Structure and dynamics determine G protein coupling specificity at a class A GPCR
- Sci Adv. 2025 Mar 21;11(12):eadq3971. doi: 10.1126/sciadv.adq3971.
- 1. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
- 2. Department of Biophysics, Medical College of Wisconsin, Milwaukee, WI, USA.
- 3. Department of Chemistry and Pharmacy, Medicinal Chemistry, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
- 4. FAU NeW, Erlangen, Germany.
- 5. Department of Medicine, Duke University Medical Center, Durham, NC, USA.
- 6. Department of Pharmacology, University of California, Davis, Davis, CA, USA.
- 7. VA Northern California Health Care System, Mather, CA, USA.
- 8. Department of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, CA, USA.
- 9. Department of Pharmacology, University of California San Diego School of Medicine, La Jolla, CA, USA.
- 10. Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Aoba, Aramaki, Aoba-ku, Sendai, Miyagi 980-8578, Japan.
- 11. Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Yoshida-Shimo-Adachi-cho, Sakyo-ku, Kyoto 606-8501, Japan.
- 12. Department of Biochemistry, Duke University Medical Center, Durham, NC, USA.
- 13. HHMI, Duke University Medical Center, Durham, NC, USA.
- 14. Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.
- 15. Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, USA.
- 16. Department of Physics and Astronomy and Department of Biological and Biomedical Biosciences, Rowan University, Glassboro, NJ, USA.
G protein-coupled receptors (GPCRs) exhibit varying degrees of selectivity for different G protein isoforms. Despite the abundant structures of GPCR-G protein complexes, little is known about the mechanism of G protein coupling specificity. The β2-adrenergic receptor is an example of GPCR with high selectivity for Gαs, the stimulatory G protein for adenylyl cyclase, and much weaker for the Gαi family of G proteins inhibiting adenylyl cyclase. By developing a Gαi-biased agonist (LM189), we provide structural and biophysical evidence supporting that distinct conformations at ICL2 and TM6 are required for coupling of the different G protein subtypes Gαs and Gαi. These results deepen our understanding of G protein specificity and bias and can accelerate the design of ligands that select for preferred signaling pathways.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Adrenergic ReceptorResearch Areas: Cardiovascular Disease
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target: Adrenergic ReceptorResearch Areas: Cardiovascular Disease