ATX-II

In contrast, the application of Toxin II from Anemonia sulcata results in the increase of the EJPS up to 40 mV causing large action potentials at the muscle fibers.

Although both sea anemone and α-scorpion toxins bind to common overlapping elements on the extracellular surface of sodium channels, they belong to distinct families and share no sequence homology.

[10] ATX-II is highly potent at voltage-gated sodium channels subtype 1.1 and 1.2 (Nav1.1 and Nav1.2) with an EC50 of approximately 7 nM when tested in human embryonic kidney 293 cells lines.

[11] Moreover, studies suggest that ATX-II interacts with glutamic acid residue (Glu-1613 and 1616 in Nav1.2) on the third and fourth transmembrane loop (S3-S4) of domain IV on the alpha-subunit of neuronal channel Nav1.2 in rats.

Studies using giant crayfish axons and myelinated fibers from frogs indicate that ATX-II acts at low doses, without changing the opening mechanism or steady-state potassium conductance.

[16] ATX-II also selectively activates A-fibers of peripheral nerves projecting to the sensory neuron of the dorsal root ganglia (DRG) by enhancing resurging currents in DRGs.

[13] In cardiac muscle tissue of various mammals, ATX-II has been shown to produce large and potentially lethal increases in heart rate.