribution of NK1-R, Galphaq/11, G-protein receptor kinase-2/3, and beta-arrestin-1/2.Molecular biology of the cell · 1998Article
- Overexpression of myocardial Gsalpha prevents full expression of catecholamine desensitization despite increased beta-adrenergic receptor kinase.The Journal of clinical investigation · 1998Article
- Restoration of beta-adrenergic signaling in failing cardiac ventricular myocytes via adenoviral-mediated gene transfer.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Receptor and G betagamma isoform-specific interactions with G protein-coupled receptor kinases.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Guanine nucleotide-binding regulatory protein (G protein)-coupled receptor kinases (GRKs) constitute a family of serine/threonine kinases that play a major role in the agonist-induced phosphorylation and desensitization of G-protein-coupled receptors. Herein we describe the generation of monoclonal antibodies (mAbs) that specifically react with GRK2 and GRK3 or with GRK4, GRK5, and GRK6. They are used in several different receptor systems to identify the kinases that are responsible for receptor phosphorylation and desensitization. The ability of these reagents to inhibit GRK- mediated receptor phosphorylation is demonstrated in permeabilized 293 cells that overexpress individual GRKs and the type 1A angiotensin II receptor. We also use this approach to identify the endogenous GRKs that are responsible for the agonist-induced phosphorylation of epitope-tagged beta2- adrenergic receptors (beta2ARs) overexpressed in rabbit ventricular myocytes that are infected with a recombinant adenovirus. In these myocytes, anti-GRK2/3 mAbs inhibit isoproterenol-induced receptor phosphorylation by 77%, while GRK4-6-specific mAbs have no effect. Consistent with the operation of a betaAR kinase-mediated mechanism, GRK2 is identified by immunoblot analysis as well as in a functional assay as the predominant GRK expressed in these cells. Microinjection of GRK2/3-specific mAbs into chicken sensory neurons, which have been shown to express a GRK3-like protein, abolishes desensitization of the alpha2AR-mediated calcium current inhibition. The intracellular inhibition of endogenous GRKs by mAbs represents a novel approach to the study of receptor specificities among GRKs that should be widely applicable to many G-protein-coupled receptors.
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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.