Cross-talks between c-Kit and PKC isoforms in HMC-1560 and HMC-1560,816 cells. Different role of PKCd in each cellular line

dc.contributor.affiliationUniversidade de Santiago de Compostela. Departamento de Farmacoloxíaes_ES
dc.contributor.affiliationUniversidade de Santiago de Compostela. Departamento de Farmacoloxía, Farmacia e Tecnoloxía Farmacéuticaes_ES
dc.contributor.authorTobío Ageitos, Araceli
dc.contributor.authorAlfonso Rancaño, María Amparo
dc.contributor.authorBotana López, Luis Miguel
dc.date.accessioned2024-10-02T12:32:18Z
dc.date.available2024-10-02T12:32:18Z
dc.date.issued2014-12-23
dc.description.abstractThe c-kit inhibitor STI571 represents one of the most important treatments for patients with mastocytosis. However, intracellular pathways modulated by this compound are not completely defined. Here, STI571 effect on Protein Kinase C (PKC) regulation is determined in HMC-1 mast cell lines. STI571 activates PKCδ isoform resulting in HMC-1560 apoptosis. The apoptosis observed is PKCδ-dependent, since PKCδ-silencing avoids STI571 effect. c-kit inhibition implies nuclear PKCδ translocation characterized by a clear dependence on actin cytoskeleton integrity in HMC-1560 cell line, but not in HMC-1560,816. Therefore, PKCδ modulations can lead to a serious decrease in STI571 treatment-effectivenesses_ES
dc.description.peerreviewedSIes_ES
dc.description.sponsorshipThe research leading to these results has received funding from the following FEDER cofunded-grants. From CDTI and Technological Funds, supported by Ministerio de Economía y Competitividad, AGL2012-40185-CO2-01 and Consellería de Cultura, Educación e Ordenación Universitaria, GRC2013-016, and through Axencia Galega de Innovación, Spain, ITC-20133020 SINTOX, IN852A 2013/16-3 MYTIGAL. From CDTI under ISIP Programme, Spain, IDI-20130304 APTAFOOD.From the European Union’s Seventh Framework Programme managed by REA – Research Executive Agency (FP7/2007-2013) under grant agreement Nos. 265409 μAQUA, 315285 CIGUATOOLS and 312184 PHARMASEA. Araceli Tobío Ageitos is supported by a fellowship from Fundación Juana de Vega, Spaines_ES
dc.identifier.citationCellular Immunology (293) 2 (2015) Pages 104-112es_ES
dc.identifier.doi10.1016/j.cellimm.2014.12.004
dc.identifier.essn1090-2163
dc.identifier.issn0008-8749
dc.identifier.urihttp://hdl.handle.net/10347/34992
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.cellimm.2014.12.004es_ES
dc.rights© 2014 The Authors. Published by Elsevier Inc. This article is available under the Creative Commons CC-BY-NC-ND licensees_ES
dc.rightsAtribución-NoComercial 4.0 Internacional
dc.rights.accessRightsopen accesses_ES
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subjectHMC-1es_ES
dc.subjectPKCes_ES
dc.subjectc-kites_ES
dc.subjectSTI571es_ES
dc.subjectPMAes_ES
dc.titleCross-talks between c-Kit and PKC isoforms in HMC-1560 and HMC-1560,816 cells. Different role of PKCd in each cellular linees_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
relation.isAuthorOfPublication91b7cd55-e565-47a8-9ea6-ee5438391839
relation.isAuthorOfPublicatione493d380-66bb-4ff9-bb05-4da21d0b21e7
relation.isAuthorOfPublication9a18ed42-77b6-4760-8303-ff4070a87ca6
relation.isAuthorOfPublication.latestForDiscovery91b7cd55-e565-47a8-9ea6-ee5438391839

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