Autoantibodies from myasthenia gravis patients bind a common core region on the nicotinic acetylcholine receptor through a largely conserved mechanism.

The protein disulphide isomerase CRELD1 controls the biosynthesis of nicotinic acetylcholine receptors in nematode and mouse muscle.

Investigation of synapse development using a single neuron system illuminates how individual neurons specify connectivity with their postsynaptic partners and the central role of the synaptic organizer neurexin in this process.

Postsynaptic MT1-MMP serves as a molecular switch to synaptogenesis by clearing the surrounding ECM environment that allows effective deposition of nerve-derived synaptogenic factors to induce postsynaptic differentiation at developing NMJs.

Signaling through nicotinic acetylcholine receptors in enterocytes impacts barrier integrity in the Drosophila intestine by regulating formation of the peritrophic matrix.

Indoxyl sulfate, a key uremic toxin in chronic kidney disease (CKD), induces trained immunity in monocytes via crosstalk between aryl hydrocarbon receptor (AhR)-dependent epigenetic reprogramming by enhancement of the arachidonic acid pathway and AhR-independent metabolic rewiring.

A novel mechanism describes how tonic activation of nicotinic acetylcholine receptors can modulate the timing of striatal output by priming feedforward inhibition.

Structural biology studies reveal the importance of protein dynamics on understanding molecular mechanisms underlying allosteric modulation of G protein-coupled receptors (GPCR) that offer insights into future GPCR research and drug discovery.

Reconstructed ancestral muscle-type acetylcholine receptor β-subunits readily form homopentameric ion channels that open spontaneously, and display functional hallmarks of the modern-day heteropentameric receptor despite being devoid of canonical agonist-binding sites.