Sudarshan Rajagopal

This study shows BCKDK inhibitors cause vasodilation by directly blocking the AT1R, independent of BCAA catabolism or BCKDK.

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 identifies small-molecule inhibitors of beta-arrestins and elucidates their mechanism, offering a framework for modulating GPCR signaling.

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

This study shows that β-arrestin conformations vary by subcellular location and influence ERK activation differently in response to agonists.

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 paper identifies beta-arrestins as key regulators of ciliary mechanotransduction in endothelial cells, showing their role in shear stress response and vascular development.

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.