Insertion of a SNS-specific tetrapeptide in S3-S4 linker of D4 accelerates recovery from inactivation of skeletal muscle voltage-gated Na channel mu1 in HEK293 cells

FEBS Lett. 1997 Oct 13;416(1):11-4. doi: 10.1016/s0014-5793(97)01154-x.

Abstract

Na channel subunits alphaSNS (PN3) and alpha mu1(SkM1) produce slowly inactivating/TTX-resistant and rapidly inactivating/TTX-sensitive currents, respectively. AlphaSNS (PN3) current recovers from inactivation (reprimes) rapidly. Sequence alignment identified the tetrapeptide SLEN, in the S3-S4 linker of D4, as alphaSNS-specific. To determine whether SLEN endows Na channels with slow kinetics and/or rapid repriming, we analyzed the transient Na current produced by a chimera mu1SLEN in HEK293 cells. Neither kinetics nor voltage dependence of activation and inactivation was affected. However, repriming was twice as fast as in the wild type at -100 mV. This suggests that SLEN may contribute to the rapid repriming of TTX-resistant Na current.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cell Line
  • Humans
  • Ion Channel Gating*
  • Molecular Sequence Data
  • Muscle, Skeletal / metabolism*
  • Mutagenesis
  • NAV1.8 Voltage-Gated Sodium Channel
  • Oligopeptides / chemistry
  • Oligopeptides / metabolism*
  • Sequence Homology, Amino Acid
  • Sodium Channel Blockers*
  • Sodium Channels / chemistry
  • Sodium Channels / metabolism

Substances

  • NAV1.8 Voltage-Gated Sodium Channel
  • Oligopeptides
  • SCN10A protein, human
  • Sodium Channel Blockers
  • Sodium Channels
  • tetrodotoxin-binding protein