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pubmed-article:17560837pubmed:abstractTextWe have previously shown that activation of the homologous recombinational repair pathway leads to a block of cell division in corrected cells, possibly through the activity of checkpoint proteins Chk1 and Chk2. In this study, we examine the long-term impact of this stalling on the growth of cells that have enabled gene repair events. Using a mutated eGFP gene as an episomal reporter, we show that corrected (eGFP-positive) cells contain only a few active replication templates 2 weeks after electroporation, yet do not display an apoptotic or senescent phenotype. By 6 weeks after electroporation, cells resume active replication with a cell cycle profile that is comparable to that of the non-corrected (eGFP-negative) population. These results indicate that the initial stalling is transient and eGFP-positive cells eventually resume a normal phenotypic growth pattern, allowing for passaging and expansion in vitro.lld:pubmed
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pubmed-article:17560837pubmed:authorpubmed-author:Parekh-Olmedo...lld:pubmed
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pubmed-article:17560837pubmed:authorpubmed-author:EngstromJulia...lld:pubmed
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pubmed-article:17560837pubmed:dateRevised2011-2-25lld:pubmed
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pubmed-article:17560837pubmed:articleTitleRecovery of cell cycle delay following targeted gene repair by oligonucleotides.lld:pubmed
pubmed-article:17560837pubmed:affiliationDepartment of Biological Sciences, University of Delaware, Delaware Biotechnology Institute, 15 Innovation Way, Newark, DE 19711, USA.lld:pubmed
pubmed-article:17560837pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17560837pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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