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Alpha-toxin Amm8  Protein, Androctonus mauritanicus, Recombinant (His & Myc)

Catalog No. TMPH-00055
Synonyms: AmmVIII, Neurotoxin 8, Alpha-anatoxin Amm VIII, Amm VIII

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.

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Alpha-toxin Amm8  Protein, Androctonus mauritanicus, Recombinant (His & Myc)
Pack Size Availability Price/USD Quantity
20 μg 20 days $ 491.00
100 μg 20 days $ 1,370.00
1 mg 20 days $ 2,750.00
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Biological Description
Technical Params
Product Properties
Description 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.
Species Androctonus mauritanicus
Expression System Baculovirus
Tag N-terminal 10xHis-tagged and C-terminal Myc-tagged
Accession Number Q7YXD3
Synonyms AmmVIII, Neurotoxin 8, Alpha-anatoxin Amm VIII, Amm VIII
Amino Acid LKDGYIVNDINCTYFCGRNAYCNELCIKLKGESGYCQWASPYGNSCYCYKLPDHVRTKGPGRCND Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Construction 20-84 aa
Protein Purity > 85% as determined by SDS-PAGE.
Molecular Weight 11.3 kDa as predicted
Formulation If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution A hardcopy of COA with reconstitution instructions is sent along with the products. Please refer to it for detailed information.
Stability & Storage

Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Shipping

In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature. Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.

Research Background 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.

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Keywords

Alpha-toxin Amm8  Protein, Androctonus mauritanicus, Recombinant (His & Myc) AmmVIII Neurotoxin 8 Alpha-anatoxin Amm VIII Amm VIII recombinant recombinant-proteins proteins protein

 

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