Cellular mechanisms of ventricular arrhythmias in a mouse model of Timothy syndrome (long QT syndrome 8).

@article{Drum2014CellularMO,
  title={Cellular mechanisms of ventricular arrhythmias in a mouse model of Timothy syndrome (long QT syndrome 8).},
  author={Benjamin M L Drum and Rose E. Dixon and Can Yuan and Edward S. Cheng and L Fernando Santana},
  journal={Journal of molecular and cellular cardiology},
  year={2014},
  volume={66},
  pages={63-71}
}
Ca(2+) flux through l-type CaV1.2 channels shapes the waveform of the ventricular action potential (AP) and is essential for excitation-contraction (EC) coupling. Timothy syndrome (TS) is a disease caused by a gain-of-function mutation in the CaV1.2 channel (CaV1.2-TS) that decreases inactivation of the channel, which increases Ca(2+) influx, prolongs APs, and causes lethal arrhythmias. Although many details of the CaV1.2-TS channels are known, the cellular mechanisms by which they induce… CONTINUE READING
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