Дисертації з теми "DNA Single-strand Repair Pathway"
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Stephanou, Nicolas Constantinos. "Mycobacterial non-homologous end-joining : molecular mechanisms and components of a novel DNA double strand break repair pathway /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528973431&sid=21&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Повний текст джерелаDemond, Marilen [Verfasser], and George [Akademischer Betreuer] Iliakis. "The influence of chromatin structure on DNA double strand break repair pathway choice / Marilen Demond ; Betreuer: George Iliakis." Duisburg, 2017. http://d-nb.info/1133478859/34.
Повний текст джерелаCaldecott, Keith. "Role of the xrs double strand break repair pathway in response to DNA damage induced by topoisomerase II-inhibiting antitumour drugs." Thesis, University College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279158.
Повний текст джерелаWang, Yu. "Mismatch ligation during non-homologous end joining pathway kinetic characterization of human DNA ligase IV/XRCC4 complex /." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1179947467.
Повний текст джерелаSaitou, Yuuichirou. "Regulatory mechanism of damage-dependent homologous recombination." Kyoto University, 2015. http://hdl.handle.net/2433/199392.
Повний текст джерела0048
新制・課程博士
博士(人間・環境学)
甲第19068号
人博第721号
新制||人||173(附属図書館)
26||人博||721(吉田南総合図書館)
32019
京都大学大学院人間・環境学研究科相関環境学専攻
(主査)教授 小松 賢志, 教授 宮下 英明, 准教授 三浦 智行
学位規則第4条第1項該当
Jaffary, Syed Ali Naqi Raza. "The human single-stranded DNA binding protein 2 (HSSB2) and its novel role in the base excision repair pathway." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/119175/1/Syed%20Ali%20Naqi%20Raza_Jaffary_Thesis.pdf.
Повний текст джерелаDean, Philip John. "Double strand break repair and DNA damage signalling pathways in Arabidopsis." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487719.
Повний текст джерелаZhang, Hongshan. "A single molecule perspective on DNA double-strand break repair mechanisms." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0177.
Повний текст джерелаDNA double-strand breaks disrupt the physical continuity of the chromosome and are one of the most severe types of DNA damage. To preserve genome integrity against the potentially deleterious effects of DNA double-strand breaks, human cells have evolved several repair mechanisms including DNA recombinational repair and Non-Homologous End Joining (NHEJ), each catalyzed by specific enzymes. In this thesis we aimed at unraveling the dynamics of protein/DNA transactions involved in DNA double-strand break repair mechanisms at single molecule level. To do this, we combined optical tweezers and microfluidics with wide-field fluorescence microscopy, which allowed us to manipulate individual DNA molecules while directly visualize fluorescently-labeled DNA repair proteins acting on them. We focused the study on three crucial proteins/complexes involved in DNA repair: (i) the human DNA annealing protein RAD52, (ii) the non-homologous end joining human proteins XRCC4 and XLF and the complex XRCC4/Ligase IV, and (iii) the human MRE11/RAD50/NBS1 complex
Iles, Natasha J. "The role of a divergent FHA domain in DNA single-strand break repair." Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487930.
Повний текст джерелаBreslin, Claire. "Investigating the importance of XRCC1 binding partners in DNA single-strand break repair." Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439658.
Повний текст джерелаChambers, Helen. "Investigating the effects of repair of DNA single-strand breaks on chromatin structure." Thesis, University of Sussex, 2011. http://sro.sussex.ac.uk/id/eprint/6332/.
Повний текст джерелаCarroll, Jean. "Investigating aprataxin function : roles in DNA single strand break repair and functional cellular effects." Thesis, University of Sussex, 2013. http://sro.sussex.ac.uk/id/eprint/46135/.
Повний текст джерелаBentle, Melissa Srougi. "INVOLVEMENT OF SINGLE- AND DOUBLE-STRAND BREAK REPAIR PROCESSES IN BETA-LAPACHONE-INDUCED CELL DEATH." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1179427756.
Повний текст джерелаCarpenter, Lucy. "DNA repair pathways involved in determining the level of cytotoxicity of environmentally relevant UV radiation." Thesis, Lancaster University, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340566.
