Journal
CELLS
Volume 10, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/cells10030555
Keywords
arrestins; GPCR; GRK; phosphorylation; signaling
Categories
Funding
- National Institutes of Health [R01GM44944, R35GM122541, R01HL142310, P01HL114471]
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Agonist activation of G protein-coupled receptors leads to sequential interaction with G proteins, GRKs, and arrestins. GRKs play a central role in mediating the switch from G protein to arrestin interaction and controlling processes like receptor desensitization. Early studies on GRK identification and cloning laid the foundation for understanding the structure and function of these enzymes.
Agonist activation of G protein-coupled receptors promotes sequential interaction of the receptor with heterotrimeric G proteins, G protein-coupled receptor kinases (GRKs), and arrestins. GRKs play a central role in mediating the switch from G protein to arrestin interaction and thereby control processes such as receptor desensitization and trafficking and arrestin-mediated signaling. In this review, I provide a historical perspective on some of the early studies that identified the family of GRKs with a primary focus on the non-visual GRKs. These studies included identification, purification, and cloning of the beta-adrenergic receptor kinase in the mid- to late-1980s and subsequent cloning and characterization of additional members of the GRK family. This helped to lay the groundwork for ensuing work focused on understanding the structure and function of these important enzymes.
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