English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/165491
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:


CtIP-specific roles during cell reprogramming have long-term consequences in the survival and fitness of induced pluripotent stem cells

AuthorsGómez-Cabello, Daniel ; Checa-Rodriguez, Cintia; Abad, María; Serrano, Manuel; Huertas Sánchez, Pablo
KeywordsGenetic instability
Cell reprogramming
DNA resection
Issue Date2017
CitationStem Cell Reports 8(2): 432-445 (2017)
AbstractAcquired genomic instability is one of the major concerns for the clinical use of induced pluripotent stem cells (iPSCs). All reprogramming methods are accompanied by the induction of DNA damage, of which double-strand breaks are the most cytotoxic and mutagenic. Consequently, DNA repair genes seem to be relevant for accurate reprogramming to minimize the impact of such DNA damage. Here, we reveal that reprogramming is associated with high levels of DNA end resection, a critical step in homologous recombination. Moreover, the resection factor CtIP is essential for cell reprogramming and establishment of iPSCs, probably to repair reprogramming-induced DNA damage. Our data reveal a new role for DNA end resection in maintaining genomic stability during cell reprogramming, allowing DNA repair fidelity to be retained in both human and mouse iPSCs. Moreover, we demonstrate that reprogramming in a resection-defective environment has long-term consequences on stem cell self-renewal and differentiation
Publisher version (URL)https://doi.org/10.1016/j.stemcr.2016.12.009
Identifiersdoi: 10.1016/j.stemcr.2016.12.009
e-issn: 2213-6711
Appears in Collections:(CABIMER) Artículos
Files in This Item:
File Description SizeFormat 
ctlpcell.pdf1,9 MBUnknownView/Open
Show full item record
Review this work

Related articles:

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.