A structural basis for how ligand binding site changes can allosterically regulate GPCR signaling and engender functional selectivity
Marta Sánchez‐Soto, Ravi Kumar Verma, Blair K. A. Willette, Elizabeth C. Gonye, Annah M. Moore, Amy E. Moritz, Comfort A. Boateng, Hideaki Yano, R. Benjamin Free, Lei Shi, David R. Sibley
Abstract
A, which is predicted to affect its interactions with β-arrestin. Our findings provide a structural basis for how ligand binding site alterations can allosterically affect GPCR-transducer interactions and result in biased signaling.
Topics & Concepts
G protein-coupled receptorFunctional selectivityArrestinCell biologyTransmembrane domainIntracellularAgonistSignal transductionBiologyReceptorAllosteric regulationBiophysicsLigand (biochemistry)G proteinChemistryBiochemistryReceptor Mechanisms and SignalingNeuropeptides and Animal PhysiologyMonoclonal and Polyclonal Antibodies Research