Biased agonists of the chemokine receptor CXCR3 differentially signal through Gα_i:β-arrestin complexes.

ABSTRACT: G protein-coupled receptors (GPCRs) are the largest family of cell surface receptors and signal through the proximal effectors, G proteins and β-arrestins, to influence nearly every biological process. The G protein and β-arrestin signaling pathways have largely been considered separable; however, direct interactions between Gα proteins and β-arrestins have been described that appear to be part of a distinct GPCR signaling pathway. Within these complexes, Gα_i/o, but not other Gα protein subtypes, directly interacts with β-arrestin, regardless of the canonical Gα protein that is coupled to the GPCR. Here, we report that the endogenous biased chemokine agonists of CXCR3 (CXCL9, CXCL10, and CXCL11), together with two small-molecule biased agonists, differentially formed Gα_i

SUBMITTER: Zheng K 

PROVIDER: S-EPMC9890572 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature