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Discontinued Productα-Conotoxin EI (Cat. No. 3124) has been withdrawn from sale for commercial reasons.
Selective antagonist of neuromuscular nicotinic receptors α1β1γδ. Displays selectivity for α/δ sites over α/γ sites in Torpedo.
Sold under license from University of Utah
(Modifications: X = Hyp, Cys-18 = C-terminal amide, Disulfide bridge between 4 - 10, 5 - 17)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Martinez et al (1995) α-Conotoxin EI, a new nicotinic acetylcholine receptor antagonist with novel selectivity. Biochemistry 34 14519 PMID: 7578057
Park et al (2001) Solution conformation of α-Conotoxin EI, a neuromuscular toxin specific for the α1/δ subunit interface of Torpedo nicotinic acetylcholine receptor. J.Biol.Chem. 276 49028 PMID: 11641403
Lopez-Vera et al (2007) Novel α-conotoxins from Conus spurius and the α-conotoxin EI share high-affinity potentiation and low-affinity inhibition of nicotinic acetylcholine receptors. FEBS Lett. 274 3972
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Keywords: alpha-Conotoxin EI, alpha-Conotoxin EI supplier, α1β1δγ, alpha1beta1deltagamma, a1b1dg, selective, nAChR, antagonists, Acetylcholine, Nicotinic, Receptors, Non-Selective, Subtypes, Other, α-conotoxin, alpha-conotoxin, EI, a-ConotoxinEI, conotoxins, venoms, (Other, Subtypes), 3124, Tocris Bioscience
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Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.