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Selective antagonist of α3β4 nicotinic acetylcholine receptors. Displays > 100-fold selectivity over other receptor subunit combinations including α2β2, α2β4, α3β2, α4β2, α4β4 and α1β1γδ.
Sold under license from University of Utah
(Modifications: Cys-15 = C-terminal amide, Disulfide bridge between 2 - 8, 3 - 15)
|Storage||Desiccate 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.
|Solubility||Soluble to 5 mg/ml in water|
References are publications that support the biological activity of the product.
Luo et al (1998) α-Conotoxin AuIB selectively blocks α3β4 nicotinic acetylcholine receptors and nicotine-evoked NE release. J.Neurosci. 18 8571 PMID: 9786965
Nai et al (2003) Relating neuronal nicotinic acetylcholine receptor subtypes defined by subunit composition and channel function. Mol.Pharmacol. 63 311 PMID: 12527802
Park et al (2006) An α3β4 subunit combination acts as a major functional nicotinic acetylcholine receptor in male rat pelvic ganglion neurons. Pflugers Arch. 452 775 PMID: 16715294
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Literature in this Area
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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.