G-Protein-Coupled Receptor Kinase 5
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Subject Areas on Research
- Clinical application of cardiovascular pharmacogenetics.
- Competing G protein-coupled receptor kinases balance G protein and β-arrestin signaling.
- Defective lymphocyte chemotaxis in beta-arrestin2- and GRK6-deficient mice.
- Different G protein-coupled receptor kinases govern G protein and beta-arrestin-mediated signaling of V2 vasopressin receptor.
- Differential regulation of dopamine D1A receptor responsiveness by various G protein-coupled receptor kinases.
- Functional antagonism of different G protein-coupled receptor kinases for beta-arrestin-mediated angiotensin II receptor signaling.
- G Protein-coupled receptor kinases phosphorylate LRP6 in the Wnt pathway.
- G protein-coupled receptor kinase 5 gene polymorphisms are associated with postoperative atrial fibrillation after coronary artery bypass grafting in patients receiving β-blockers.
- G protein-coupled receptor kinase 5 regulates airway responses induced by muscarinic receptor activation.
- G protein-coupled receptor kinase 5 regulates beta 1-adrenergic receptor association with PSD-95.
- G protein-coupled receptor kinase-5 attenuates atherosclerosis by regulating receptor tyrosine kinases and 7-transmembrane receptors.
- G-protein-coupled receptor (GPCR) kinase phosphorylation and beta-arrestin recruitment regulate the constitutive signaling activity of the human cytomegalovirus US28 GPCR.
- G-protein-coupled receptor kinase specificity for beta-arrestin recruitment to the beta2-adrenergic receptor revealed by fluorescence resonance energy transfer.
- Gene signatures of postoperative atrial fibrillation in atrial tissue after coronary artery bypass grafting surgery in patients receiving β-blockers.
- Grk5l controls heart development by limiting mTOR signaling during symmetry breaking.
- Human substance P receptor undergoes agonist-dependent phosphorylation by G protein-coupled receptor kinase 5 in vitro.
- Hybrid transgenic mice reveal in vivo specificity of G protein-coupled receptor kinases in the heart.
- Identification of the G protein-coupled receptor kinase phosphorylation sites in the human beta2-adrenergic receptor.
- Identification, purification, and characterization of GRK5, a member of the family of G protein-coupled receptor kinases.
- Mechanism of beta-adrenergic receptor desensitization in cardiac hypertrophy is increased beta-adrenergic receptor kinase.
- Muscarinic supersensitivity and impaired receptor desensitization in G protein-coupled receptor kinase 5-deficient mice.
- Myocardial G protein-coupled receptor kinases: implications for heart failure therapy.
- Myocardial overexpression of adrenergic receptors and receptor kinases.
- Overlapping and opposing functions of G protein-coupled receptor kinase 2 (GRK2) and GRK5 during heart development.
- Phosphatidylinositol 4,5-bisphosphate (PIP2)-enhanced G protein-coupled receptor kinase (GRK) activity. Location, structure, and regulation of the PIP2 binding site distinguishes the GRK subfamilies.
- Phosphorylation and desensitization of human endothelin A and B receptors. Evidence for G protein-coupled receptor kinase specificity.
- Quantitative label-free phosphoproteomics strategy for multifaceted experimental designs.
- Receptor and G betagamma isoform-specific interactions with G protein-coupled receptor kinases.
- Receptor-specific in vivo desensitization by the G protein-coupled receptor kinase-5 in transgenic mice.
- Reciprocal regulation of the platelet-derived growth factor receptor-beta and G protein-coupled receptor kinase 5 by cross-phosphorylation: effects on catalysis.
- Regulation of G protein-coupled receptor kinase 5 (GRK5) by actin.
- Regulation of the platelet-derived growth factor receptor-beta by G protein-coupled receptor kinase-5 in vascular smooth muscle cells involves the phosphatase Shp2.
- The GRK4 subfamily of G protein-coupled receptor kinases. Alternative splicing, gene organization, and sequence conservation.
- The platelet-derived growth factor receptor-beta phosphorylates and activates G protein-coupled receptor kinase-2. A mechanism for feedback inhibition.
- alpha-Actinin is a potent regulator of G protein-coupled receptor kinase activity and substrate specificity in vitro.
- beta-arrestin-dependent, G protein-independent ERK1/2 activation by the beta2 adrenergic receptor.
- β-arrestin1-biased β1-adrenergic receptor signaling regulates microRNA processing.
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Keywords of People
- Milano, Carmelo Alessio, Professor of Surgery, Surgery, Cardiovascular and Thoracic Surgery