Altered Na+ channels promote pause-induced spontaneous diastolic activity in long QT syndrome type 3 myocytes.

@article{Fredj2006AlteredNC,
  title={Altered Na+ channels promote pause-induced spontaneous diastolic activity in long QT syndrome type 3 myocytes.},
  author={Sandra Fredj and Nicolas Lindegger and Kevin J. Sampson and Peter Carmeliet and Robert S. Kass},
  journal={Circulation research},
  year={2006},
  volume={99 11},
  pages={1225-32}
}
Long QT syndrome (LQTS) type 3 (LQT3), typified by the DeltaKPQ mutation (LQT3 mutation in which amino acid residues 1505 to 1507 [KPQ] are deleted), is caused by increased sodium entry during the action potential plateau resulting from mutation-altered inactivation of the Na(v)1.5 channel. Although rare, LQT3 is the most lethal of common LQTS variants. Here we tested the hypothesis that cellular electrical dysfunction, caused not only by action potential prolongation but also by mutation… CONTINUE READING

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