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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
131

AtZDP, a plant 3' DNA phosphatase, involved in DNA repair /

Valsecchi, Isabel, January 2008 (has links)
Diss. (sammanfattning) Uppsala : Uppsala universitet, 2008. / Härtill 3 uppsatser.
132

REV7-mediated polyubiquitination and degration of human REV1

Chun, Chiu-shun. January 2009 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 114-136). Also available in print.
133

Transcription and DNA repair in immunoglobulin gene somatic hypermutations /

Kim, Nayun. January 2000 (has links)
Thesis (Ph. D.)--University of Chicago, Dept. of Biochemistry and Molecular Biology. / Includes bibliographical references. Also available on the Internet.
134

Mycobacterial non-homologous end-joining : molecular mechanisms and components of a novel DNA double strand break repair pathway /

Stephanou, Nicolas Constantinos. January 2008 (has links)
Thesis (Ph. D.)--Cornell University, May, 2008. / Vita. Includes bibliographical references (leaves 162-177).
135

Photoreactivation in yeast : a test of how lesions in DNA are recognized /

Zhang, Wei. January 2005 (has links)
Thesis (M.Sc.)--York University, 2005. Graduate Programme in Biology. / Typescript. Includes bibliographical references. Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url%5Fver=Z39.88-2004&res%5Fdat=xri:pqdiss &rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR11935
136

Exploring DNA destabilization induced by the thymine dimer lesion using base modifying probes and thermodynamic techniques /

Rumora, Amy. January 2007 (has links) (PDF)
Undergraduate honors paper--Mount Holyoke College, 2007. Program in Biochemistry. / Includes bibliographical references (leaves 107-108).
137

Ultrafast dynamics of energy and electron transfer in DNA-photolyase

Saxena, Chaitanya, January 2007 (has links)
Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 131-146).
138

Involvement of single-and double-strand break repair processes in beta-lapachone-induced cell death

Bentle, Melissa Srougi. January 2007 (has links)
Thesis (Ph. D.)--Case Western Reserve University, 2007. / [School of Medicine] Department of Pharmacology. Includes bibliographical references. Available online via OhioLINK's ETD Center.
139

Pol [kappa] : a novel DNA polymerase required for sister chromatid cohesion and DNA repair /

Wang, Zhenghe. January 2001 (has links)
Thesis (Ph. D.)--University of Virginia, 2001. / In title: the [kappa] is the Greek symbol. Includes bibliographical references (leaves 129-140). Also available online through Digital Dissertations.
140

Investigation into the relationship between PARPs in DNA repair and synthetic lethality with homologous recombination deficiency

Ronson, George January 2017 (has links)
The genome of each cell is under constant threat from various forms of DNA damage. In order to protect themselves from this danger, cells possess a number of pathways able to resolve DNA lesions. The addition of poly(ADPribose) is a post-translational modification produced by attaching successive ADP-ribose moieties to a protein acceptor, forming long chains. Enzymes called poly(ADP-ribose) polymerases (PARPs) catalyse the production of these modifications, and a number of different PARPs have been linked to the process of DNA repair, including PARP1, PARP2 and PARP3. How these enzymes might function together to facilitate the repair of different lesions is unclear. Furthermore, inhibitors that target these enzymes are in clinical use for their ability to kill homologous recombination deficient tumour cells, through a mechanism of synthetic lethality. Which subset of PARPs is necessary to inhibit to achieve maximum efficacy of these agents has not been assessed. I use genome editing to generate cells disrupted for these PARPs in different combinations. Whilst loss of PARP1 compromises cellular tolerance to homologous recombination deficiency, this is independent of the status of PARP2 and PARP3, indicating the development of PARP1-specific inhibitors may hold therapeutic potential. In contrast to these observations, I uncover strong redundancy between PARP1 and PARP2 in the repair of damaged DNA bases through the base excision repair (BER) pathway. I also identify BER independent roles of both PARP1 and PARP2 in resolving replication forks that have collided with BER-intermediates, through promoting the stability of Rad51 nucleofilaments via an Fbh1-dependent mechanism. Thus PARP1 and PARP2 perform two closely-linked functions in response to cellular base damage promoting resolution of these lesions directly through BER, and stabilising replication forks which have encountered BER intermediates.

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