The β3-subunit modulates the effect of venom peptides ProTx-II and OD1 on Na_V 1.7 gating.

ABSTRACT: The voltage-gated sodium channel Na_V 1.7 is involved in various pain phenotypes and is physiologically regulated by the Na_V -β3-subunit. Venom toxins ProTx-II and OD1 modulate Na_V 1.7 channel function and may be useful as therapeutic agents and/or research tools. Here, we use patch-clamp recordings to investigate how the β3-subunit can influence and modulate the toxin-mediated effects on Na_V 1.7 function, and we propose a putative binding mode of OD1 on Na_V 1.7 to rationalise its activating effects. The inhibitor ProTx-II slowed the rate of Na_V 1.7 activation, whilst the activator OD1 reduced the rate of fast inactivation and accelerated recovery from inactivation. The β3-subunit partially abrogated these effects. OD1 induce

SUBMITTER: Salvage SC 

PROVIDER: S-EPMC10953403 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature