Tesis sobre el tema "DNA strand"
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Lo, Allen Tak Yiu. "Protein dynamics on the lagging strand during DNA synthesis". Thesis, School of Chemistry, 2012. https://ro.uow.edu.au/theses/3684.
Texto completoTingey, Andrew Philip. "Strand passage in DNA gyrase". Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/35173.
Texto completoHo, F. M. "Strand exchange for duplex DNA detection". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604106.
Texto completoWashbrook, Elinor. "Alternate strand DNA triple helix formation". Thesis, University of Southampton, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242223.
Texto completoLansita, Janice A. (Janice Ann) 1975. "Physicochemical characterization of immortal strand DNA". Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/18038.
Texto completoIncludes bibliographical references.
Adult tissue differentiation involves the generation of distinct cell types from adult stem cells (ASCs). Current understanding of tissue differentiation mechanisms is based on studies of protein and RNAs that asymmetrically segregate between daughter cells during embryogenesis. Whether or not other types of biomolecules segregate asymmetrically has not been widely studied. In 1975, John Cairns proposed that ASCs preferentially segregate the oldest parental template DNA strands to themselves and pass on newly replicated DNA strands to their differentiating progeny in order to protect the stem cell from inheriting DNA replication mutations. This laboratory has shown non-random chromosome segregation in murine fetal fibroblasts that model asymmetric self-renewal like ASCs. In these cells, chromosomes that contain the oldest DNA strands co-segregate to the cycling daughter stem-like cells, while chromosomes with more recently replicated DNA segregate to the non-stem cell daughters. Previously, cytological methods were reported to elucidate non-random segregation in these cells. This dissertation research provides additional confirmation of the mechanism using physicochemical methods. Specifically, buoyant density-shift experiments in equilibrium CsCl density gradients were used to detect co-segregated "immortal DNA strands" based on incorporation of the thymidine base analogue bromodeoxyuridine. In addition, DNA from cells undergoing non-random mitotic chromosome segregation was analyzed for unique DNA base modifications and global structural modifications (by HPLC and melting temperature analyses). To date, these studies show no significant differences compared to control randomly segregated DNA. Components of the mitotic chromosome separation
(cont.) apparatus that might play a role in the co-segregation mechanism were also evaluated. Two homologous proteins, essential for proper chromosome segregation and cytokinesis, Aurora A kinase and Aurora B kinase, were highly reduced in expression in cells retaining immortal DNA strands and may indicate a role for them in the immortal strand mechanism. These studies independently confirm the immortal strand mechanism and provide methods for its detection in other cell lines. In addition, observed changes in chromosome segregation proteins that are potential candidates for involvement in the mechanism have revealed a new area of investigation in the laboratory. These findings are relevant to understanding normal tissue development, cancer, and aging.
y Janice A. Lansita.
Ph.D.
Absalon, Michael Joseph. "DNA double-strand cleavage mediated by bleomycin". Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/11927.
Texto completoMorant, Nick. "Novel thermostable DNA polymerases for isothermal DNA amplification". Thesis, University of Bath, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667735.
Texto completoTatavarthi, Haritha. "Action of Tyrosyl DNA Phosphodiesterase on 3'-Phosphoglycolate Terminated DNA Strand Breaks". VCU Scholars Compass, 2006. http://hdl.handle.net/10156/1799.
Texto completoRazavy, Haide. "Single-strand DNA ends in recombination in vivo". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq22661.pdf.
Texto completoFan, Saijun. "DNA strand breaks induced by gamma-ray irradiation". Thesis, University of Leicester, 1992. http://hdl.handle.net/2381/33667.
Texto completoMahalingam, Kalpana. "Involution codes with application to DNA strand design". [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000409.
Texto completoKrietsch, Jana. "PARP-1 activation regulates the DNA damage response to DNA double-strand breaks". Thesis, Université Laval, 2014. http://www.theses.ulaval.ca/2014/30722/30722.pdf.
