G Protein-Coupled Receptor Kinase (GRK)

Sino Biological provides a comprehensive set of tools for G protein-coupled receptor kinase (GRK) related studies, including proteins, antibodies (rabbit mAbs, mouse mAbs, and rabbit pAbs), ELISA kits, and ORF cDNA clones. G protein-coupled receptor kinases (GRKs) are a family of serine/threonine kinases, which regulate the activity of G protein-coupled receptors (GPCRs) by phosphorylating their intracellular domains after their associated G proteins have been released and activated. So far seven G protein-coupled receptor kinases have been discovered, which are named GRK1 to GRK7.

G Protein-Coupled Receptor Kinase (GRK) Products

• GRK1
• GRK3 / ADRBK2
• GRK6
• GRK2 / ADRBK1
• GRK5

G Protein-Coupled Receptor Kinase (GRK) Background

G protein-coupled receptor kinases (GRKs) are a family of serine/threonine protein kinases. GRKs regulate the activity of G protein-coupled receptors (GPCRs) by phosphorylating their intracellular domains after their associated G proteins have been released and activated. GRK family is so far composed of seven cloned members, named GRK1 to GRK7.

Despite the diversity of GPCRs, the process of GPCR homologous desensitization is intrinsically related to the function of GRKs. After binding to its agonist, a GPCR assumes a conformation that allows it to bind one or more of the GRKs and, in doing so, becomes phosphorylated at residues on its intracellular loops and carboxyl terminus. Phosphorylation of the receptor promotes the high-affinity binding of the arrestin family of proteins to the receptor, which physically interdicts further coupling to G proteins. This hindrance of coupling can result in as much as an 80% diminution of receptor signaling.

G Protein-Coupled Receptor Kinase (GRK) Related Studies

1. Krupnick JG, et al. (1998) The role of receptor kinases and arrestins in G protein-coupled receptor regulation. Annu Rev Pharmacol Toxicol. 38:289-319.
2. Kohout TA, et al. (2003) Regulation of G Protein-Coupled Receptor Kinases and Arrestins During Receptor Desensitization. Molecular Pharmacology. 63(1):9-18.
3. Nogués L, et al. (2011) Multiple scaffolding functions of {beta}-arrestins in the degradation of G protein-coupled receptor kinase 2. J Biol Chem. 286(2):1165-73.