| Literature DB >> 28223524 |
Thomas J Cahill1,2, Alex R B Thomsen1, Jeffrey T Tarrasch3,4, Bianca Plouffe5, Anthony H Nguyen1,6, Fan Yang7, Li-Yin Huang1, Alem W Kahsai1, Daniel L Bassoni8, Bryant J Gavino8, Jane E Lamerdin8, Sarah Triest9,10, Arun K Shukla1, Benjamin Berger2, John Little2, Albert Antar2, Adi Blanc2, Chang-Xiu Qu7, Xin Chen11, Kouki Kawakami12, Asuka Inoue12,13, Junken Aoki12,14, Jan Steyaert9,10, Jin-Peng Sun7, Michel Bouvier5, Georgios Skiniotis3,4, Robert J Lefkowitz15,2,6.
Abstract
β-Arrestins (βarrs) interact with G protein-coupled receptors (GPCRs) to desensitize G protein signaling, to initiate signaling on their own, and to mediate receptor endocytosis. Prior structural studies have revealed two unique conformations of GPCR-βarr complexes: the "tail" conformation, with βarr primarily coupled to the phosphorylated GPCR C-terminal tail, and the "core" conformation, where, in addition to the phosphorylated C-terminal tail, βarr is further engaged with the receptor transmembrane core. However, the relationship of these distinct conformations to the various functions of βarrs is unknown. Here, we created a mutant form of βarr lacking the "finger-loop" region, which is unable to form the core conformation but retains the ability to form the tail conformation. We find that the tail conformation preserves the ability to mediate receptor internalization and βarr signaling but not desensitization of G protein signaling. Thus, the two GPCR-βarr conformations can carry out distinct functions.Keywords: GPCR; arrestin; desensitization; endocytosis; signaling
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Year: 2017 PMID: 28223524 PMCID: PMC5347553 DOI: 10.1073/pnas.1701529114
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205