Texto completoDNA double-strand breaks are potentially lethal lesions, which if not repaired correctly, can have harmful consequences such as carcinogenesis promoted by chromosome deletions and rearrangements. Poly(ADP-ribosyl)ation carried out by poly(ADP-ribose) polymerase 1 (PARP-1) is one of the first posttranslational modifications occurring in response to DNA damage. In brief, PARP-1 uses nicotinamide to generate a negatively charged polymer called poly(ADP-ribose) polymer (PAR), that can be attached to acceptor proteins, which is to a large extent PARP-1 itself. PAR has recently been recognized as a recruitment signal for key DNA repair proteins to sites of DNA damage but the precise role of PARP-1 and its catalytic product PAR in the DNA damage response are still a matter of ongoing debate. Throughout my doctoral work, we confirmed that the proteins in complex with PAR promptly after DNA damage are mostly DNA repair proteins, whereas during the period of recovery from DNA damage, the PAR interactome is highly enriched with RNA processing factors. Interestingly, one of the most abundant RNA-binding proteins detected in the PAR interactome, namely NONO, did not follow these kinetics as it was highly enriched immediately after DNA damage in the DNA repair protein complexes centered on PAR. Our subsequent investigation of NONO in the DNA damage response to double-strand breaks strikingly revealed a direct implication for NONO in repair by nonhomologous end joining (NHEJ). Moreover, we found that NONO strongly and specifically binds to PAR through its RNA-recognition motif 1 (RRM1), highlighting competition between PAR and RNA for the same binding site. Remarkably, the in vivo recruitment of NONO to DNA damage sites completely depends on PAR and requires the RRM1 motif. In conclusion, our results establish NONO as a new protein implicated in the DNA damage response to double-strand break and in broader terms add another layer of complexity to the cross-talk between RNA-biology and DNA repair.
Zabolotnaya, Ekaterina. "DNA double-strand break repair studied by atomic force microscopy". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275890.
Texto completoCouto, Claudia Anne-Marie. "Investigating DNA double-strand break repair in Dictyostelium discoideum". Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558280.
Texto completoWardrope, Laura. "Repair of double-strand DNA breaks in Escherichia coli". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/13208.
Texto completoAmato, Nicholas J. "Impact of DNA Structure and Aeropyrum pernix Single-Strand DNA Binding Protein on Oxidative Damage to DNA". University of Toledo / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1372296254.
Texto completoVILLA, MATTEO. "Regulation of DNA-end resection at DNA double strand breaks and stalled replication forks". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/198950.
Texto completoGenome instability is an hallmark of cancer cells and can be due to DNA damage or replication stress. DNA double strand breaks (DSBs) are the most dangerous type of damage that cells have to manage. In response to DSBs, cells activate an highly conserved mechanism known as DNA damage checkpoint (DDC), whose primary effect is to halt the cell cycle until the damage is repaired. DDC is activated by the apical kinases Tel1/ATM and Mec1/ATR, which phosphorylate and activate the effector kinases Rad53/CHK2 and Chk1/CHK1. The Homologous Recombination (HR)-mediated repair of a DSB starts with the nucleolytic degradation (resection) of the 5’ ends to create long ssDNA tails. In Saccharomyces cerevisiae, resection starts with an endonucleolytic cleavage catalyzed by the MRX complex together with Sae2. More extensive resection relies on two parallel pathways that involve the nucleases Exo1 and Dna2, together with the helicase Sgs1. Resection must be tightly controlled to avoid excessive ssDNA creation. The Ku complex and the checkpoint protein Rad9 negatively regulate resection. While Ku inhibits Exo1, Rad9 restrains nucleolytic degradation by an unknown mechanism. The absence of Sae2 impairs DSB resection and causes prolonged MRX binding at DSB that leads to persistent Tel1 and Rad53-dependent DNA damage checkpoint. SAE2 deleted strains are sensitive to DSBs inducing agents, like camptothecin (CPT). This sensitivity has been associated to the resection defect of sae2∆ cells, but what causes this resection defect and if the enhanced checkpoint signaling contributes to the DNA damage sensitivity of sae2∆ cells is unknown. For these reasons, we tried to identify other possible mechanisms regulating MRX/Sae2 requirement in DSB resection by searching extragenic mutations that suppressed the sensitivity to DNA damaging agents of sae2Δ cells. We identified three mutant alleles (SGS1-G1298R, rad53-Y88H and tel1-N2021D) that suppress both the DNA damage hypersensitivity and the resection