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dc.contributor.authorMartin, Pilar 
dc.contributor.authorMoscat, Jorge
dc.date.accessioned2019-06-13T09:10:09Z
dc.date.available2019-06-13T09:10:09Z
dc.date.issued2012
dc.identifier.citationFront Immunol. 2012; 3:241es_ES
dc.identifier.issn1664-3224es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7776
dc.description.abstractThe members of the atypical Protein Kinase Cs (aPKC) kinase subfamily, PKCζ and PKCλ/ɩ, as well as their adapters, p62 and Par-6, form part of the PB1-domain-containing group of signaling regulators. Both adapters serve to locate through heterotypic interactions the aPKCs into the NF-κB and cell polarity pathways, respectively. Both signaling cascades have been critically implicated in T cell function in vitro and in vivo. The analysis of gene-knockout (KO) mice deficient in the different PB1 molecules is providing more definitive information on the actual role that the aPKCs and other PB1-containing molecules play in B cell biology and T cell polarity, survival, and differentiation toward the different effector lineages in vivo and at the cellular ex vivo level. Here we discuss recent data generated from the analysis of KO mice linking the control of cell polarity by PKCλ/ɩ and PKCζ, their adapter p62, and the Par-4 inhibitor, in the control of B and T cell signaling and differentiation. Altogether, these genetic and biochemical evidences reveal the existence of a PB1-orchestrated signaling network that acts to control Th2 differentiation in vitro and in vivo, and the gene transcriptional programs that are essential during the B cell maturation and function and Th2 differentiation.es_ES
dc.description.sponsorshipThis work was funded by grants SAF2011-27330 and INDISNET 01592006 from the Spanish Ministry of Economy and Competitiveness, and Comunidad de Madrid, respectively, to Pilar Martín, and R01AI072581 from the National Institutes of Health to Jorge Moscat.es_ES
dc.language.isoenges_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectB cellses_ES
dc.subjectT cellses_ES
dc.subjectTh1es_ES
dc.subjectTh2es_ES
dc.subjectadaptive immune responseses_ES
dc.subjectasthmaes_ES
dc.subjectatypical PKCses_ES
dc.titleTh1/Th2 Differentiation and B Cell Function by the Atypical PKCs and Their Regulatorses_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID22888333es_ES
dc.format.volume3es_ES
dc.format.page241es_ES
dc.identifier.doi10.3389/fimmu.2012.00241es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderComunidad de Madrid
dc.contributor.funderNational Institutes of Health (United States)
dc.description.peerreviewedes_ES
dc.identifier.e-issn1664-3224es_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fimmu.2012.00241es_ES
dc.identifier.journalFrontiers in immunologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Moléculas Reguladoras de los Procesos Inflamatorioses_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2011-27330es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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