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Depletion of LRRC8A provides genetic evidence for the importance of Cl^- channels in NLRP3 activation.

Mambalgin1 binds to the thumb domain of human ASIC1a channel and inhibits the channel through hindering the proton-induced transitions from the resting closed state to the active and/or desensitized state.

A functional link between representative family members of the CLCA channel regulator family and TMEM16 channels suggests that these protein families may cooperate in influencing multiple homeostatic and disease physiologies.

Whole endosome recording shows that chloride interacts with vesicular glutamate transporters as both allosteric activator and permeant ion, and although the mode of permeation differs, chloride and glutamate use a related conduction pathway.

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.

The characterization of a previously unidentified “outward-facing open” conformational state provides a new framework for understanding the CLC transport mechanism.

A concerted approach employing equilibrium and biased molecular simulations, electrophysiology, mutagenesis, and functional assays reveals, in atomic details, the mechanism and pathway for transport of phospholipids and ions by a lipid scramblase.

A newly characterized calcium-activated chloride channel has been implicated in the immune system of Drosophila, shedding light on an enigmatic family of transmembrane proteins that are ubiquitous in nature.

A high axonal chloride concentration explains why activation of light-gated chloride channels causes neurotransmitter release, and a novel hybrid somatodendritic targeting motif ameliorates this phenomenon and improves their inhibitory function.

TMEM206 proteins are identified as constituting the pore of the widely expressed acid-activated chloride channel PAORAC/ASOR, which is important in acid toxicity.