Channel Openings Are Necessary but not Sufficient for Use-dependent Block of Cardiac Na+ Channels by Flecainide

@article{Liu2002ChannelOA,
  title={Channel Openings Are Necessary but not Sufficient for Use-dependent Block of Cardiac Na+ Channels by Flecainide},
  author={Huajun Liu and Michihiro Tateyama and Colleen E. Clancy and H. Abriel and Robert S. Kass},
  journal={The Journal of General Physiology},
  year={2002},
  volume={120},
  pages={39 - 51}
}
Na(+) channel blockers such as flecainide have found renewed usefulness in the diagnosis and treatment of two clinical syndromes arising from inherited mutations in SCN5A, the gene encoding the alpha subunit of the cardiac voltage-gated Na(+) channel. The Brugada syndrome (BrS) and the LQT-3 variant of the Long QT syndrome are caused by disease-linked SCN5A mutations that act to change functional and pharmacological properties of the channel. Here we have explored a set of SCN5A mutations… CONTINUE READING

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The cardiac persistent sodium current: an appealing therapeutic target?

British journal of pharmacology • 2008
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Flecainide sensitivity of a Na channel long QT mutation shows an open-channel blocking mechanism for use-dependent block.

American journal of physiology. Heart and circulatory physiology • 2006
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