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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Castillo Acosta, Víctor M. | es_ES |
dc.contributor.author | Ruiz-Pérez, Luis Miguel | es_ES |
dc.contributor.author | Van Damme, Els J. M. | es_ES |
dc.contributor.author | Balzarini, Jan | es_ES |
dc.contributor.author | González-Pacanowska, Dolores | es_ES |
dc.date.accessioned | 2017-09-20T10:13:11Z | - |
dc.date.available | 2017-09-20T10:13:11Z | - |
dc.date.issued | 2015-03-06 | - |
dc.identifier.citation | PLoS Neglected Tropical Diseases | es_ES |
dc.identifier.issn | 1935-2727 | - |
dc.identifier.uri | http://hdl.handle.net/10261/155345 | - |
dc.description.abstract | Trypanosoma brucei variant surface glycoproteins (VSG) are glycosylated by both paucimannose and oligomannose structures which are involved in the formation of a protective barrier against the immune system. Here, we report that the stinging nettle lectin (UDA), with predominant N-acetylglucosamine-binding specificity, interacts with glycosylated VSGs and kills parasites by provoking defects in endocytosis together with impaired cytokinesis. Prolonged exposure to UDA induced parasite resistance based on a diminished capacity to bind the lectin due to an enrichment of biantennary paucimannose and a reduction of triantennary oligomannose structures. Two molecular mechanisms involved in resistance were identified: VSG switching and modifications in N-glycan composition. Glycosylation defects were correlated with the down-regulation of the TbSTT3A and/or TbSTT3B genes (coding for oligosaccharyltransferases A and B, respectively) responsible for glycan specificity. Furthermore, UDA-resistant trypanosomes exhibited severely impaired infectivity indicating that the resistant phenotype entails a substantial fitness cost. The results obtained further support the modification of surface glycan composition resulting from down-regulation of the genes coding for oligosaccharyltransferases as a general resistance mechanism in response to prolonged exposure to carbohydrate-binding agents | es_ES |
dc.description.sponsorship | This work was supported by grants from the VI Plan Nacional de Investigación Científica, Desarrollo e Innovación Tecnológica 2008-2011, Instituto de Salud Carlos III - Subdirección General de Redes y Centros de Investigación Cooperativa, Red de Investigación Cooperativa en Enfermedades Tropicales (RICET) (RD06/0021), the Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016 (SAF2010-20059) (http://www.idi.mineco.gob.es), and the Junta de Andalucía (BIO-199, P09-CVI-5367) to DGP. Research of JB was supported by the Katholieke Universiteit Leuven (GOA 10/14 and PF 10/18) and the Flemish Research Foundation - Flanders (Flemish FWO) (www.fwo.be), (G.0485.08). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Public Library of Science | es_ES |
dc.relation.isversionof | Publisher's version | es_ES |
dc.rights | openAccess | es_ES |
dc.title | Exposure of Trypanosoma brucei to an N-acetylglucosamine-Binding Lectin Induces VSG Switching and Glycosylation Defects Resulting in Reduced Infectivity | es_ES |
dc.type | artículo | es_ES |
dc.identifier.doi | 10.1371/journal.pntd.0003612 | - |
dc.description.peerreviewed | Peer reviewed | es_ES |
dc.relation.publisherversion | http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0003612#ack | es_ES |
dc.identifier.e-issn | 1935-2735 | - |
dc.rights.license | https://creativecommons.org/licenses/by/4.0/ | es_ES |
dc.relation.csic | Sí | es_ES |
oprm.item.hasRevision | no ko 0 false | * |
dc.identifier.pmid | 25746926 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
item.languageiso639-1 | en | - |
item.openairetype | artículo | - |
Aparece en las colecciones: | (IPBLN) Artículos |
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Exposure_pntd.PDF | 1,28 MB | Adobe PDF | Visualizar/Abrir |
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