%0 Journal Article %1 Bunemann1999a %A Bunemann, M. %A Hosey, M. M. %D 1999 %J J Physiol %K Animals Arrestin/metabolism Biological Cell Conformation Endocytosis GTP-Binding Humans Kinases/chemistry/*metabolism M2 Models, Muscarinic Muscarinic/metabolism Protein Protein-Tyrosine Receptor Signal Surface/*metabolism Transduction beta-2/metabolism Proteins/metabolism Adrenergic %P 5-23 %T G-protein coupled receptor kinases as modulators of G-protein signalling %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10226145 %V 517 ( Pt 1) %X G-protein coupled receptors (GPCRs) comprise one of the largest classes of signalling molecules. A wide diversity of activating ligands induce the active conformation of GPCRs and lead to signalling via heterotrimeric G-proteins and downstream effectors. In addition, a complex series of reactions participate in the 'turn-off' of GPCRs in both physiological and pharmacological settings. Some key players in the inactivation or 'desensitization' of GPCRs have been identified, whereas others remain the target of ongoing studies. G-protein coupled receptor kinases (GRKs) specifically phosphorylate activated GPCRs and initiate homologous desensitization. Uncoupling proteins, such as members of the arrestin family, bind to the phosphorylated and activated GPCRs and cause desensitization by precluding further interactions of the GPCRs and G-proteins. Adaptor proteins, including arrestins, and endocytic machinery participate in the internalization of GPCRs away from their normal signalling milieu. In this review we discuss the roles of these regulatory molecules as modulators of GPCR signalling.

@article{Bunemann1999a, abstract = {G-protein coupled receptors (GPCRs) comprise one of the largest classes of signalling molecules. A wide diversity of activating ligands induce the active conformation of GPCRs and lead to signalling via heterotrimeric G-proteins and downstream effectors. In addition, a complex series of reactions participate in the 'turn-off' of GPCRs in both physiological and pharmacological settings. Some key players in the inactivation or 'desensitization' of GPCRs have been identified, whereas others remain the target of ongoing studies. G-protein coupled receptor kinases (GRKs) specifically phosphorylate activated GPCRs and initiate homologous desensitization. Uncoupling proteins, such as members of the arrestin family, bind to the phosphorylated and activated GPCRs and cause desensitization by precluding further interactions of the GPCRs and G-proteins. Adaptor proteins, including arrestins, and endocytic machinery participate in the internalization of GPCRs away from their normal signalling milieu. In this review we discuss the roles of these regulatory molecules as modulators of GPCR signalling.}, added-at = {2010-12-14T18:12:02.000+0100}, author = {Bunemann, M. and Hosey, M. M.}, biburl = {https://www.bibsonomy.org/bibtex/2ee3397b279371f4b6bf11b1e0213b1b7/pharmawuerz}, endnotereftype = {Journal Article}, interhash = {cd454233ccce32134a97e7d8342b941f}, intrahash = {ee3397b279371f4b6bf11b1e0213b1b7}, issn = {0022-3751 (Print) 0022-3751 (Linking)}, journal = {J Physiol}, keywords = {Animals Arrestin/metabolism Biological Cell Conformation Endocytosis GTP-Binding Humans Kinases/chemistry/*metabolism M2 Models, Muscarinic Muscarinic/metabolism Protein Protein-Tyrosine Receptor Signal Surface/*metabolism Transduction beta-2/metabolism Proteins/metabolism Adrenergic}, month = {May 15}, note = {Bunemann, M Hosey, M M Review England The Journal of physiology J Physiol. 1999 May 15;517 ( Pt 1):5-23.}, pages = {5-23}, shorttitle = {G-protein coupled receptor kinases as modulators of G-protein signalling}, timestamp = {2010-12-14T18:22:39.000+0100}, title = {G-protein coupled receptor kinases as modulators of G-protein signalling}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10226145}, volume = {517 ( Pt 1)}, year = 1999 }