Повний текст джерелаSmith, Christopher E. "Insights into the structure and function of Red beta: the unique single-strand annealing protein of bacteriophage lambda." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1449183321.
Повний текст джерелаYuan, Ying. "Modulation of DNA double strand breaks end-joining pathway choice by single stranded oligonucleotides in mammalian cells." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30091.
Повний текст джерелаIn response to DNA damage, the choice made by the cells between DNA repair mechanisms is crucial for mutagenic and survival outcomes. In humans, DNA double-strand breaks are repaired by two mutually-exclusive mechanisms, homologous recombination or end-joining. Among end-joining mechanisms, the main process is classical non-homologous end-joining (C-NHEJ) which relies on Ku binding to DNA ends and DNA Ligase IV (Lig4)-mediated ligation. Mostly under Ku- or Lig4-defective conditions, an alternative end-joining process (A-EJ) can operate and exhibits a trend toward microhomology usage at the break junction. Homologous recombination relies on an initial MRN-dependent nucleolytic degradation of one strand at DNA ends. This process, named DNA resection generates 3' single-stranded tails necessary for homologous pairing with the sister chromatid. While it is believed from the current literature that the balance between joining and recombination processes at DSBs ends is mainly dependent on the initiation of resection, it has also been shown that MRN activity can generate short single-stranded DNA oligonucleotides (ssO) that may also be implicated in repair regulation. In this work, we evaluate the effect of ssO on end-joining at DSB sites both in vitro and in cells. Under both conditions, we report that ssO inhibit C-NHEJ through binding to Ku and favor repair by the Lig4-independent microhomology-mediated A-EJ process. Our data bring new clues in the understanding of the cellular response to DNA double-strand breaks
El-Khamisy, Sherif F. "Biochemical characterisation of a novel DNA single-strand break repair process and its defect in a neurodegenerative disease." Thesis, University of Sussex, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412689.
Повний текст джерелаVerkhedkar, Ketki Dinesh. "Quantitative Analysis of DNA Repair and p53 in Individual Human Cells." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10660.
Повний текст джерелаWang, Jinglong. "Insights into the mechanism of DNA double-strand breaks and classic NHEJ by single-molecule magnetic tweezers." Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7063.
Повний текст джерелаRepairing DNA double-strand breaks (DSBs) by non-homologous end-joining (NHEJ) requires multiple proteins to recognize and bind DNA ends, process them for compatibility, and ligate them together. We constructed novel DNA substrates for single-molecule nano-manipulation allowing us to mechanically detect, probe, and rupture in real-time DSB synapsis by specific human NHEJ components. DNA-PKcs and Ku allow DNA end synapsis on the sub second timescale, and addition of PAXX extends this lifetime to ~2s. Further addition of XRCC4, XLF and Ligase IV resulted in minute-scale synapsis and led to robust repair of both strands of the nanomanipulated DNA. In contrast with PAXX, a long non-coding RNA LINP1 can also help DNA-PK to tether DNA ends together, which could be more required when DNA ends falling apart in distance. Moreover, we also interrogate the bacteria Bacillus subtilis NHEJ system, which just composed Ku and Ligase D, bacteria Ku also can tether DNA together and introducing the Ligase D strengthen the synapsis and lead to ligation. The energetic contribution of the different components to synaptic stability is typically small, on the scale of a few kCal/mol. Our combined results define assembly rules for NHEJ machinery and unveil the importance of weak interactions, rapidly ruptured even at sub-picoNewton forces, in regulating this multicomponent chemomechanical system for genome integrity. Moreover, we also identify a novel the DNA double strand cleavage pattern regulated by Cas9 PAM. In sum, this PhD work investigates the DSB generation and the detailed process from DNA end tethering to ligation
Pfitzer, Lisa [Verfasser], and Stefan [Akademischer Betreuer] Zahler. "The role of nuclear actin in distinctive DNA double strand break repair pathways - actin as a novel target for combination chemotherapy / Lisa Pfitzer ; Betreuer: Stefan Zahler." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1163534234/34.
