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dc.contributor.authorEscudero Hernández, Celia
dc.date.accessioned2017-03-15T08:38:41Z
dc.date.available2017-03-15T08:38:41Z
dc.date.issued2017
dc.identifier.citationInnate Immunity, 2017 Vol. 23(1), pp. 44-53es
dc.identifier.issn1753-4259es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/22616
dc.descriptionProducción Científicaes
dc.description.abstractIL-15 is a pleiotropic cytokine related to IL-2 which acts at a broader level than its counterpart. It is presented through its specific high-affinity receptor, IL-15Ra. Both cytokine and receptor are tightly regulated at multiple levels and are widely distributed. Thus, deregulation of their expression leads to an inflammatory immune response. Variants of splicing of IL-15Ra have been described in immune and barrier cells; however, their presence has not been focused on intestinal epithelial cells. In this study, we describe five new alternative variants of splicing of IL-15Ra in Caco-2 cells. Four of them were expressed into proteins inside Caco-2 cells, but these were unable to bind IL-15 or to follow the secretory pathway. However, the expression of mRNA itself might be relevant to diseases such as celiac disease, inflammatory bowel disease or colorectal cancer.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherInternational Endotoxin and Innate Immunity Societyes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.classificationCáncer colorrectales
dc.subject.classificationEnfermedad celíacaes
dc.subject.classificationColon irritablees
dc.titleNew IL-15 receptor-α splicing variants identified in intestinal epithelial Caco-2 cellses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1177/175342 5916674263es
dc.relation.publisherversionhttps://journals.sagepub.com/doi/10.1177/1753425916674263
dc.identifier.publicationfirstpage1es
dc.identifier.publicationlastpage10es
dc.identifier.publicationtitleInnate Immunityes
dc.identifier.publicationvolume2es
dc.peerreviewedSIes
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International


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