Pharmacological activation of normal and arrhythmia-associated mutant KCNQ1 potassium channels.

@article{Seebohm2003PharmacologicalAO,
  title={Pharmacological activation of normal and arrhythmia-associated mutant KCNQ1 potassium channels.},
  author={Guiscard Seebohm and Michael Pusch and Jun Chen and Michael C Sanguinetti},
  journal={Circulation research},
  year={2003},
  volume={93 10},
  pages={941-7}
}
KCNQ1 alpha-subunits coassemble with KCNE1 beta-subunits to form channels that conduct the slow delayed rectifier K+ current (IKs) important for repolarization of the cardiac action potential. Mutations in KCNQ1 reduce IKs and cause long-QT syndrome, a disorder of ventricular repolarization that predisposes affected individuals to arrhythmia and sudden death. Current therapy for long-QT syndrome is inadequate. R-L3 is a benzodiazepine that activates IKs and has the potential to provide gene… CONTINUE READING
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