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dc.contributor.authorTorres-Ruiz Raul, Raul 
dc.contributor.authorMartinez-Lage, Marta
dc.contributor.authorMartin, Maria C
dc.contributor.authorGarcia, Aida
dc.contributor.authorBueno, Clara
dc.contributor.authorCastaño, Julio
dc.contributor.authorRamirez, Juan C
dc.contributor.authorMenendez, Pablo
dc.contributor.authorCigudosa, Juan C
dc.contributor.authorRodriguez Perales, Sandra 
dc.date.accessioned2019-02-26T12:56:37Z
dc.date.available2019-02-26T12:56:37Z
dc.date.issued2017
dc.identifier.citationStem Cell Reports. 2017;8(5):1408-1420.es_ES
dc.identifier.issn22136711es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7238
dc.description.abstractEfficient methodologies for recreating cancer-associated chromosome translocations are in high demand as tools for investigating how such events initiate cancer. The CRISPR/Cas9 system has been used to reconstruct the genetics of these complex rearrangements at native loci while maintaining the architecture and regulatory elements. However, the CRISPR system remains inefficient in human stem cells. Here, we compared three strategies aimed at enhancing the efficiency of the CRISPR-mediated t(11;22) translocation in human stem cells, including mesenchymal and induced pluripotent stem cells: (1) using end-joining DNA processing factors involved in repair mechanisms, or (2) ssODNs to guide the ligation of the double-strand break ends generated by CRISPR/Cas9; and (3) all-in-one plasmid or ribonucleoprotein complex-based approaches. We report that the generation of targeted t(11;22) is significantly increased by using a combination of ribonucleoprotein complexes and ssODNs. The CRISPR/Cas9-mediated generation of targeted t(11;22) in human stem cells opens up new avenues in modeling Ewing sarcoma.es_ES
dc.description.sponsorshipThis work was supported by funds from the Spanish National Research and Development Plan, Instituto de Salud Carlos III, and FEDER (PI14/01884 to S.R.-P. and PI12/00425 to J.C.C.). R.T.-R. was supported by an international fellowship from Lady Tata Memorial Trust during 2016–2017.es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCRISPRes_ES
dc.subjectCas9es_ES
dc.subjectEwing sarcomaes_ES
dc.subjectMSCes_ES
dc.subjectcancer modelinges_ES
dc.subjectcancer translocationes_ES
dc.subjectdisease modeles_ES
dc.subjectgenome engineeringes_ES
dc.subjecthuman stem cellses_ES
dc.subjectiPSCes_ES
dc.subject.meshGene Targeting es_ES
dc.subject.meshHEK293 Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshInduced Pluripotent Stem Cells es_ES
dc.subject.meshMesenchymal Stem Cells es_ES
dc.subject.meshOncogene Proteins, Fusion es_ES
dc.subject.meshSarcoma, Ewing es_ES
dc.subject.meshCRISPR-Cas Systems es_ES
dc.subject.meshTranslocation, Genetices_ES
dc.titleEfficient Recreation of t(11;22) EWSR1-FLI1+ in Human Stem Cells Using CRISPR/Cas9es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID28494941es_ES
dc.format.volume8es_ES
dc.format.number5es_ES
dc.format.page1408-1420es_ES
dc.identifier.doi10.1016/j.stemcr.2017.04.014es_ES
dc.contributor.funderInstItuto de Salud Carlos III (España)es_ES
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)es_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn2213-6711es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.stemcr.2017.04.014.es_ES
dc.identifier.journalStem cell reportses_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Unidades técnicas::Unidad de Citogenética Moleculares_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI14/01884es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI12/00425es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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