The human skeletal muscle Na channel mutation R669H associated with hypokalemic periodic paralysis enhances slow inactivation.

@article{Struyk2000TheHS,
  title={The human skeletal muscle Na channel mutation R669H associated with hypokalemic periodic paralysis enhances slow inactivation.},
  author={Arie F. Struyk and Kylie A. Scoggan and Dennis E. Bulman and Stephen C Cannon},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2000},
  volume={20 23},
  pages={
          8610-7
        }
}
Missense mutations of the human skeletal muscle voltage-gated Na channel (hSkM1) underlie a variety of diseases, including hyperkalemic periodic paralysis (HyperPP), paramyotonia congenita, and potassium-aggravated myotonia. Another disorder of sarcolemmal excitability, hypokalemic periodic paralysis (HypoPP), which is usually caused by missense mutations of the S4 voltage sensors of the L-type Ca channel, was associated recently in one family with a mutation in the outermost arginine of the… CONTINUE READING

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