The role of receptor kinases and arrestins in G protein-coupled receptor regulation. Export

@article{citeulike:2870321, abstract = {G protein-coupled receptors (GPRs) play a key role in controlling hormonal regulation of numerous second-messenger pathways. However, following agonist activation, most GPRs rapidly lose their ability to respond to hormone. For many GPRs, this process, commonly referred to as desensitization, appears to be primarily mediated by two protein families: G protein-coupled receptor kinases (GRKs) and arrestins. GRKs specifically bind to the agonist-occupied receptor, thereby promoting receptor phosphorylation, which in turn leads to arrestin binding. Arrestin binding precludes receptor/G protein interaction leading to functional desensitization. Many GPRs are then removed from the plasma membrane via clathrin-mediated endocytosis. Recent studies have implicated endocytosis in the resensitization of GPRs and have linked both GRKs and arrestins to this process. In this review, we discuss the role of GRKs and arrestins in regulating agonist-specific signaling and trafficking of GPRs.}, address = {Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.}, author = {Krupnick, J. G. and Benovic, J. L.}, citeulike-article-id = {2870321}, citeulike-linkout-0 = {http://dx.doi.org/10.1146/annurev.pharmtox.38.1.289}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/9597157}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=9597157}, doi = {10.1146/annurev.pharmtox.38.1.289}, issn = {0362-1642}, journal = {Annual review of pharmacology and toxicology}, keywords = {grk, intro}, pages = {289--319}, posted-at = {2008-06-06 20:54:29}, priority = {2}, title = {The role of receptor kinases and arrestins in G protein-coupled receptor regulation.}, url = {http://dx.doi.org/10.1146/annurev.pharmtox.38.1.289}, volume = {38}, year = {1998} }

TY - JOUR ID - citeulike:2870321 L3 - citeulike-article-id:2870321 N2 - G protein-coupled receptors (GPRs) play a key role in controlling hormonal regulation of numerous second-messenger pathways. However, following agonist activation, most GPRs rapidly lose their ability to respond to hormone. For many GPRs, this process, commonly referred to as desensitization, appears to be primarily mediated by two protein families: G protein-coupled receptor kinases (GRKs) and arrestins. GRKs specifically bind to the agonist-occupied receptor, thereby promoting receptor phosphorylation, which in turn leads to arrestin binding. Arrestin binding precludes receptor/G protein interaction leading to functional desensitization. Many GPRs are then removed from the plasma membrane via clathrin-mediated endocytosis. Recent studies have implicated endocytosis in the resensitization of GPRs and have linked both GRKs and arrestins to this process. In this review, we discuss the role of GRKs and arrestins in regulating agonist-specific signaling and trafficking of GPRs. JF - Annual review of pharmacology and toxicology SN - 0362-1642 AD - Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. EP - 319 TI - The role of receptor kinases and arrestins in G protein-coupled receptor regulation. VL - 38 SP - 289 KW - grk KW - intro AU - Krupnick, JG AU - Benovic, JL PY - 1998/// UR - http://dx.doi.org/10.1146/annurev.pharmtox.38.1.289 ER -