defect of sae2∆ cells. We show that Sgs1-G1298R-mediated suppression depends on Dna2 but not on Exo1. Furthermore, not only Sgs1-G1298R suppresses the resection defect of sae2∆ cells but also increases resection efficiency even in a wild type context by escaping Rad9-mediated inhibition. In fact, Rad9 negatively regulates the binding/persistence of Sgs1 at the DSB ends. When inhibition by Rad9 is abolished by the Sgs1-G1298R mutant variant, the requirement for MRX/Sae2 in DSBs resection is reduced. Rad53-Y88H and Tel1-N2021 are loss of function mutant variants that suppress sae2∆ cells sensitivity in a Sgs1-Dna2 dependent manner. Furthermore, abolishing Rad53 and Tel1 kinase activity results in a similar suppression phenotype which does not involve the escape from the checkpoint mediated cell cycle arrest. Rather, defective Rad53 or Tel1 signaling bypasses Sae2 function in DSBs resection by decreasing the amount of Rad9 bound at DSBs. This increases the Sgs1-Dna2 activity that, in turn, can compensate for the lack of Sae2. We propose that persistent Tel1 and Rad53 checkpoint signaling in sae2∆ cells causes DNA damage hypersensitivity and defective DSB resection by increasing the amount of Rad9 that, in turn, inhibits Sgs1-Dna2. Replication stress can induce fork stalling and controlled resection can be a relevant mechanism to allow repair/restart of stalled replication forks. We show that loss of the inhibition that Rad9 exerts on resection exacerbates the sensitivity to replication stress of Mec1 defective yeast cells by exposing stalled replication forks to Dna2-dependent degradation. This Rad9 protective function is independent of checkpoint activation and relies mainly on Rad9-Dpb11 interaction. We propose that Rad9 not only regulates the action of Sgs1-Dna2 at DSBs but also at stalled replication forks, supporting cell viability when the S-phase checkpoint is not fully functional.
Tentner, Andrea R. (Andrea Ruth). "Quantitative measurement and modeling of the DNA damage signaling network : DNA double-strand breaks". Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/61234.
Texto completo"September 2009." Cataloged from PDF version of thesis.
Includes bibliographical references (p. 218-229).
DNA double-strand breaks (DSB) are one of the major mediators of chemotherapy-induced cytotoxicity in tumors. Cells that experience DNA damage can initiate a DNA damage-mediated cell-cycle arrest, attempt to repair the damage and, if successful, resume the cell-cycle (arrest/repair/resume). Cells can also initiate an active cell-death program known as apoptosis. However, it is not known what "formula" a cell uses to integrate protein signaling molecule activities to determine which of these paths it will take, or what protein signaling-molecules are essential to the execution of that decision. A better understanding of how these cellular decisions are made and mediated on a molecular level is essential to the improvement of existing combination and targeted chemotherapies, and to the development of novel targeted and personalized therapies. Our goal has been to gain an understanding of how cells responding to DSB integrate protein signaling-molecule activities across distinct signaling networks to make and execute binary cell-fate decisions, under conditions relevant to tumor physiology and treatment. We created a quantitative signal-response dataset, measuring signals that widely sample the response of signaling networks activated by the induction of DSB, and the associated cellular phenotypic responses, that together reflect the dynamic cellular responses that follow the induction of DSB. We made use of mathematical modeling approaches to systematically discover signal-response relationships within the DSB-responsive protein signaling network. The structure and content of the signal-response dataset is described, and the use of mathematical modeling approaches to analyze the dataset and discover specific signal-response relationships is illustrated. As a specific example, we selected a particularly strong set of identified signal-response correlations between ERK1/2 activity and S phase cell-cycle phenotype, identified in the mathematical data analysis, to posit a causal relationship between ERK1/2 and S phase cell cycle phenotype. We translated this posited causal relationship into an experimental hypothesis and experimentally test this hypothesis. We describe the validation of an experimental hypothesis based upon model-derived signal response relationships, and demonstrate a dual role for ERK1/2 in mediating cell-cycle arrest and apoptosis following DNA damage. Directions for the extension of the signal-response dataset and mathematical modeling approaches are outlined.
by Andrea R. Tentner.
Ph.D.
MARSELLA, ANTONIO. "Functions and regulation of the MRX complex at DNA double strand breaks". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/310478.
