ADRBK1 Antibody – Rabbit Polyclonal

The product of this gene phosphorylates the beta-2-adrenergic receptor and appears to mediate agonist-specific desensitization observed at high agonist concentrations. This protein is an ubiquitous cytosolic enzyme that specifically phosphorylates the activated form of the beta-adrenergic and related G-protein-coupled receptors. Abnormal coupling of beta-adrenergic receptor to G protein is involved in the pathogenesis of the failing heart. [provided by RefSeq, Jul 2008]

GRK2: a ubiquitous protein kinase of the GRK family. Phosphorylates the beta-2-adrenergic receptor and related G-protein-coupled receptors. Appears to mediate agonist-specific desensitization observed at high agonist concentrations. Expression level is consistently elevated in chronic human heart failure. Mouse models of severe heart failure have been used to demonstrate that inhibition of BARK1 with a peptide inhibitor is sufficient to increase mean survival, reduce dialation and improve cardiac function.

Protein type: Kinase, protein; EC 2.7.11.15; Protein kinase, Ser/Thr (non-receptor); Protein kinase, AGC; AGC group; GRK family; BARK subfamily

Chromosomal Location of Human Ortholog: 11q13.1

Cellular Component: membrane; cytoplasm; plasma membrane; cytosol

Molecular Function: G-protein coupled receptor kinase activity; protein binding; Edg-2 lysophosphatidic acid receptor binding; beta-adrenergic receptor kinase activity; alpha-2A adrenergic receptor binding; ATP binding; protein kinase activity

Biological Process: epidermal growth factor receptor signaling pathway; desensitization of G-protein coupled receptor protein signaling pathway; tachykinin signaling pathway; fibroblast growth factor receptor signaling pathway; acetylcholine receptor signaling, muscarinic pathway; nerve growth factor receptor signaling pathway; heart development; peptidyl-threonine phosphorylation; signal transduction; negative regulation of striated muscle contraction; peptidyl-serine phosphorylation; negative regulation of the force of heart contraction by chemical signal; phospholipase C activation; receptor internalization; positive regulation of catecholamine secretion; innate immune response; cardiac muscle contraction