G-Protein-Coupled Receptor Kinases

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  Subject Areas on Research

  • Arrestins come of age: a personal historical perspective. 
  • Beta-arrestins: multifunctional cellular mediators. 
  • Cardiopulmonary bypass decreases G protein-coupled receptor kinase activity and expression in human peripheral blood mononuclear cells. 
  • Chemerin-activated functions of CMKLR1 are regulated by G protein-coupled receptor kinase 6 (GRK6) and β-arrestin 2 in inflammatory macrophages. 
  • 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. 
  • Distinct phosphorylation sites on the β(2)-adrenergic receptor establish a barcode that encodes differential functions of β-arrestin. 
  • Dopaminergic supersensitivity in G protein-coupled receptor kinase 6-deficient mice. 
  • Enhanced Uterine Contractility and Stillbirth in Mice Lacking G Protein-Coupled Receptor Kinase 6 (GRK6): Implications for Oxytocin Receptor Desensitization. 
  • G Protein-coupled receptor kinases phosphorylate LRP6 in the Wnt pathway. 
  • G protein-coupled receptor kinase 6A phosphorylates the Na(+)/H(+) exchanger regulatory factor via a PDZ domain-mediated interaction. 
  • G protein-coupled receptor kinase-2 (GRK-2) regulates serotonin metabolism through the monoamine oxidase AMX-2 in Caenorhabditis elegans. 
  • G protein-coupled receptor kinases (GRKs) orchestrate biased agonism at the β2-adrenergic receptor. 
  • G-protein-coupled receptor kinase specificity for beta-arrestin recruitment to the beta2-adrenergic receptor revealed by fluorescence resonance energy transfer. 
  • Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN). 
  • Increased acute inflammation, leukotriene B4-induced chemotaxis, and signaling in mice deficient for G protein-coupled receptor kinase 6. 
  • Monoclonal antibodies reveal receptor specificity among G-protein-coupled receptor kinases. 
  • Novel roles for β-arrestins in the regulation of pharmacological sequestration to predict agonist-induced desensitization of dopamine D3 receptors. 
  • Palmitoylation increases the kinase activity of the G protein-coupled receptor kinase, GRK6. 
  • Palmitoylation of G protein-coupled receptor kinase, GRK6. Lipid modification diversity in the GRK family. 
  • Phosphorylation and desensitization of human endothelin A and B receptors. Evidence for G protein-coupled receptor kinase specificity. 
  • Regulation of β2-adrenergic receptor function by conformationally selective single-domain intrabodies. 
  • Selective engagement of G protein coupled receptor kinases (GRKs) encodes distinct functions of biased ligands. 
  • Seven transmembrane receptors: something old, something new. 
  • The GRK4 subfamily of G protein-coupled receptor kinases. Alternative splicing, gene organization, and sequence conservation. 
  • The association of single-nucleotide polymorphisms in the oxytocin receptor and G protein-coupled receptor kinase 6 (GRK6) genes with oxytocin dosing requirements and labor outcomes. 
  • The cloning of GRK7, a candidate cone opsin kinase, from cone- and rod-dominant mammalian retinas. 
  • The role of GRK6 in animal models of Parkinson's disease and L-DOPA treatment. 
  • Understanding the mechanism of bias signaling of the insulin-like growth factor 1 receptor: Effects of LL37 and HASF. 
  • beta-Arrestin mediates beta1-adrenergic receptor-epidermal growth factor receptor interaction and downstream signaling. 
  • beta-arrestin-dependent, G protein-independent ERK1/2 activation by the beta2 adrenergic receptor. 
  • beta2-adrenergic receptor signaling and desensitization elucidated by quantitative modeling of real time cAMP dynamics. 
  • β-arrestin1-biased β1-adrenergic receptor signaling regulates microRNA processing.