Voltage-dependent L-type calcium channel subunit alpha-1 egl-19 (EGL-19) (EGL-19)

EGL-19 is the pore-forming alpha-1 subunit of the L-type voltage-gated calcium channel (VGCC) in the nematode Caenorhabditis elegans. It is the primary mediator of voltage-dependent calcium influx in excitable tissues, including body-wall muscles, the pharynx, and specific neurons. EGL-19 is highly homologous to the human CACNA1C (Cav1.2) channel, making it a prominent model for studying human channelopathies such as Timothy syndrome, which is caused by gain-of-function mutations in the orthologous human gene. In C. elegans, EGL-19 is essential for vital processes such as muscle contraction, egg-laying, and proper axon termination during development. Pharmacologically, the channel is sensitive to dihydropyridines like nifedipine and the nematode-specific antagonist nemadipine A. Gain-of-function mutations in egl-19 lead to myotonia and prolonged muscle contraction, while loss-of-function mutations result in paralysis or embryonic lethality. Because of its well-defined genetics and physiological roles, EGL-19 serves as a critical target for high-throughput drug screening and basic research into calcium-dependent signaling and neurodevelopmental disorders. It also plays a role in sensory adaptation and glial-neuron interactions in the nematode nervous system.

Other names

egl-19L-type voltage-gated calcium channel alpha-1 subunitCaV1-like calcium channel

Antagonist of the L-type voltage-gated calcium channel, blocking the pore of the alpha-1 subunit to prevent calcium ion influx during membrane depolarization.