ArticleTheoretical biology & medical modelling2009
Binding of long-chain alpha-neurotoxin would stabilize the resting state of nAChR: a comparative study with alpha-conotoxin.
Article in Theoretical biology & medical modelling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
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- High-throughput immuno-profiling of mamba (Dendroaspis) venom toxin epitopes using high-density peptide microarrays.Scientific reports · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe details of interaction in a complex between potent antagonists such as long chain alpha-neurotoxins and alpha-conotoxins with nicotinic acetylcholine receptor (nAChR), and conformational changes induced by these antagonists, are not yet clear. MODELING: In order to uncover some of these critical structural features, we conducted a docking simulation and a molecular dynamics simulation (MD) of a model of the ligand binding domain of nAChR in complex with a long-chain alpha-neurotoxin and an alpha-conotoxin.
resultsOur docking results confirm the claim that T.nAChR is in the basal or resting state, which favors binding to the alpha-neurotoxins. Moreover, more correct "hits" for the alpha/gamma interface upon docking for conotoxin-nAChR confirm the preference of conotoxin GI for the alpha/gamma interface. More importantly, upon binding of alpha-neurotoxin, ligand-bonded nAChR is less dynamic in certain domains than the apo form of the conotoxin-AChR complex. Some critical interactions in the binding site such as the salt bridge formed between K145/D200 in the neurotoxin-nAChR complex is further stabilized during the MD simulation, while it is obviously more labile in the apo form.
conclusionThese observations could support the claim that alpha neurotoxins stabilize the nAChR resting state.
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