Graham Ladds

This study compares the functional and structural properties of the intracellular agonist PCO371 with the extracellular peptide agonist PTH 1-34 at the PTH1R, revealing PCO371's non-biased signaling profile and lower potency.

This paper designs a pathway-selective P2Y1R inverse agonist that suppresses inflammation without affecting hemostasis, demonstrating its functional selectivity in vitro and in vivo.

This study shows that reducing foetal bovine serum from 10% to 5% in culture conditions does not significantly affect cell growth or GPCR signalling.

RAMP3 complexes with GLP-1R at the plasma membrane, shifts signalling toward Ca2+ mobilisation, and enhances insulin secretion in INS-1 832/3 cells; Ramp3 loss blunts GLP-1 responses in mice.

This study shows that agonist efficacy at the {beta}2AR is determined by differences in receptor affinity for Gs protein, not ligand binding kinetics.

This study shows that activating GPR65 on fibroblast-like synoviocytes leads to inflammatory mediator release, contributing to joint pain in mice and humans.

The paper shows that an optimal ER-mitochondria distance of ~20 nm is critical for efficient Ca2+ transfer and mitochondrial oxidative metabolism, with reduced distances observed in Parkinson's disease astrocytes.

This study investigates rare disease variants in Gs, a G protein, using multidimensional approaches to reveal how mutations affect receptor-Gs coupling and signaling defects.

The paper compares the effects of BnOCPA, an A1R agonist, in rat and mouse hippocampal neurons, finding differences in its functional selectivity between pre- and postsynaptic receptors.

This paper identifies that GLP-1(9-36) inhibits glucagon secretion via the glucagon receptor, while GLP-1(7-36) uses the GLP-1 receptor, revealing distinct mechanisms for glucagon suppression.

The paper constructs a synthetic GPCR signaling system in yeast to predictably tune cellular responses to stimuli using computational and experimental methods.