Anti-Alpha-toxin Amm8

Make to order. Production time: 70-80 business days. Deliverables: 1. 200 µg antigen (used as positive control), 2. 1 ml pre-immune serum (used as negative control) , 3. Rabbit polyclonal antibody, antigen affinity purified. Quality Guarantee: 1. Antibody purity > 90% confirmed by SDS-PAGE, 2. Antibody titer > 1: 64,000 confirmed by ELISA, 3. WB positive with the immunogen protein (not applicable for synthetic peptide). Applications: ELISA, WB (positive for the recombinant immunogen protein/peptide). Buffer: Preservative: 0.03% Proclin 300, Constituents: 50% Glycerol, 0.01M PBS, pH 7.4. Protein function: Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission (PubMed:12911331). The toxin principally slows the inactivation process of TTX-sensitive sodium channels (PubMed:23685008). 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) (PubMed:12911331). It also shows a weak activity on Nav1.7/SCN9A (EC(50)=1.76 uM) (PubMed:23685008). 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 (PubMed:20619318). This paradoxical analgesic action, is significantly suppressed by opioid receptor antagonists, suggesting a pain-induced analgesia mechanism that involves an endogenous opioid system (PubMed:20619318). 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 (PubMed:20619318). [The UniProt Consortium]