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.
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.
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.
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.
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.
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.