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dc.contributor.authorChung, Jung Hwaen_US
dc.date.accessioned2008-04-22T02:41:30Z
dc.date.available2008-04-22T02:41:30Z
dc.date.issued2008-04-22T02:41:30Z
dc.date.submittedDecember 2007en_US
dc.identifier.otherDISS-1933en_US
dc.identifier.urihttp://hdl.handle.net/10106/743
dc.description.abstractReovirus is a ubiquitous virus with demonstrated oncolytic properties. In this study, we investigate the pathways which reovirus produces a lytic infection in SV-40 transformed WI-38 cells and the noncytocidal infection of normal WI-38 cells using microarray technology. The analysis revealed that reovirus infection induced changes in 178 genes, of which 112 genes were up regulated and 66 genes down regulated. Of the 112 up regulated genes, 13 of the WI-38 2RA genes were shown to be involved in apoptosis or inhibition of cellular DNA synthesis. Of the 66 genes down regulated, seven of the WI-38 genes displayed effects involved in apoptosis or inhibition of cell cycle progression, suggesting that inhibition of these genes prevented death in these cells. Additionally, five of the 62 up regulated WI-38 genes were found to be involved in cell survival. Reovirus caused lysis of transformed cells by over inducing a multitude of cellular targets.en_US
dc.description.sponsorshipRoner, Michaelen_US
dc.language.isoENen_US
dc.publisherBiologyen_US
dc.titleCellular Targets Involved In Reovirus-induced Oncolysis Of RAs-transformed Cellsen_US
dc.typeM.S.en_US
dc.contributor.committeeChairRoner, Michaelen_US
dc.degree.departmentBiologyen_US
dc.degree.disciplineBiologyen_US
dc.degree.grantorUniversity of Texas at Arlingtonen_US
dc.degree.levelmastersen_US
dc.degree.nameM.S.en_US
dc.identifier.externalLinkhttps://www.uta.edu/ra/real/editprofile.php?onlyview=1&pid=36
dc.identifier.externalLinkDescriptionLink to Research Profiles


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