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.
Source:Recombinant protein corresponding to aa20-84 from Androctonus mauritanicus mauritanicus Alpha-toxin Amm8, fused to 10X His-Tag at N-terminal and Myc-Tag at C-terminal, expressed in Baculovirus.
Storage and Stability:May be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for 6 months after receipt at -20°C. 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.
仕様
Size：20ug
Source Antigen：Recombinant, Baculovirus
Grade：Purified
Purity：≥85% (SDS-PAGE)
Form：Supplied as a liquid in Tris, pH 8.0, 6% trehalose, 50% glycerol
