11032-79-4

Single polypeptide weight; molecular weight of 8000.

Nuerotoxic.

A polypeptide composed of 74 amino acids containing 5 disulfide bridges. Blocks neuromuscular transmission by irreversible binding to the motor end-plate acetylcholine receptor (K_d = 1 nM to 1 pM) but does not depress acetylcholine release from motor nerve endings. Blocks nicotine-induced augmentation in intracellular Ca²⁺ in PC12 cells (IC₅₀ = 310 nM). Prevents opening of nicotinic receptor-associated ion channels. Reconstitution experiments in Xenopus oocytes have shown the effects of α-Bungarotoxin on neuronal nAChR to be highly specific for the α₇-subtype (IC₅₀ = 1.6 nM), but not for the α₃β₄-subtype (IC₅₀ >3 µM).
Blocks neuromuscular transmission by irreversible binding to motor end-plate acetylcholine receptor (K_d = 1 pM to 1 nM) but does not depress acetylcholine release from motor nerve endings. Blocks nicotine-induced increase of intracellular Ca²⁺ in PC12 cells (IC₅₀ = 310 nM), and prevents opening of nicotinic receptor-associated ion channels. Reconstitution experiments in Xenopus oocytes have shown the effects of α-bungarotoxin on neuronal nAChR to be highly specific for the α₇-subtype (IC₅₀ = 1.6 nM), but not for the α₃β₄-subtype (IC₅₀ >3 µM).

Blocks neuromuscular transmission by irreversible binding to motor end-plate acetylcholine receptor (K_d = 1 pM to 1 nM) but does not depress acetylcholine release from motor nerve endings. Blocks nicotine-induced increase of intracellular Ca²⁺ in PC12 cells (IC₅₀ = 310 nM), and prevents opening of nicotinic receptor-associated ion channels. Reconstitution experiments in Xenopus oocytes have shown the effects of α-bungarotoxin on neuronal nAChR to be highly specific for the α₇-subtype (IC₅₀ = 1.6 nM), but not for the α₃β₄-subtype (IC₅₀ >3 μM).

Product does not compete with ATP.

-20°C (desiccate)