Targeting voltage sensors in sodium channels with spider toxins.
Voltage-activated sodium (Nav) channels are essential in generating and propagating nerve impulses, placing them amongst the most widely targeted ion channels by toxins from venomous organisms. An increasing number of spider toxins have been shown to interfere with the voltage-driven activation process of mammalian Nav channels, possibly by interacting with one or more of their voltage sensors. This review focuses on our existing knowledge of the mechanism by which spider toxins affect Nav channel gating and the possible applications of these toxins in the drug discovery process.
Bosmans
Frank
F
Molecular Physiology and Biophysics Section, Porter Neuroscience Research Center National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 USA. bosmansf@ninds.nih.gov <bosmansf@ninds.nih.gov>
Swartz
Kenton J
KJ
D000595:Amino Acid Sequence; D000818:Animals; D016503:Drug Delivery Systems / Q000379:methods*; D006801:Humans; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D008969:Molecular Sequence Data; D026941:Sodium Channel Blockers / Q000008:administration & dosage / Q000737:chemistry; D015222:Sodium Channels / Q000235:genetics / Q000378:metabolism*; D013111:Spider Venoms / Q000008:administration & dosage*
D026941:Sodium Channel Blockers; D015222:Sodium Channels; D013111:Spider Venoms