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Voltage-gated calcium channels present in the tegument of parasitic helminths (notably *Schistosoma* spp.) are essential for parasite survival, playing critical roles in calcium ion influx, muscle contraction, neuromuscular signaling, and the maintenance of tegumental structure and function. These channels are the major molecular target of praziquantel, the frontline drug for schistosomiasis and related parasitic infections: praziquantel triggers rapid calcium influx through these channels, leading to sustained muscle contraction, paralysis, and rapid damage to the tegument, which results in parasite death. Parasite resistance to praziquantel is associated with altered calcium channel function. Calcium channel blockers can antagonize drug action or themselves disrupt parasite viability, emphasizing the essential nature of these channels for parasite physiology and tegument integrity. No unified single protein sequence is implied by the term: it covers a class of parasite voltage-gated calcium channels believed to be functionally distinct from, though evolutionarily related to, their mammalian counterparts. They are regarded as validated antiparasitic drug targets, although the exact molecular identity and diversity of all subtypes are still under study.
Induction of calcium influx leading to paralysis and tegument disruption by praziquantel; Blockade of calcium entry, reducing parasite viability (calcium channel blockers)
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