Sylvain F. Feliciangeli

This study shows that gain- and loss-of-function mutations in KCNK9 cause perinatal lethality in mice, indicating BBS pathogenesis involves mechanisms beyond channel activity.

This study investigates the role of THIK2 channels in pain regulation through molecular, electrophysiological, and behavioral analyses in knock-out mice, revealing their involvement in limiting neuronal hyperexcitability and suggesting therapeutic potential for chronic pain.

The paper identifies a network of residues responsible for TWIK1 channel's pH-dependent shift in ionic selectivity from K+ to Na+ using MD simulations, mutagenesis, and electrophysiology.

The paper shows that TALK2 forms functional heterodimers with TALK1 and TASK2 in pancreatic β cells, enhancing their sensitivity to alkalosis and conductance.