Texto completoDNA double strand breaks (DSBs) are among the most severe DNA lesions. If not properly repaired, DSBs could lead to loss of genetic information and genome instability, which is one of the hallmarks of cancer cells. Eukaryotic cells repair DSBs by non-homologous end joining (NHEJ), which directly re-ligates the DNA broken ends, and homologous recombination (HR), which uses the intact homologous DNA sequence as a template to repair the DSB. HR requires a nucleolytic degradation of the broken DNA ends, in a process called resection. In Saccharomyces cerevisiae, the MRX (Mre11, Rad50 and Xrs2) complex, aided by Sae2, initiates resection of the DSB ends by performing an endonucleolytic cleavage on the 5’-ended strands. This cleavage, catalyzed by the Mre11 subunit, allows the access of Exo1 and Dna2 nucleases that elongate the ssDNA ends. In NHEJ, the two broken ends need to be physically connected to allow their correct religation. This function, called end tethering, depends on the Rad50 subunit, which binds and hydrolyses ATP. A transitions between an ATP-bound state to a post-hydrolysis cutting state regulates MRX DNA binding and processing activities. The MRX complex is also essential in DNA damage checkpoint activation because it recruits the checkpoint kinase Tel1 at the break site. In this thesis, we studied functions and regulation of the MRX complex in DSB repair. We found mre11 alleles that suppress the hypersensitivity of sae2Δ cells to genotoxic agents. The mutations in the Mre11 N-terminus suppress the resection defect of sae2Δ cells by lowering MRX and Tel1 association to DSBs. The diminished Tel1 persistence potentiates Dna2 resection activity by decreasing Rad9 association to DSBs. By contrast, the mre11 mutations localized at the C-terminus bypass Sae2 function in end-tethering but not in DSB resection, possibly by destabilizing the Mre11–Rad50 open conformation. These findings unmask the existence of structurally distinct Mre11 domains that support resistance to genotoxic agents by mediating different processes. In vitro Tel1 activation by MRX requires ATP binding to Rad50, suggesting a role for the MR subcomplex in Tel1 activation. In this thesis, we describe two separation-of-functions alleles, mre11-S499P and rad50-A78T, which we show to specifically affect Tel1 activation without impairing MRX functions in DSB repair. Both Mre11-S499P and Rad50-A78T reduce Tel1–MRX interaction leading to low Tel1 association at DSBs that reduces Tel1 activation. Molecular dynamics simulations show that the wild type MR subcomplex bound to ATP lingers in a tightly ‘closed’ conformation, while ADP presence leads to the destabilization of Rad50 dimer and of Mre11–Rad50 association, both events being required for MR conformational transition to an open state. By contrast, MRA78T undertakes complex opening even if Rad50 is bound to ATP, indicating that defective Tel1 activation caused by MRA78T results from destabilization of the ATP- bound conformational state. The lack of Sae2 increases MRX persistence at DSBs and checkpoint activation. In this thesis, we also show that the telomeric protein Rif2, which stimulates ATP hydrolysis by Rad50, inhibits the Mre11 endonuclease activity and is responsible for the increased MRX retention at DSBs in sae2Δ cells. We identified a Rad50 residue that is important for Rad50-Rif2 interaction and Rif2-mediated inhibition of Mre11 nuclease. This residue is located nearby a Rad50 surface that binds Sae2 and is important to stabilize the Mre11-Rad50 interaction in the cutting state. We propose that Sae2 stimulates MRX endonuclease activity by stabilizing the cutting state, whereas Rif2 inhibits it by antagonizing Sae2 binding to Rad50 and stabilizing a MR conformation that is not competent for DNA cleavage. The results described in this PhD thesis contribute to the understanding of the molecular mechanisms supporting functions and regulation of the MRX complex at DSBs.
Lempidaki, Styliani. "Study of DNA double strand break repair in Dictyostelium discoideum". Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:3d0035a5-6f17-435d-990f-22ec24ec441e.
Texto completoDickman, Rebekah. "Thermodynamic Effects of 5' and 3' Single Strand Dangling Ends on Short Duplex DNA". PDXScholar, 2010. https://pdxscholar.library.pdx.edu/open_access_etds/94.
