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DNA mismatch repair and hypermutability in the physiology and pathogenesis of Haemophilus influenzaeWatson, Michael E., January 2004 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2004. / Typescript. Vita. Includes bibliographical references (leaves 156-180). Also issued on the Internet.
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DNA damage response activated by anti-cancer agent, irofulvenWiltshire, Timothy D. January 2007 (has links)
Thesis (Ph. D.)--West Virginia University, 2007. / Title from document title page. Document formatted into pages; contains ix, 227 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Formation and genotoxicity of novel oxidatively generated tandem DNA lesions and N2-(1-carboxyethyl)-2'-deoxyguanosineJiang, Yong. January 2009 (has links)
Thesis (Ph. D.)--University of California, Riverside, 2009. / Includes abstract. Available via ProQuest Digital Dissertations. Title from first page of PDF file (viewed March 16, 2010). Includes bibliographical references. Also issued in print.
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Impact of KU80 in genomic stability, cancer and aging: a dissertation /Li, Han. January 2007 (has links)
Dissertation (Ph.D.).--University of Texas Graduate School of Biomedical Sciences at San Antonio, 2007. / Vita. Includes bibliographical references.
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Base excision repair (BER) of 7, 8-dihydro-8-oxoguanine (8-oxoG) in DNA mismatch repair proficient and mismatch repair deficient human cellsLi, Tai. January 2007 (has links)
Thesis (M.S.)--University of Toledo, 2007. / "In partial fulfillment of the requirements for the degree of Master of Science in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 50-55.
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DNA mismatch repair and hypermutability in the physiology and pathogenesis of Haemophilus influenzae /Watson, Michael E., January 2004 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2004. / "May 2004." Typescript. Vita. Includes bibliographical references (leaves 156-180). Also issued on the Internet.
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The role of human Rev7, the accessory subunit of human DNA polymerase zeta, in cell survival and DNA damage induced mutagenesisNeal, Jessica A. January 2008 (has links)
Thesis (PH. D.)--Michigan State University. Biochemistry and Molecular Biology, 2008. / Title from PDF t.p. (viewed on Sept. 2, 2009) Includes bibliographical references. Also issued in print.
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Examining kinetic and thermodynamic DNA destabilization caused by the cis-syn thymine dimer lesion using small molecule probes /Malhowski, Anne M. January 2005 (has links) (PDF)
Undergraduate honors paper--Mount Holyoke College, 2005. Dept. of Chemistry. / Includes bibliographical references (leaves 107-111).
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An investigation of a rapid fluorescence microtiter plate methodology for measuring chemically-induced DNA damage, suitable for use in development of a primary DNA damage databaseBrockmann, William G. Eick, J. David January 2004 (has links)
Thesis (Ph. D.)--School of Dentistry and School of Pharmacy. University of Missouri--Kansas City, 2004. / "A dissertation in oral biology and pharmacology." Advisor: J. David Eick. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed Feb. 22, 2006. Includes bibliographical references (leaves 176-189). Online version of the print edition.
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Deciphering the molecular mechanism by which Fml1 promotes and constrains homologous recombinationNandi, Saikat January 2011 (has links)
Homologous Recombination (HR) can promote genome stability through its capacity to faithfully repair DNA gouble 2trand !;!reak2 (DSBs) and preventing the demise of stalled replication forks in part by catalysing template switching to enable DNA polymerase to bypass lesions. Despite these beneficial roles, inappropriate or untimely HR events can have deleterious consequences. HR can cause genome instability by recombining "inappropriate" homologous sequences, especially if the recombination intermediates are resolved to form crossovers. Over the past few years, study of the rare inherited chromosome instability disorder, Eanconi Anaemia (FA), has uncovered a novel DNA damage response pathway. Although the FA pathway is required primarily for interstrand DNA cross link repair, its precise role in DNA repair reactions is still unclear. FA.Qomplementation group M (FANCM) is the sole component within the FA core complex which possesses a DNA helicase/ATPase domain and an endonuclease domain (albeit non-functional), suggesting that FANCM could translocate along DNA and target the FA core complex to blocked replication forks. To further elucidate the role of FANCM in HR, I have purified Fm11, the FANCM orthologue in the fission yeast Schizosaccharomyces pombe and tested its activity on a range of synthetic replication and recombination intermediates in vitro. Fml1 binds both replication forks and Holliday Junctions (HJs) which are key intermediates of HR.
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