pubmed-article:17560837 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17560837 | lifeskim:mentions | umls-concept:C0007586 | lld:lifeskim |
pubmed-article:17560837 | lifeskim:mentions | umls-concept:C0028953 | lld:lifeskim |
pubmed-article:17560837 | lifeskim:mentions | umls-concept:C2004454 | lld:lifeskim |
pubmed-article:17560837 | lifeskim:mentions | umls-concept:C1720855 | lld:lifeskim |
pubmed-article:17560837 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
pubmed-article:17560837 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:17560837 | pubmed:dateCreated | 2007-9-17 | lld:pubmed |
pubmed-article:17560837 | pubmed:abstractText | We 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:17560837 | pubmed:language | eng | lld:pubmed |
pubmed-article:17560837 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17560837 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17560837 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17560837 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17560837 | pubmed:month | Oct | lld:pubmed |
pubmed-article:17560837 | pubmed:issn | 1568-7864 | lld:pubmed |
pubmed-article:17560837 | pubmed:author | pubmed-author:Parekh-Olmedo... | lld:pubmed |
pubmed-article:17560837 | pubmed:author | pubmed-author:KmiecEric BEB | lld:pubmed |
pubmed-article:17560837 | pubmed:author | pubmed-author:FerraraLucian... | lld:pubmed |
pubmed-article:17560837 | pubmed:author | pubmed-author:EngstromJulia... | lld:pubmed |
pubmed-article:17560837 | pubmed:author | pubmed-author:SchwartzTimot... | lld:pubmed |
pubmed-article:17560837 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17560837 | pubmed:day | 1 | lld:pubmed |
pubmed-article:17560837 | pubmed:volume | 6 | lld:pubmed |
pubmed-article:17560837 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17560837 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17560837 | pubmed:pagination | 1529-35 | lld:pubmed |
pubmed-article:17560837 | pubmed:dateRevised | 2011-2-25 | lld:pubmed |
pubmed-article:17560837 | pubmed:meshHeading | pubmed-meshheading:17560837... | lld:pubmed |
pubmed-article:17560837 | pubmed:meshHeading | pubmed-meshheading:17560837... | lld:pubmed |
pubmed-article:17560837 | pubmed:meshHeading | pubmed-meshheading:17560837... | lld:pubmed |
pubmed-article:17560837 | pubmed:meshHeading | pubmed-meshheading:17560837... | lld:pubmed |
pubmed-article:17560837 | pubmed:meshHeading | pubmed-meshheading:17560837... | lld:pubmed |
pubmed-article:17560837 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17560837 | pubmed:articleTitle | Recovery of cell cycle delay following targeted gene repair by oligonucleotides. | lld:pubmed |
pubmed-article:17560837 | pubmed:affiliation | Department of Biological Sciences, University of Delaware, Delaware Biotechnology Institute, 15 Innovation Way, Newark, DE 19711, USA. | lld:pubmed |
pubmed-article:17560837 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17560837 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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