Regulation of GPCR Trafficking by Ubiquitin. Prog Mol Biol Transl Sci 2015;132:15-38
Date
06/10/2015Pubmed ID
26055053Pubmed Central ID
PMC4699176DOI
10.1016/bs.pmbts.2015.02.005Scopus ID
2-s2.0-84942193272 (requires institutional sign-in at Scopus site) 47 CitationsAbstract
G protein-coupled receptor (GPCR)-promoted signaling mediates cellular responses to a variety of stimuli involved in diverse physiological processes. In addition, GPCRs are also the largest class of target for many drugs used to treat a variety of diseases. Despite the role of GPCR signaling in health and disease, the molecular mechanisms governing GPCR signaling remain poorly understanding. Classically, GPCR signaling is tightly regulated by GPCR kinases and β-arrestins, which act in a concerted fashion to govern GPCR desensitization and also GPCR trafficking. Ubiquitination has now emerged as an important posttranslational modification that has multiple roles, either directly or indirectly, in governing GPCR trafficking. Recent studies have revealed a mechanistic link between GPCR phosphorylation, β-arrestins, and ubiquitination. Here, we review recent developments in our understanding of how ubiquitin regulates GPCR trafficking within the endocytic pathway.
Author List
Kennedy JE, Marchese AAuthor
Adriano Marchese PhD Professor in the Biochemistry department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsArrestins
Cell Membrane
Endosomes
Gene Expression Regulation
Humans
Lysosomes
Phosphorylation
Protein Binding
Protein Transport
Receptors, G-Protein-Coupled
Signal Transduction
Ubiquitin
Ubiquitination
beta-Arrestins
