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Engineered anion-conducting channelrhodopsins with enhanced red-light sensitivity and accelerated kinetics enable precise, low-intensity optical silencing of neurons, advancing optogenetic control in neuroscience research.

Substrate-induced structural changes in GtACR1 provide new insight into the chemical mechanism of natural light-gated anion conductance and facilitate its optimization for photoinhibition of neuron firing in optogenetics.

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.

Oculocutaneous albinism II (OCA2) contributes to a melanosome-specific anion channel that modulates organellar pH and is critical for melanin synthesis.

An anion-selective ligand gated channel acts as a presynaptic auto-receptor to modulate vesicle release and neuronal excitation.

The basis for small-molecule block, insights into gating, and an unexpected architectural role for the lipid membrane are revealed in structures of the volume regulated anion channel LRRC8A.

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.

A conformational switch in the Casein Kinase 1 activation loop controls substrate preference to regulate the abundance of the clock protein PERIOD2 and circadian timekeeping.

The cryo-EM structure and functional characterization of the chloride-selective ion transporter Slc26a9 defines its oligomeric architecture and transport mechanism.

Cortical microtubule pulling forces influence nuclear envelope breakdown, while nuclear envelope remodeling, particularly lamina depolymerization, impacts mitotic spindle length during mitosis.