Chanpreet Jassal

The paper identifies novel GPCR interacting proteins independent of G proteins and β-arrestins using proximity labeling in cells lacking β-arrestin.

This study shows that G proteins and β-arrestins can directly interact, with Gi family members differing in their association with β-arrestin, and this selectivity is located in the alpha helical domain of Gi.

This study shows β-arrestin condensates regulate GPCR function through liquid-liquid phase separation, influencing internalization and signaling.

The paper shows that CXCL1 acts as a G protein-biased partial agonist at CXCR1 but a balanced full agonist at CXCR2, revealing receptor bias in chemokine signaling.

This study evaluates a beta-arrestin-biased AT1R agonist in PAH models, finding it fails to improve survival compared to AngII but promotes vascular remodeling.