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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Human HT-29 colon carcinoma cells contain muscarinic M3 receptors coupled to phosphoinositide metabolism.

Five different muscarinic receptor subtypes can be distinguished by the differences in their amino acid sequence, the coupled signal transduction system, pharmacological binding properties and activation of ionic fluxes. The present study served to characterize the binding profile of muscarinic receptors in human colon carcinoma cells (HT-29) using selective muscarinic antagonists. The affinities of the compounds were compared with their potency to inhibit cholinergically-activated phosphoinositide metabolism. Pirenzepine displaced [3H]N-methyl-scopolamine binding and inhibited inositolphosphate (IP) release with potencies typical of those of non-M1 receptors. The M3 subtype-selective antagonists sila-hexocyclium and hexahydro-sila-difenidol had high affinity to the muscarinic receptors in HT-29 cells (KD = 3.1 nM and 27 nM, respectively) and inhibited IP release at nanomolar concentrations. The M2 receptor antagonists, AF-DX 116 and methoctramine, had low antimuscarinic potencies. Our results demonstrate that HT-29 human colon carcinoma cells contain an apparently pure population of M3 receptors. These cells could serve as a model system for further investigations concerning regulatory and signal transduction mechanisms associated with glandular muscarinic M3 receptors.[1]


  1. Human HT-29 colon carcinoma cells contain muscarinic M3 receptors coupled to phosphoinositide metabolism. Kopp, R., Lambrecht, G., Mutschler, E., Moser, U., Tacke, R., Pfeiffer, A. Eur. J. Pharmacol. (1989) [Pubmed]
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