Michel Bouvier

This study shows ACKR3 is released on extracellular vesicles under both basal and ligand-induced conditions, sequestering chemokines and opioid peptides and modulating their signaling.

This study shows that GRKs are essential for ACKR3 endocytosis and chemokine scavenging, while β-arrestins and receptor phosphorylation are not required.

This study identifies a novel mechanism where Gq/11 and G12/13 activation causes SH2 domain-containing proteins to translocate from the plasma membrane to the nucleus, reducing RTK signaling activity.

This study shows that targeting protease-activated receptor 2 (PAR2) signaling in organelles using nanomedicines provides sustained analgesia in preclinical models of inflammatory bowel disease.

This study shows that MRAP2 modifies MC4R signaling and oligomerization, enhancing G protein signaling while reducing beta-arrestin2 recruitment and receptor internalization.

The paper investigates how multiple triggers on an allosteric communication network influence preferential coupling of the CB2R to Gi2 over β-arrestin1, revealing insights into GPCR signaling mechanisms.

The paper identifies structural elements in Gαs that prevent interactions with RGS proteins, showing three residues in the GTPase domain are necessary and sufficient for this resistance.

This study identifies and characterizes synthetic ligands for HCAR1 using ebBRET, revealing its activation of Gi/o and Gs pathways without β-arrestin recruitment.

This study identifies residue-level differences in G13 interactions with p115RhoGEF and PDZRhoGEF, revealing molecular determinants of their differential recruitment and providing insights for targeted therapeutic strategies.

The paper develops BRET biosensors to monitor ERM protein activation in real-time and identifies a cortical reserve pool of inactive ERMs that rapidly activates upon stimulation.

The paper identifies 138 associations between common protein-altering variants in GPCR genes and various phenotypes using UK Biobank data.