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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/33336
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dc.contributor.authorFerrés-Masó, Montse-
dc.contributor.authorIovanna, Juan Lucio-
dc.contributor.authorClosa, Daniel-
dc.contributor.authorFolch-Puy, Emma-
dc.date.accessioned2011-03-11T14:11:31Z-
dc.date.available2011-03-11T14:11:31Z-
dc.date.issued2009-05-12-
dc.identifier.citationCellular and Molecular Life Sciences 66(13): 2195-2204 (2009)es_ES
dc.identifier.issn1420-682X-
dc.identifier.urihttp://hdl.handle.net/10261/33336-
dc.descriptionEl pdf del artículo es la versión post-print.-- et al.-
dc.description.abstractPancreatitis-associated protein 1 (PAP1) belongs to the Reg family of secretory proteins. Several important biological roles have been attributed to PAP1 but the signaling pathways activated by this protein remain only partially understood. Here, we describe the intracellular pathways triggered by PAP1 in a pancreatic acinar cell line. Taking advantage of the fact that PAP1 induces its own transcription, we performed ChIP assays to analyze the recruitment of transcriptional factors on its promoter. Our results show that PAP1 increased the transactivation activity of pap1 and the binding on its promoter of the nuclear factors C/EBPβ, P-CREB, P-ELK1, EGR1, STAT3, and ETS2, which are downstream targets of MAPK signaling. p44/42, p38, and JNK MAPKs activity increased after PAP1 treatment. In addition, pharmacological inhibition of these kinases markedly inhibited the induction of pap1 mRNA. Taken together, these results indicated that the mechanism of PAP1 action involves the activation of the MAPK superfamily.es_ES
dc.description.sponsorshipThis work was supported by the FIS PI050599 and FIS PI081608 projects to E. Folch-Puy, Acción Integrada HF2006-0092 and CIBERehd to D. Closa and Spanish Ministry of Science and Technology BFU2007-63120 and CSD2006-49 to G. López-Rodas. CIBERehd is funded by the Instituto de Salud Carlos III. E. Folch-Puy is the recipient of a Ramón y Cajal contract from the Spanish Ministry of Education and Science. M. Ferrés-Masó is the recipient of a FIS-Instituto de Salud Carlos III contract PI050599.-
dc.language.isoenges_ES
dc.publisherSpringer Naturees_ES
dc.relation.isversionofPostprint-
dc.rightsopenAccesses_ES
dc.subjectPAP1es_ES
dc.subjectMAPKes_ES
dc.subjectTranscriptional factorses_ES
dc.subjectAR42Jes_ES
dc.subjectChromatin immunoprecipitationes_ES
dc.subjectRNApol ChIPes_ES
dc.titlePAP1 signaling involves MAPK signal transductiones_ES
dc.typeartículoes_ES
dc.identifier.doi10.1007/s00018-009-0040-4-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1007/s00018-009-0040-4-
dc.identifier.e-issn1420-9071-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.grantfulltextopen-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.languageiso639-1en-
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