Ion conduction in the calcium-activated chloride channel TMEM16A is directly regulated by calcium, which binds to a site close to the pore thereby shaping the electrostatics at its intracellular entrance.
The chloride channel Ano1/Tmem16a plays an essential and non-redundant role in the developing airway by inhibiting mucus cell hyperplasia and promoting proper immune function of the airway mucosal barrier.
Drosophila nociceptive neurons convert high-intensity stimuli into characteristic fluctuations of firing rates, quiescent periods of which are regulated by hyperpolarization through small conductance Ca2+-activated K+ channels.
Single-particle cryo-EM and electrophysiology studies of the chloride channel TMEM16A reveals the structural basis for anion conduction and uncover its relationship to lipid scramblases of the same family.
The amino acids that are necessary for phospholipid scrambling by ANO6/TMEM16F can, via domain swapping, confer scrambling activity to the chloride ion channel ANO1 that normally does not scramble phospholipids.
A function-based genetic screen using the Caenorhabditis elegans axotomy model identifies new regulators and an inhibitory role for NAD+ in axon regeneration, expanding the understanding of axon injury responses and regeneration.