Filip Liebsch

This study shows that ROS-induced oxidation of gephyrin cysteines promotes synaptic multimerization and enhances inhibitory receptor clustering through disulfide bridges.

The paper identifies a de novo G134R mutation in gephyrin that impairs oligomerization, phase separation, and synaptic clustering, contributing to developmental epileptic encephalopathy.

This study shows that SOX deficiency leads to persulfidation loss and increased H2S release, with thiosulfate accumulation and metabolic rewiring in a mouse model.

This study investigates a specific gephyrin microdeletion (Δ199-233) in a mouse model, showing disrupted synaptic function and neurological deficits linked to reduced inhibitory signal transmission.

This study identifies the molecular mechanism of gephyrin clustering at GABAergic synapses, showing collybistin and phosphoinositides drive high-molecular weight complex formation, while gephyrin phosphorylation at Ser325 disrupts it.

This study shows that AP-2 maintains Purkinje cell function by balancing synaptic inputs from parallel and climbing fibers, preventing degeneration and motor dysfunction.

This study shows that autophagy regulator ATG5 protects cerebellar Purkinje cells by maintaining glycolytic activity, preventing neurodegeneration through regulation of glucose transporter 2.