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Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors
Nicotinic acetylcholine receptors (nAChRs) play essential roles in transmitting acetylcholine-mediated neural signals across synapses and neuromuscular junctions, and are also closely linked to various diseases and clinical conditions. Therefore, novel nAChR-specific compounds have great potential f...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585798/ https://www.ncbi.nlm.nih.gov/pubmed/26395518 http://dx.doi.org/10.1038/srep14261 |
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author | Xu, Shaoqiong Zhang, Tianlong Kompella, Shiva N. Yan, Mengdi Lu, Aiping Wang, Yanfang Shao, Xiaoxia Chi, Chengwu Adams, David J. Ding, Jianping Wang, Chunguang |
author_facet | Xu, Shaoqiong Zhang, Tianlong Kompella, Shiva N. Yan, Mengdi Lu, Aiping Wang, Yanfang Shao, Xiaoxia Chi, Chengwu Adams, David J. Ding, Jianping Wang, Chunguang |
author_sort | Xu, Shaoqiong |
collection | PubMed |
description | Nicotinic acetylcholine receptors (nAChRs) play essential roles in transmitting acetylcholine-mediated neural signals across synapses and neuromuscular junctions, and are also closely linked to various diseases and clinical conditions. Therefore, novel nAChR-specific compounds have great potential for both neuroscience research and clinical applications. Conotoxins, the peptide neurotoxins produced by cone snails, are a rich reservoir of novel ligands that target receptors, ion channels and transporters in the nervous system. From the venom of Conus generalis, we identified a novel dimeric nAChR-inhibiting αD-conotoxin GeXXA. By solving the crystal structure and performing structure-guided dissection of this toxin, we demonstrated that the monomeric C-terminal domain of αD-GeXXA, GeXXA-CTD, retains inhibitory activity against the α9α10 nAChR subtype. Furthermore, we identified that His7 of the rat α10 nAChR subunit determines the species preference of αD-GeXXA, and is probably part of the binding site of this toxin. These results together suggest that αD-GeXXA cooperatively binds to two inter-subunit interfaces on the top surface of nAChR, thus allosterically disturbing the opening of the receptor. The novel antagonistic mechanism of αD-GeXXA via a new binding site on nAChRs provides a valuable basis for the rational design of new nAChR-targeting compounds. |
format | Online Article Text |
id | pubmed-4585798 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-45857982015-09-29 Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors Xu, Shaoqiong Zhang, Tianlong Kompella, Shiva N. Yan, Mengdi Lu, Aiping Wang, Yanfang Shao, Xiaoxia Chi, Chengwu Adams, David J. Ding, Jianping Wang, Chunguang Sci Rep Article Nicotinic acetylcholine receptors (nAChRs) play essential roles in transmitting acetylcholine-mediated neural signals across synapses and neuromuscular junctions, and are also closely linked to various diseases and clinical conditions. Therefore, novel nAChR-specific compounds have great potential for both neuroscience research and clinical applications. Conotoxins, the peptide neurotoxins produced by cone snails, are a rich reservoir of novel ligands that target receptors, ion channels and transporters in the nervous system. From the venom of Conus generalis, we identified a novel dimeric nAChR-inhibiting αD-conotoxin GeXXA. By solving the crystal structure and performing structure-guided dissection of this toxin, we demonstrated that the monomeric C-terminal domain of αD-GeXXA, GeXXA-CTD, retains inhibitory activity against the α9α10 nAChR subtype. Furthermore, we identified that His7 of the rat α10 nAChR subunit determines the species preference of αD-GeXXA, and is probably part of the binding site of this toxin. These results together suggest that αD-GeXXA cooperatively binds to two inter-subunit interfaces on the top surface of nAChR, thus allosterically disturbing the opening of the receptor. The novel antagonistic mechanism of αD-GeXXA via a new binding site on nAChRs provides a valuable basis for the rational design of new nAChR-targeting compounds. Nature Publishing Group 2015-09-23 /pmc/articles/PMC4585798/ /pubmed/26395518 http://dx.doi.org/10.1038/srep14261 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Xu, Shaoqiong Zhang, Tianlong Kompella, Shiva N. Yan, Mengdi Lu, Aiping Wang, Yanfang Shao, Xiaoxia Chi, Chengwu Adams, David J. Ding, Jianping Wang, Chunguang Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
title | Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
title_full | Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
title_fullStr | Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
title_full_unstemmed | Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
title_short | Conotoxin αD-GeXXA utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
title_sort | conotoxin αd-gexxa utilizes a novel strategy to antagonize nicotinic acetylcholine receptors |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585798/ https://www.ncbi.nlm.nih.gov/pubmed/26395518 http://dx.doi.org/10.1038/srep14261 |
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