A molecular basis for gating mode transitions in human skeletal muscle Na+ channels

Paul B. Bennett*, Naomasa Makita, Alfred L. George

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

73 Scopus citations


Recombinant sodium channel α subunits expressed in Xenopus oocytes display an anomalously slow rate of inactivation that arises from channels that predominantly exist in a slow gating mode [1,2]. Co-expression of Na- channel β1 subunit with the human skeletal muscle Na+ channel α subunit increases the Na+ current and induces normal gating behavior in Xenopus laevis oocytes. The effects of the β1 subunit can be explained by an allosterically induced conformational switch of the α subunit protein that occurs upon binding the β1 subunit. This binding alters the free energy barriers separating distinct conformational states of the channel. The results illustrate a fundamental modulation of ion channel gating at the molecular level, and specifically demonstrate the importance of the β1 subunit for gating mode changes of Na+ channels.

Original languageEnglish (US)
Pages (from-to)21-24
Number of pages4
JournalFEBS Letters
Issue number1-3
StatePublished - Jul 1993


  • Gating
  • I
  • Inactivation
  • Na channel
  • Subunit

ASJC Scopus subject areas

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


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