ArticleThe EMBO journal2004
GRK2 is an endogenous protein inhibitor of the insulin signaling pathway for glucose transport stimulation.
Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 88 citations in OpenAlex.
- The impact of paroxetine on insulin secretion and sensitivity through AKT/GLUT4 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Role of G Protein-Coupled Receptors and Receptor Kinases in PancreaticPharmacological reviews · 2024Review
- Characterizing Adrenergic Regulation of Glucose Transporter 4-Mediated Glucose Uptake and Metabolism in the Heart.JACC. Basic to translational science · 2023Article
- Novel inhibitors of phosphorylation independent activity of GRK2 modulate cAMP signaling.Pharmacology research & perspectives · 2022Article
- Review
- Article
- G protein-coupled receptor kinase 2 regulates mitochondrial bioenergetics and impairs myostatin-mediated autophagy in muscle cells.American journal of physiology. Cell physiology · 2019Article
- Antidiabetic and Cardioprotective Effects of Pharmacological Inhibition of GRK2 in db/db Mice.International journal of molecular sciences · 2019Article
- Cdc42: A Novel Regulator of Insulin Secretion and Diabetes-Associated Diseases.International journal of molecular sciences · 2019Review
- GRKs and β-Arrestins: "Gatekeepers" of Mitochondrial Function in the Failing Heart.Frontiers in pharmacology · 2019Review
- Of mice and men: models and mechanisms of diabetic cardiomyopathy.Basic research in cardiology · 2018Review
- Is GRK2 a new target for cardiovascular disease?Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- Noncanonical Roles of G Protein-coupled Receptor Kinases in Cardiovascular Signaling.Journal of cardiovascular pharmacology · 2017Review
- Insulin receptor substrate signaling controls cardiac energy metabolism and heart failure.The Journal of endocrinology · 2017Review
- β-Adrenergic Receptor and Insulin Resistance in the Heart.Biomolecules & therapeutics · 2017Review
- G protein-coupled receptor kinases as regulators of dopamine receptor functions.Pharmacological research · 2016Review
- Endothelin-1 suppresses insulin-stimulated Akt phosphorylation and glucose uptake via GPCR kinase 2 in skeletal muscle cells.British journal of pharmacology · 2016Article
- Kinome Screen Identifies PFKFB3 and Glucose Metabolism as Important Regulators of the Insulin/Insulin-like Growth Factor (IGF)-1 Signaling Pathway.The Journal of biological chemistry · 2015Article
- GRK3 suppresses L-DOPA-induced dyskinesia in the rat model of Parkinson's disease via its RGS homology domain.Scientific reports · 2015Article
- The evolving impact of g protein-coupled receptor kinases in cardiac health and disease.Physiological reviews · 2015Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
G protein-coupled receptor kinases (GRKs) represent a class of proteins that classically phosphorylate agonist-activated G protein-coupled receptors, leading to uncoupling of the receptor from further G protein activation. Recently, we have reported that the heterotrimeric G protein alpha-subunit, Galphaq/11, can mediate insulin-stimulated glucose transport. GRK2 contains a regulator of G protein signaling (RGS) domain with specificity for Galphaq/11. Therefore, we postulated that GRK2 could be an inhibitor of the insulin signaling cascade leading to glucose transport in 3T3-L1 adipocytes. In this study, we demonstrate that microinjection of anti-GRK2 antibody or siRNA against GRK2 increased insulin-stimulated insulin-responsive glucose transporter 4 (GLUT4) translocation, while adenovirus-mediated overexpression of wild-type or kinase-deficient GRK2 inhibited insulin-stimulated GLUT4 translocation as well as 2-deoxyglucose uptake. Importantly, a mutant GRK2 lacking the RGS domain was without effect. Taken together, these results indicate that through its RGS domain endogenous GRK2 functions as a negative regulator of insulin-stimulated glucose transport by interfering with Galphaq/11 signaling to GLUT4 translocation. Furthermore, inhibitors of GRK2 can lead to enhanced insulin sensitivity.
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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.