Highly potent and selective competitive antagonist for α3β2 subunit-containing nicotinic receptors (IC50 = 0.5 - 3.5 nM at α3β2 expressed in Xenopus oocytes). Also potently blocks β3-containing neuronal nicotinic receptors. Displays > 200-fold selectivity for α3β2 over α2β2, α4β2 and α3β4.
Sold under license from the University of Utah.
(Modifications: Disulfide bridge between 2 - 8, 3 - 16, Cys-16 = C-terminal amide)
|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 1 mg/ml in water|
References are publications that support the biological activity of the product.
Cartier et al (1996) A new α-conotoxin which targets α3β2 nicotinic acetylcholine receptors. J.Biol.Chem. 271 7522 PMID: 8631783
Harvey et al (1997) Determinants of specificity for α-conotoxin MII on α3β2 neuronal nicotinic receptors. Mol.Pharmacol. 51 336 PMID: 9203640
McIntosh et al (2000) Conus peptides: novel probes for nicotinic acetylcholine receptor structure and function. Eur.J.Pharmacol. 393 205 PMID: 10771014
David et al (2010) Biochemical and functional properties of distinct nicotinic acetylcholine receptors in the superior cervical ganglion of mice with targeted deletions of nAChR subunit genes. Eur.J.Neurosci. 31 978 PMID: 20377613
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Keywords: alpha-Conotoxin MII, alpha-Conotoxin MII supplier, Potent, α3β2, alpha3beta2, a3b2, b3, β3, beta3, subunit, selective, nicotinic, antagonist, Acetylcholine, ACh, Receptors, Non-Selective, Subtypes, nAChR, α-conotoxin, alpha-conotoxin, MII, a-ConotoxinMII, venoms, Nicotinic, (Other, Subtypes), 1340, Tocris Bioscience
1 Citation for α-Conotoxin MII
Citations are publications that use Tocris products. Selected citations for α-Conotoxin MII include:
Krais et al (2011) CHRNA5 as negative regulator of nicotine signaling in normal and cancer bronchial cells: effects on motility, migration and p63 expression. Carcinogenesis 32 1388 PMID: 21586512
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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.