Texto completoLiu, Nan. "Hypersensitivity of ataxia telangiectasia cells to DNA double strand breaks". Thesis, University of St Andrews, 1994. http://hdl.handle.net/10023/13905.
Texto completoChoudhury, Sibgat Ahmed. "Role of TRM2RNC1 endo-exonuclease in DNA double strand break repair". Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103373.
Texto completoIn this dissertation, we provided compelling biochemical and genetic evidence that linked TRM2/RNC1 to the DNA end processing role in HRR. Trm2/Rnc1p purified with a small calmodulin binding peptide (CBP) tag displayed single strand (ss) specific endonuclease and double strand (ds) specific 5' to 3' exonuclease activity characteristic of endo-exonucleases involved in HRR. Intriguingly, purified Trm2/Rnc1p deleted for its C-terminal methyl transferase domain retained its nuclease activity but not the methyl transferase activity indicating that the C-terminal part responsible for its methyl transferase function is not required for its nuclease activity.
Our genetic and functional studies with S. cerevisiae trm2/rnc1 single mutants alone or in combination with other DNA DSB repair mutants after treatment with the DNA damaging drug methyl methane sulfonate (MMS) or IR that is believed to produce DSBs, or with specific induction of DNA DSBs at the MAT locus by HO-endonuclease demonstrated an epistatic relationship of TRM2/RNC1 with the major recombination factor RAD52. These studies suggested that TRM2/RNC1 probably acts at an earlier step than RAD52 in the HRR pathway. The genetic evidence also indicated a possible functional redundancy with the bona fide endo-exonuclease EXO1 in the processing of DNA ends at the DSB sites.
In a recent report, the immuno-purified mouse homologue of TRM2/RNC1 exhibited similar enzymatic properties as the endo-exonucleases involved in HRR. A small molecular inhibitor pentamidine specifically inhibited the nuclease activity of the mouse EE and sensitized various cancer cells to DNA damaging agents commonly used in cancer chemotherapy. We specifically suppressed expression of the mouse EE using small interfering RNA (siRNA) that conferred sensitivity of B16F10 melanoma cells to a variety of DNA damaging drugs often used in cancer treatment. This further validated our earlier claim of the endo-exonuclease as a potential therapeutic target in treating cancer.
Song, Daqing. "Homologous Strand Exchange and DNA Helicase Activities in Plant Mitochondria". Diss., CLICK HERE for online access, 2005. http://contentdm.lib.byu.edu/ETD/image/etd931.pdf.
Texto completoKegel, Andreas. "Silencing and DNA double-strand break repair in budding yeast /". Stockholm : Department of Developmental Biology, Wenner-Gren Institute, Stockholm University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-1059.
Texto completoHarer, Christine Joan. "DNA double strand break rejoining by NHEJ and interfacing components". Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437460.
Texto completoSawlekar, Rucha. "Programming dynamic nonlinear biomolecular devices using DNA strand displacement reactions". Thesis, University of Warwick, 2016. http://wrap.warwick.ac.uk/91757/.
Texto completoAzeroglu, Benura. "DNA synthesis during double-strand break repair in Escherichia coli". Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/16213.
Texto completoMawer, Julia Sofia Pamela. "Intermediates of DNA double strand break repair in Escherichia coli". Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6258.
Texto completoDever, Seth. "The Role of BRCA1 in DNA Double-strand Break Repair". VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1741.
Texto completoWang, Xin. "PTIP promotes DNA double-strand break repair through homologous recombination". Kyoto University, 2010. http://hdl.handle.net/2433/120541.
Texto completoDamit, Michael James. "Condensin recruitment to the DNA double-strand break in meiosis". Tallahassee, Fla. : Florida State University, 2008. http://purl.fcla.edu/fsu/lib/digcoll/undergraduate/honors-theses/341780.
Texto completoAdvisor: Dr. Hong-Guo Yu, Florida State University, College of Arts and Sciences, Dept. of Chemistry and Biochemistry. Includes bibliographical references.
Wechsler, Thomas. "Characterization of new interaction partners of the DNA double-strand break repair protein DNA-PKcs". Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-42460.
