Myotonic dystrophy kinase modulates skeletal muscle but not cardiac voltage-gated sodium channels

Mohamed Chahine, Alfred L. George

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Altered modulation of skeletal muscle voltage-gated sodium channels by myotonic dystrophy kinase (DMPK) has been proposed as a possible mechanism underlying myotonia in this disease. We examined the effect of a recombinant mouse DMPK on the functional properties of human skeletal muscle (hSkM1) and cardiac (hH1) voltage-gated sodium channels in the Xenopus oocyte expression system. Co-expression of DMPK with hSkM1 in oocytes resulted in significantly lower peak sodium current amplitude as compared to cells expressing hSkM1 alone in agreement with a previous report. By contrast, DMPK had no effect on the level of expressed sodium current in cells expressing hH1. Similarly, there mere no measurable effects of the kinase on the kinetics or steady-state properties of activation or inactivation. Our findings support the previous observations made with rat muscle sodium channels and demonstrate that the effect of DMPK on sodium channels is isoform specific despite conservation of a putative phosphorylation site between the two isoforms.

Original languageEnglish (US)
Pages (from-to)621-624
Number of pages4
JournalFEBS Letters
Issue number3
StatePublished - Aug 4 1997


  • Ion channel
  • Myotonic dystrophy
  • Phosphorylation
  • Skeletal muscle

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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