Article
Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channel.
Nature communications - 1 Jan 2012
Yang Yang, Dib-Hajj Sulayman D, Zhang Jian, Zhang Yang, Tyrrell Lynda, Estacion Mark, Waxman Stephen G
Abstract excerpt
Sodium channel Na(V)1.7 is critical for human pain signalling. Gain-of-function mutations produce pain syndromes including inherited erythromelalgia, which is usually resistant to pharmacotherapy, but carbamazepine normalizes activation of Na(V)1.7-V400M mutant channels from a family with carbama...
Topics
- Action Potentials
- Animals
- Carbamazepine
- Dimethyl Sulfoxide
- Ganglia, Spinal
- HEK293 Cells
- Humans
- Ion Channel Gating
- Models, Molecular
- Mutant Proteins
- Mutation
- NAV1.7 Voltage-Gated Sodium Channel
- Neurons
- Protein Structure, Tertiary
- Rats