Proteolytic cleavage of the voltage-gated Ca2+ channel alpha2delta subunit: structural and functional features.

Proteolytic cleavage of the voltage - gated Ca 2 + channel α 2 δ subunit : structural and functional features

Ca2+ signalling, voltage-gated Ca2+ channels and praziquantel in flatworm neuromusculature.

Transient changes in calcium (Ca2+) levels regulate a wide variety of cellular processes, and cells employ both intracellular and extracellular sources of Ca2+ for signalling. Praziquantel, the drug of choice against schistosomiasis, disrupts Ca2+ homeostasis in adult worms. This review will focus on voltage-gated Ca2+ channels, which regulate levels of intracellular Ca2+ by coupling membrane d...

Mutations in a Drosophila alpha2delta voltage-gated calcium channel subunit reveal a crucial synaptic function.

Voltage-dependent calcium channels regulate many aspects of neuronal biology, including synaptic transmission. In addition to their alpha1 subunit, which encodes the essential voltage gate and selective pore, calcium channels also contain auxiliary alpha2delta, beta, and gamma subunits. Despite progress in understanding the biophysical properties of calcium channels, the in vivo functions of th...

Proteolytic cleavage of the voltage - gated Ca 2 + channel subunit : α 2 δ structural and functional features

By mediating depolarization-induced Ca influx high voltage-activated (HVA) Ca channels control a variety of cellular events. 2+ 2+ These heteromultimeric proteins are composed of an ion-conducting ( ) and three auxiliary ( , and ) subunits. The subunit α1 α2δ β γ α2δ enhances the trafficking of the channel complex to the cell surface and increases channel open probability. To exert these effect...

Traumatic axonal injury induces proteolytic cleavage of the voltage-gated sodium channels modulated by tetrodotoxin and protease inhibitors.

We demonstrated previously that dynamic stretch injury of cultured axons induces structural changes and Ca2+ influx modulated by tetrodotoxin (TTX)-sensitive voltage-gated sodium channels (NaChs). In the present study, we evaluated potential damage to the NaCh alpha-subunit, which can cause noninactivation of NaChs. In addition, we explored the effects of pre-injury and post-injury treatment wi...