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Selective antagonist of α3β2 nAChR receptors (IC50 values are 9.56 and 252 nM for α3β2 and α7 receptors respectively).
Sold under license from University of Utah
(Modifications: Cys-16 = C-terminal amide, Disulfide bridge between 2 - 8, 3 - 16)
|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.
Fainzilber et al (1994) New mollusc-specific α-conotoxins block Aplysia neuronal acetylcholine receptors. Biochemistry 33 9523 PMID: 8068627
Luo et al (1999) Single-residue alteration in α-conotoxin PnIA switches its nAChR subtype selectivity. Biochemistry 38 14542 PMID: 10545176
Everhart et al (2003) Identification of residues that confer α-conotoxin-PnIA sensitivity on the α3 subunit of neuronal nicotinic acetylcholine receptors. J.Pharmacol.Exp.Ther. 306 664 PMID: 12734390
If you know of a relevant reference for α-Conotoxin PnIA, please let us know.
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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.