pubmed-article:17284323 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17284323 | lifeskim:mentions | umls-concept:C1516334 | lld:lifeskim |
pubmed-article:17284323 | lifeskim:mentions | umls-concept:C0947647 | lld:lifeskim |
pubmed-article:17284323 | lifeskim:mentions | umls-concept:C1947976 | lld:lifeskim |
pubmed-article:17284323 | lifeskim:mentions | umls-concept:C0376249 | lld:lifeskim |
pubmed-article:17284323 | lifeskim:mentions | umls-concept:C1720856 | lld:lifeskim |
pubmed-article:17284323 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
pubmed-article:17284323 | pubmed:dateCreated | 2007-2-14 | lld:pubmed |
pubmed-article:17284323 | pubmed:abstractText | Single-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:17284323 | pubmed:language | eng | lld:pubmed |
pubmed-article:17284323 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17284323 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17284323 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17284323 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17284323 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17284323 | pubmed:issn | 1471-2199 | lld:pubmed |
pubmed-article:17284323 | pubmed:author | pubmed-author:KmiecEric BEB | lld:pubmed |
pubmed-article:17284323 | pubmed:author | pubmed-author:EngstromJulia... | lld:pubmed |
pubmed-article:17284323 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17284323 | pubmed:volume | 8 | lld:pubmed |
pubmed-article:17284323 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17284323 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17284323 | pubmed:pagination | 9 | lld:pubmed |
pubmed-article:17284323 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:17284323 | pubmed:meshHeading | pubmed-meshheading:17284323... | lld:pubmed |
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pubmed-article:17284323 | pubmed:meshHeading | pubmed-meshheading:17284323... | lld:pubmed |
pubmed-article:17284323 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17284323 | pubmed:articleTitle | Manipulation of cell cycle progression can counteract the apparent loss of correction frequency following oligonucleotide-directed gene repair. | lld:pubmed |
pubmed-article:17284323 | pubmed:affiliation | Department 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:17284323 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17284323 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |