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dc.contributor | Facultad de Ciencias Biologicas y Ambientales | es_ES |
dc.contributor.author | López Ferreras, Lorena | |
dc.contributor.author | Martínez-García, Nicole | |
dc.contributor.author | Maeso Alonso, Laura | |
dc.contributor.author | Martín López, Marta | |
dc.contributor.author | Díez Matilla, Ángela | |
dc.contributor.author | Villoch-Fernández, Javier | |
dc.contributor.author | Alonso-Olivares, Hugo | |
dc.contributor.author | Marqués Martínez, Margarita | |
dc.contributor.author | Marín Vieira, María Carmen | |
dc.contributor.other | Bioquimica y Biologia Molecular | es_ES |
dc.date | 2021-06-25 | |
dc.date.accessioned | 2024-01-18T11:59:12Z | |
dc.date.available | 2024-01-18T11:59:12Z | |
dc.identifier.citation | López-Ferreras, L., Martínez-García, N., Maeso-Alonso, L., Martín-López, M., Díez-Matilla, Á., Villoch-Fernandez, J., Alonso-Olivares, H., Marques, M. M., & Marin, M. C. (2021). Deciphering the nature of trp73 isoforms in mouse embryonic stem cell models: Generation of isoform-specific deficient cell lines using the crispr/cas9 gene editing system. Cancers, 13(13), Article e3182. https://doi.org/10.3390/CANCERS13133182 | es_ES |
dc.identifier.other | https://www.mdpi.com/2072-6694/13/13/3182 | es_ES |
dc.identifier.uri | https://hdl.handle.net/10612/17669 | |
dc.description | This article belongs to the Special Issue The Isoforms of the p53 Gene Family and Their Role in Cancer and Aging:Selection Papers from International p53/p63/p73 Isoforms Workshop | es_ES |
dc.description.abstract | [EN] The p53 family has been widely studied for its role in various physiological and pathological processes. Imbalance of p53 family proteins may contribute to developmental abnormalities and pathologies in humans. This family exerts its functions through a profusion of isoforms that are generated by different promoter usage and alternative splicing in a cell type dependent manner. In particular, the Trp73 gene gives rise to TA and DN-p73 isoforms that confer p73 a dual nature. The biological relevance of p73 does not only rely on its tumor suppression effects, but on its pivotal role in several developmental processes. Therefore, the generation of cellular models that allow the study of the individual isoforms in a physiological context is of great biomedical relevance. We generated specific TA and DN-p73-deficient mouse embryonic stem cell lines using the CRISPR/Cas9 gene editing system and validated them as physiological bona fide p73-isoform knockout models. Global gene expression analysis revealed isoform-specific alterations of distinctive transcriptional networks. Elimination of TA or DN-p73 is compatible with pluripotency but prompts naïve pluripotent stem cell transition into the primed state, compromising adequate lineage differentiation, thus suggesting that differential expression of p73 isoforms acts as a rheostat during early cell fate determination | es_ES |
dc.language | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.rights | Atribución 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | Bioquímica | es_ES |
dc.subject | Biotecnología | es_ES |
dc.subject | Genética | es_ES |
dc.subject.other | p73 isoforms | es_ES |
dc.subject.other | TAp73 | es_ES |
dc.subject.other | DNp73 | es_ES |
dc.subject.other | Mouse embryonic stem cells (mESC) | es_ES |
dc.subject.other | Gene editing | es_ES |
dc.subject.other | Pluripotency | es_ES |
dc.subject.other | Differentiation | es_ES |
dc.subject.other | Cell fate | es_ES |
dc.subject.other | Self-renewal | es_ES |
dc.subject.other | CRISPR/Cas9 | es_ES |
dc.title | Deciphering the Nature of Trp73 Isoforms in Mouse Embryonic Stem Cell Models: Generation of Isoform-Specific Deficient Cell Lines Using the CRISPR/Cas9 Gene Editing System | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.identifier.doi | 10.3390/cancers13133182 | |
dc.description.peerreviewed | SI | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/AEI/Programa Estatal de Generación de Conocimiento y Fortalecimiento Científico y Tecnológico del Sistema de I+D+i/PID2019-105169RB-I00/ES/FUNCION DE P73 EN EL ADHESOMA CELULAR: IMPLICACIONES EN MORFOGENESIS VASCULAR, ANGIOGENESIS Y CANCER | es_ES |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es_ES |
dc.identifier.essn | 2072-6694 | |
dc.journal.title | Cancers | es_ES |
dc.volume.number | 13 | es_ES |
dc.issue.number | 13 | es_ES |
dc.page.initial | 3182 | es_ES |
dc.type.hasVersion | info:eu-repo/semantics/publishedVersion | es_ES |
dc.subject.unesco | 2410.07 Genética Humana | es_ES |
dc.subject.unesco | 2415 Biología Molecular | es_ES |
dc.subject.unesco | 3201.01 Oncología | es_ES |
dc.subject.unesco | 2409.02 Ingeniería Genética | es_ES |
dc.subject.unesco | 2407 Biología Celular | es_ES |
dc.description.project | This work was supported by Grants PID2019-105169RB-I00 from Spanish Ministerio de Ciencia e Innovación cofinanced by FEDER funds (to M.C.M.) and LE021P17 from Junta de Castilla y Leon. L.L.-F. was a holder of a postdoctoral contract “Juan de de la Cierva-Incorporacion” from Ministerio de Ciencia e Innovación. N.M.-G. and H.A.-O. are supported by a predoctoral scholarship from the Asociación Española contra el Cáncer (AECC). M.M.-L. was a recipient of a Torres Quevedo contract from Ministerio de Ciencia e Innovación at Biomar Microbial Technologies. Á.D.-M., J.V.-F. and L.M.-A. are funded by Junta de Castilla y León | es_ES |
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