Mutant channels contribute ,50% to Na1 current in paramyotonia congenita muscle

نویسندگان

  • Nenad Mitrovic
  • Alfred L. George
  • Reinhardt Rüdel
  • Frank Lehmann-Horn
  • Holger Lerche
چکیده

An important question in the pathophysiology of dominantly inherited diseases, such as channelopathies, is the level of expression of the mutant protein. In our study, we address this issue by comparing the gating defects of two human muscle NaF channel mutants (R1448C and R1448P) causing paramyotonia congenita in native muscle specimens from two patients with those of the same mutant recombinant channels expressed in human embryonic kidney (HEK-293) cells. Patch-clamp recordings of transfected HEK-293 cells revealed a pronounced slowing of the NaF current decay, a leftshifted and decreased voltage dependence of steadystate inactivation, and an increased frequency of channel reopenings for mutant compared with wild-type channels.

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Mutant channels contribute <50% to Na+ current in paramyotonia congenita muscle.

An important question in the pathophysiology of dominantly inherited diseases, such as channelopathies, is the level of expression of the mutant protein. In our study, we address this issue by comparing the gating defects of two human muscle Na+ channel mutants (R1448C and R1448P) causing paramyotonia congenita in native muscle specimens from two patients with those of the same mutant recombina...

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Pii: S0960-8966(99)00060-7

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تاریخ انتشار 1999