Sea anemone toxin and scorpion toxin share a common receptor site associated with the action potential sodium ionophore.
Toxin II isolated from the sea anemone Anemonia sulcata enhances activation of the action potential sodium ionophore of electrically excitable neuroblastoma cells by veratridine and batrachotoxin. This heterotropic cooperative effect is identical to that observed previously with scorpion toxin but occurs at a 110-fold higher concentration. Depolarization of the neuroblastoma cells inhibits the effect of sea anemone toxin as observed previously for scorpion toxin. Specific scorpion toxin binding is inhibited by sea anemone toxin with KD approximately equal to 90 nM. These results show that the polypeptides scorpion toxin and sea anemone toxin II share a common receptors site associated with action potential sodium ionophores.
D000200:Action Potentials; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002460:Cell Line; D003064:Cnidarian Venoms / Q000378:metabolism* / Q000494:pharmacology; D007476:Ionophores / Q000378:metabolism*; D007700:Kinetics; D009498:Neurotoxins / Q000378:metabolism; D011955:Receptors, Drug / Q000378:metabolism*; D012604:Scorpion Venoms / Q000378:metabolism* / Q000494:pharmacology; D012615:Sea Anemones; D012964:Sodium / Q000378:metabolism*
D003064:Cnidarian Venoms; D007476:Ionophores; D009498:Neurotoxins; D011955:Receptors, Drug; D012604:Scorpion Venoms; D012964:Sodium