Article
Loss of Na+ channel inactivation by anemone toxin (ATX II) mimics the myotonic state in hyperkalaemic periodic paralysis.
The Journal of physiology - 1 Jul 1993
Cannon S C, Corey D P
Abstract excerpt
1. Mutations that impair inactivation of the sodium channel in skeletal muscle have recently been postulated to cause several heritable forms of myotonia in man. A peptide toxin from Anemonia sulcata (ATX II) selectively disrupts the inactivation mechanism of sodium channels in a way that mimics these mutations. We applied ATX II to rat skeletal muscle to test the hypothesis that myotonia is inducible by altered...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
