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dc.contributor.supervisor Kovalchuk, Igor
dc.contributor.author Wickersham, Stephanie
dc.date.accessioned 2014-04-16T23:35:45Z
dc.date.available 2014-04-16T23:35:45Z
dc.date.issued 2012
dc.identifier.uri https://hdl.handle.net/10133/3401
dc.description xv, 168 leaves : ill. ; 29 cm en_US
dc.description.abstract DNA double strand breaks (DSBs) are primarily repaired in eukaryotic cells by two different mechanisms – non-homologous end joining (NHEJ) or homologous recombination (HR). In mammalian somatic cells the balance between the two highly favours NHEJ. Gene targeting is a technique that exploits HR repair to alter a defined gene locus. While it holds potential to be implemented as a treatment option for several diseases, the outlook for using it in a clinical setting has been obstructed by a low gene targeting efficiency. This has been coupled to the low frequency of HR in mammalian cells. With the intention of shifting the repair balance, antibodies against DSB repair proteins will be introduced into mammalian cells. It is predicted that by targeting key repair proteins with antibodies, a compensatory increase in the frequency of HR can be fostered, ultimately resulting in improved gene targeting. en_US
dc.language.iso en_CA en_US
dc.publisher Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2012 en_US
dc.subject DNA damage -- Research en_US
dc.subject DNA repair -- Research en_US
dc.subject Gene targeting -- Research en_US
dc.subject Protein kinases en_US
dc.subject NAD-ADP-ribosyltransferase en_US
dc.title The down-regulation of Ku70, DNA-PKcs, and Parp-1 in mammalian cell lines en_US
dc.type Thesis en_US
dc.publisher.faculty Arts and Science en_US
dc.publisher.department Department of Biological Sciences en_US
dc.degree.level Masters


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