Abstract
The ability to design 'biased' drugs that selectively activate G protein-coupled receptor (GPCR) signaling pathways beneficial in treating a disease, while limiting their side effects, is of broad significance. Lee et al. move us a step closer to this important goal by identifying structural differences in the β1-adrenoceptor in complex with β-arrestin 1 versus a G protein-mimicking nanobody.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
