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. Note: This description may include information from UniProtKB.
Protein type: EC 188.8.131.52; Kinase, protein; Protein kinase, AGC; Protein kinase, Ser/Thr (non-receptor); AGC group; GRK family; BARK subfamily
Molecular Function: beta-adrenergic receptor kinase activity; Edg-2 lysophosphatidic acid receptor binding; G-protein coupled receptor kinase activity; protein binding; protein kinase activity; protein serine/threonine kinase activity
Biological Process: cardiac muscle contraction; desensitization of G-protein coupled receptor protein signaling pathway; entry of virus into host cell; follicle-stimulating hormone signaling pathway; G-protein coupled receptor protein signaling pathway; heart development; negative regulation of G-protein coupled receptor protein signaling pathway; negative regulation of striated muscle contraction; negative regulation of the force of heart contraction by chemical signal; peptidyl-serine phosphorylation; peptidyl-threonine phosphorylation; positive regulation of catecholamine secretion; protein amino acid phosphorylation; receptor internalization; regulation of the force of heart contraction; response to organic cyclic substance; response to oxidative stress; tachykinin signaling pathway; viral genome replication
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.