Munc13, a protein that is essential for exocytosis, controls the behavior of voltage gated calcium channels and shapes synaptic plasticity on fast time scales.

A novel Mendelian disease featuring early-onset hypertension is caused by a recurrent gain of function mutation in CACNA1H, which encodes the voltage-gated calcium channel Cav3.2.

A novel engineered protein that uncouples electrical signals from downstream biological responses in excitable cells provides a unique investigative tool with potential therapeutic applications.

FlpStop is a generalizable tool for conditional gene disruption and rescue and enables critical experiments examining the interactions between genes, circuits, and computation.

Super-resolution imaging reveals a novel multi-channel arrangement that explains how big potassium (BK) channel activation closely tracks the opening of low-voltage-activated L-type calcium channels.

Engineered E3 ubiquitin ligases are utilized to elucidate mechanisms underlying ubiquitin regulation of membrane proteins, and to achieve robust post-translational functional knockdown of ion channels.

The Ca²⁺-driven functional coupling of CaV1.2 channels is a mechanism of channel memory that may modulate the amplification of Ca²⁺ influx.

NG2 glial cells respond to synaptic input with calcium signals in the absence of action potentials and process synaptic depolarizations with somatic and dendritic voltage gated channels.

Direct patch clamp of ependymal motile cilia reveals that voltage-gated calcium channels in the cell body dominate their electrical and calcium signaling properties.

Proteolytic maturation of auxiliary α2δ subunits of voltage-gated calcium channels increases neuronal communication by controlling the synaptic release of neurotransmitter.