VRAC activation, observed with a FRET sensor of intracellular LRRC8-domains movement during gating and by fluorometry, requires plasma membrane localization and diacylglycerol signaling, but is independent of intracellular ionic strength.
SWELL1 is required for basal, stretch, and flow-mediated endothelial AKT-eNOS signaling in vitro and protects against angiotensin-induced hypertension and diabetes-associated vascular dysfunction in vivo.
A multidisciplinary platform featured by patient-derived RPEs is established to study the disease-causing mechanisms of BEST1 mutations, and demonstrates gene-supplemented rescue of the mutation-caused deficiency in Ca2+-dependent Cl- current in human RPE.
In the extremely selective fluoride channels from the bacterial Fluc family, fluoride ions access the pore via two points, an electropositive vestibule and a triad of conserved residues involved in anion recognition.
Mathematical models with experimental validation show that chloride transporters in the cell membrane, and not negatively charged impermeant molecules, generate the driving force used by GABA receptors to silence neurons.