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dc.contributor.authorVico Barranco, Inmaculada
dc.contributor.authorArbulo-Echevarria, Mikel. M.
dc.contributor.authorSerrano-García, Isabel
dc.contributor.authorPérez-Linaza, Alba
dc.contributor.authorMiranda-Sayago, José M.
dc.contributor.authorMiazek, Arkadiusz
dc.contributor.authorNarbona Sánchez, Isaac
dc.contributor.authorAguado Vidal, Enrique
dc.contributor.otherBiomedicina, Biotecnología y Salud Públicaes_ES
dc.date.accessioned2021-04-16T06:47:33Z
dc.date.available2021-04-16T06:47:33Z
dc.date.issued2021-02
dc.identifier.issn2073-4409
dc.identifier.urihttp://hdl.handle.net/10498/24707
dc.description.abstractIntracellular signaling through the T cell receptor (TCR) is essential for T cell development and function. Proper TCR signaling requires the sequential activities of Lck and ZAP-70 kinases, which result in the phosphorylation of tyrosine residues located in the CD3 ITAMs and the LAT adaptor, respectively. LAT, linker for the activation of T cells, is a transmembrane adaptor protein that acts as a scaffold coupling the early signals coming from the TCR with downstream signaling pathways leading to cellular responses. The leukemic T cell line Jurkat and its derivative mutants J.CaM1.6 (Lck deficient) and J.CaM2 (LAT deficient) have been widely used to study the first signaling events upon TCR triggering. In this work, we describe the loss of LAT adaptor expression found in a subline of J.CaM1.6 cells and analyze cis-elements responsible for the LAT expression defect. This new cell subline, which we have called J.CaM1.7, can re-express LAT adaptor after Protein Kinase C (PKC) activation, which suggests that activation-induced LAT expression is not affected in this new cell subline. Contrary to J.CaM1.6 cells, re-expression of Lck in J.CaM1.7 cells was not sufficient to recover TCR-associated signals, and both LAT and Lck had to be introduced to recover activatory intracellular signals triggered after CD3 crosslinking. Overall, our work shows that the new LAT negative J.CaM1.7 cell subline could represent a new model to study the functions of the tyrosine kinase Lck and the LAT adaptor in TCR signaling, and their mutual interaction, which seems to constitute an essential early signaling event associated with the TCR/CD3 complex.es_ES
dc.description.sponsorshipThis research was funded by Consejeria de Salud de Andalucia, Junta de Andalucia (grant PI-0055-2017 to E.A.), and Fundacion Biomedica Cadiz Proyectos INIBICA 2019 (grant LI19/I14NCO15 to E.A. and M.M.A.-E.).es_ES
dc.formatapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.sourceCells 2021, 10(2), 343es_ES
dc.subjectLckes_ES
dc.subjectLATes_ES
dc.subjectJes_ES
dc.subjectCaM1es_ES
dc.subject6es_ES
dc.subjectTCRes_ES
dc.subjectsignalinges_ES
dc.titleA Novel, LAT/Lck Double Deficient T Cell Subline J.CaM1.7 for Combined Analysis of Early TCR Signalinges_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.3390/cells10020343
dc.relation.projectIDConsejería de Salud. Junta de Andalucia [PI-0055-2017]es_ES
dc.relation.projectIDInstituto de Investigación e Innovación Biomedica de Cádiz. INIBICA [LI19/I14NCO15]es_ES


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Atribución 4.0 Internacional
This work is under a Creative Commons License Atribución 4.0 Internacional