Повний текст джерелаSerra, Heïdi. "Etude des acteurs et des interactions entre les voies de recombinaison chez Arabidopsis thaliana." Thesis, Clermont-Ferrand 2, 2014. http://www.theses.fr/2014CLF22483/document.
Повний текст джерелаThe repair of DNA double-strand breaks (DSB) by recombination is essential for the maintenance of genome integrity of all living organisms. However, recombination must be finely regulated as it can generate mutations or chromosomal rearrangements, sometimes extremely deleterious to the cell. DSB can be repaired by two classes of recombination mechanism: non-homologous recombination (or DNA End Joining) or homologous recombination (implicating DNA sequence homology between the recombining molecules). In somatic cells, the two main pathways of homologous recombination (HR) are RAD51-dependent Synthesis Dependent Strand Annealing (SDSA) and RAD51-independent Single Strand Annealing (SSA). Our results have demonstrated an unexpected role of XRCC2, RAD51B and RAD51D - three RAD51 paralogues – in the SSA pathway. We confirmed that the function of XRCC2 in SSA does not depend upon RAD51, thus demonstrating that some RAD51 paralogues have acquired RAD51 recombinase-independent functions. The different severities of individual mutant phenotypes and epistasis analyses carried out on the double and triple mutants suggest individual functions of these proteins in SSA recombination. We propose that they facilitate hybridization of the two complementary sequences located on both sides of the break, although this remains to be confirmed by in vitro experiments. Study of the roles of XPF-ERCC1 - a complex involved in the cleavage of non-homologous DNA ends during HR - revealed an inhibitory role of this complex on the SDSA pathway. This is dependent on its endonuclease activity and is probably due to the cleavage of long 3' ends performing the homologous DNA duplex invasion, the initial step of the SDSA pathway. Our analyses also confirmed that the role of the complex depends on the length of the nonhomologous ends, as seen in mammals and yeasts. Although XPF-ERCC1 is essential for the cleavage of long nonhomologous DNA ends, it is not required for the elimination of short ends during HR
Paul, Katja [Verfasser], George [Akademischer Betreuer] Iliakis, and Hemmo [Akademischer Betreuer] Meyer. "Function of DNA Ligase III in the Repair of Radiation induced DNA Double Strand Breaks via alternative Pathways of Non-homologous End Joining functioning as Backup / Katja Paul. Gutachter: Hemmo Meyer. Betreuer: George Iliakis." Duisburg, 2013. http://d-nb.info/1035066394/34.
Повний текст джерелаMagin, Simon [Verfasser], George [Akademischer Betreuer] Iliakis, and Jürgen [Akademischer Betreuer] Thomale. "A balance shift between error-free and error-prone DNA double-strand break repair pathways as a novel mechanism of radiosensitization by nucleoside analogs / Simon Magin. Gutachter: Jürgen Thomale. Betreuer: George Iliakis." Duisburg, 2014. http://d-nb.info/1053913613/34.
Повний текст джерелаHancock, Janelle Louise. "Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1." Thesis, Queensland University of Technology, 2008. https://eprints.qut.edu.au/28603/1/Janelle_Hancock_Thesis.pdf.
Повний текст джерелаHancock, Janelle Louise. "Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1." Queensland University of Technology, 2008. http://eprints.qut.edu.au/28603/.
Повний текст джерелаMishra, Anup. "Targeting RAD51C Pathological Mutants by Synthetic Lethality and Extended Functions of RAD51C/XRCC3 in Mitochondrial Genome Maintenance." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4155.
Повний текст джерелаSingh, Amandeep. "Exploration of the Recombination Repair Pathway in Mycobacteria : Identification and Characterization of New Proteins." Thesis, 2018. https://etd.iisc.ac.in/handle/2005/4259.
Повний текст джерелаStauropoulos, Dimitrios James. "An analysis of the interplay between telomeric factors and DNA repair proteins, in the human ALT pathway and cellular response to genomic double strand breaks." 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=478811&T=F.
Повний текст джерелаZheng, Haihua. "Radiation-induced DNA single-strand break induction and repair in murine tissues measured by the comet assay." Thesis, 1996. http://hdl.handle.net/2429/4534.
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