Mapping the receptor site for hanatoxin, a gating modifier of voltage-dependent K+ channels

Neuron. 1997 Apr;18(4):675-82. doi: 10.1016/s0896-6273(00)80307-4.

Abstract

Hanatoxin (HaTx) binds to multiple sites on the surface of the drk1 voltage-gated K+ channel and modifies channel gating. We set out to identify channel residues that contribute to form these HaTx binding sites. Chimeras constructed using the drk1 and shaker K+ channels suggest that the S3-S4 linker may contain influential residues. Alanine scanning mutagenesis of the region extending from the C terminal end of S3 through S4 identified a number of residues that likely contribute to form the HaTx binding sites. The pore blocker Agitoxin2 and the gating modifier HaTx can simultaneously bind to individual K+ channels. These results suggest that residues near the outer edges of S3 and S4 form the HaTx binding sites and are eccentrically located at least 15 A from the central pore axis on the surface of voltage-gated K+ channels.

Publication types

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

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Binding, Competitive
  • Chimera
  • Chromosome Mapping*
  • Drosophila / genetics
  • Electrophysiology
  • Female
  • Ion Channel Gating / drug effects*
  • Molecular Sequence Data
  • Mutation
  • Peptides / metabolism*
  • Peptides / pharmacology*
  • Potassium Channel Blockers
  • Potassium Channels / genetics
  • Potassium Channels / metabolism*
  • Receptors, Cell Surface / genetics*
  • Scorpion Venoms / metabolism
  • Toxins, Biological / metabolism

Substances

  • Peptides
  • Potassium Channel Blockers
  • Potassium Channels
  • Receptors, Cell Surface
  • Scorpion Venoms
  • Toxins, Biological
  • hanatoxin
  • agitoxin 2