Molecular basis for pore blockade of human Na+ channel Nav1.2 by the μ-conotoxin KIIIA

Science. 2019 Mar 22;363(6433):1309-1313. doi: 10.1126/science.aaw2999. Epub 2019 Feb 14.

Abstract

The voltage-gated sodium channel Nav1.2 is responsible for the initiation and propagation of action potentials in the central nervous system. We report the cryo-electron microscopy structure of human Nav1.2 bound to a peptidic pore blocker, the μ-conotoxin KIIIA, in the presence of an auxiliary subunit, β2, to an overall resolution of 3.0 angstroms. The immunoglobulin domain of β2 interacts with the shoulder of the pore domain through a disulfide bond. The 16-residue KIIIA interacts with the extracellular segments in repeats I to III, placing Lys7 at the entrance to the selectivity filter. Many interacting residues are specific to Nav1.2, revealing a molecular basis for KIIIA specificity. The structure establishes a framework for the rational design of subtype-specific blockers for Nav channels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Conotoxins / chemistry*
  • Cryoelectron Microscopy
  • HEK293 Cells
  • Humans
  • NAV1.2 Voltage-Gated Sodium Channel / chemistry*
  • Protein Conformation
  • Voltage-Gated Sodium Channel Blockers / chemistry*
  • Voltage-Gated Sodium Channel beta-2 Subunit / chemistry

Substances

  • Conotoxins
  • NAV1.2 Voltage-Gated Sodium Channel
  • SCN2B protein, human
  • Voltage-Gated Sodium Channel Blockers
  • Voltage-Gated Sodium Channel beta-2 Subunit
  • mu-conotoxin KIIIA, Conus kinoshitai