Texto completoCoogan, Christian P. "Reduced fidelity of E. coli leading strand DNA replication opposite ENU-induced thymine adducts in the transcribed strand /". Available to subscribers only, 2005. http://proquest.umi.com/pqdweb?did=1079660821&sid=4&Fmt=2&clientId=1509&RQT=309&VName=PQD.
Texto completoHiller, Natalie. "H2A.Z-dependent cellular responses to a persistent DNA double-strand break". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-124885.
Texto completoZhang, Hongshan. "A single molecule perspective on DNA double-strand break repair mechanisms". Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0177.
Texto completoDNA 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
Hudson, Jessica. "The conservation of DNA double strand repair proteind in Dictyostelium discoideum". Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442763.
Texto completoShaheen, Fadhel Sulaiman. "Targeting the DNA double strand break repair machinery in prostate cancer". Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500921.
Texto completoDean, 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.
Texto completoRenkawitz, Jörg. "Monitoring homology search during DNA double-strand break repair in vivo". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-169454.
Texto completoGolding, Sarah E. "DNA double-strand break repair and signalling in human glioma cells". Thesis, University of the West of England, Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431304.
Texto completoBlunt, Tracy. "The identification of genes involved in DNA double strand break repair". Thesis, University of Sussex, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320363.
Texto completoMonteiro, Emanuela. "Dynamics of p53 signalling in response to single-strand DNA damage". Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/dynamics-of-p53-signalling-in-response-to-singlestrand-dna-damage(ddb35d2e-98ac-4e17-a620-c8a047878477).html.
Texto completoMills, Kevin D. (Kevin David) 1972. "Silencing, heterochromatin, and DNA double strand break repair in Saccharomyces cerevisiae". Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/84768.
Texto completoRoy, Rajat. "Functional analysis of the DNA double-strand break repair protein Ku". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619963.
Texto completoRakhimova, Alina. "Role of histones in DNA double-strand break repair in Dictyostelium". Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:f6ae6f6a-9f83-4326-89e3-719ea9c43cc0.
Texto completoMa, Yue. "Double-strand breaks (DSBs) and structure transition on genome-sized DNA". Thesis, https://doors.doshisha.ac.jp/opac/opac_link/bibid/BB13097333/?lang=0, 2018. https://doors.doshisha.ac.jp/opac/opac_link/bibid/BB13097333/?lang=0.
Texto completoThe protective effect of ascorbic acid (AA) and DMSO against double-strand breaks (DSBs) in DNA was evaluated by single-molecule observation of giant DNA (T4 DNA; 166kbp) through fluorescence microscopy. Samples were exposed to three different forms of radiation: visible light, γ-ray, and ultrasound or freeze/thawing. The change of the higher-order structure of genomic DNA molecules in the presence of alcohols by use of single DNA observation with fluorescence microscopy, by focusing our attention to unveil the different effect between 1-propanol and 2-propanol.
博士(工学)
Doctor of Philosophy in Engineering
同志社大学
Doshisha University
Khalil, Ashraf. "ATM-Dependent ERK Signaling in Response to DNA Double Strand Breaks". VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/760.
Texto completoSinha, Manisha. "Recombinational Repair of a Chromosomal DNA Double Strand Break: A Dissertation". eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/412.
Texto completoPhipps, Jamie. "Cohesin and maintenance of genome integrity at DNA double-strand breaks". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL005.
Texto completoDNA double-strand breaks (DSB) must be repaired to ensure genome stability. Crucially, DSB ends must be kept together for timely repair. In Saccharomyces cerevisiae, two poorly understood pathways mediate DSB end-tethering. One employs the Mre11-Rad50-Xrs2 (MRX) complex to physically bridge DSB ends. Another requires the conversion of DSB ends into single-strand DNA (ssDNA) by Exo1, but the bridging proteins are unknown. We uncover that cohesin, its loader and Smc5/6 act with Exo1 to tether DSB ends. Remarkably, cohesin specifically impaired in oligomerization fails to tether DSB ends, revealing a new function for cohesin oligomerization. In addition to the known importance of sister chromatid cohesion, microscopy-based microfluidic experiments unveil a new role for cohesin in repair by ensuring DSB end-tethering. Altogether, our findings demonstrate that oligomerization of cohesin prevents DSB end separation and promotes DSB repair, revealing a novel mode of action and role for cohesin in safeguarding genome integrity