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pubmed-article:17284323pubmed:abstractTextSingle-stranded oligonucleotides (ssODN) are used routinely to direct specific base alterations within mammalian genomes that result in the restoration of a functional gene. Despite success with the technique, recent studies have revealed that following repair events, correction frequencies decrease as a function of time, possibly due to a sustained activation of damage response signals in corrected cells that lead to a selective stalling. In this study, we use thymidine to slow down the replication rate to enhance repair frequency and to maintain substantial levels of correction over time.lld:pubmed
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pubmed-article:17284323pubmed:authorpubmed-author:KmiecEric BEBlld:pubmed
pubmed-article:17284323pubmed:authorpubmed-author:EngstromJulia...lld:pubmed
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pubmed-article:17284323pubmed:articleTitleManipulation of cell cycle progression can counteract the apparent loss of correction frequency following oligonucleotide-directed gene repair.lld:pubmed
pubmed-article:17284323pubmed:affiliationDepartment of Biological Sciences, University of Delaware, Delaware Biotechnology Institute, 15 Innovation Way, Newark, DE 19711, USA. juliaeng@udel.edu <juliaeng@udel.edu>lld:pubmed
pubmed-article:17284323pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17284323pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed