Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission. The toxin principally slows the inactivation process of TTX-sensitive sodium channels. It discriminates neuronal versus muscular sodium channel, as it is more potent on rat brain Nav1.2/SCN2A (EC(50)=29 nM) than on rat skeletal muscle Nav1.4/SCN4A (EC(50)=416 nM). It also shows a weak activity on Nav1.7/SCN9A (EC(50)=1.76 uM). In vivo, the toxin produces pain hypersensibility to mechanical and thermal stimuli.(PubMed:23685008). It also exhibits potent analgesic activity (when injected intraperitoneally), increasing hot plate and tail flick withdrawal latencies in a dose-dependent fashion. This paradoxical analgesic action, is significantly suppressed by opioid receptor antagonists, suggesting a pain-induced analgesia mechanism that involves an endogenous opioid system. This led to hypothesis that pain relief induced by peripheral administration of Amm VIII may result from sensitization of primary afferent neurons and subsequent activation of an opioid-dependent noxious inhibitory control. Hide more Source: Recombinant protein corresponding to aa20-84 from Androctonus mauretanicus mauretanicus Alpha-toxin Amm8, fused to 6X His-Tag at N-terminal, expressed in Yeast. Molecular Weight: ~9.4kD Amino Acid Sequence: LKDGYIVNDINCTYFCGRNAYCNELCIKLKGESGYCQWASPYGNSCYCYKLPDHVRTKGPGRCND Storage and Stability: Lyophilized and reconstituted products are stable for 6 months after receipt at -20C. Reconstitute with sterile ddH2O. Aliquot to avoid repeated freezing and thawing. Store at -20C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.
Supplied as a lyophilized powder from 20mM Tris-HCl, 0.5M sodium chloride, pH 8.0, 6% trehalose. Reconstitute with sterile ddH2O to a concentration of 0.1-1mg/ml.
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