Дисертації з теми "Genotoxic stress response"
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Konstantinidou, C. "Stage-specific response of NC lineages to genotoxic stress." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1458881/.
Повний текст джерелаPurmessur, Nadia Sheree. "The regulation of p53-dependent microRNA expression in response to genotoxic stress." Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/28637.
Повний текст джерелаVickridge, Elise. "Management of E. coli sister chromatid cohesion in response to genotoxic stress." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS172/document.
Повний текст джерелаMaintaining genome integrity through replication is an essential process for the cell cycle. However, many factors can compromise this replication and thus the genome integrity. Mitomycin C is a genotoxic agent that creates a covalent link between the two DNA strands. When the replication fork encounters the DNA crosslink, it breaks and creates a DNA double strand break (DSB). Escherichia coli (E.coli) is a widely used model for studying complex DNA mechanisms. When facing a DNA DSB, E. coli activates the SOS response pathway. The SOS response comprises over 50 genes that are under the control of a LexA-repressed promoter. Upon a DSB induction, RecA, a central protein of the SOS response will trigger the degradation of LexA and all the SOS genes will be expressed.We have developed a novel molecular biology tool that reveals contacts between sister chromatids that are cohesive. It has been shown in the lab (Lesterlin et al. 2012) that during a regular cell cycle, the two newly replicated sister chromatids stay in close contact for 10 to 20 min before segregating to separate cell halves thanks to the action of Topoisomerase IV. This step is called sister chromatid cohesion. We have used this molecular biology tool to study sister chromatid cohesion upon a genotoxic stress induced by mitomycin C (MMC). We have shown that sister chromatid cohesion is maintained and prolonged when the cell is facing a DSB. Moreover, this sister chromatid cohesion is dependent on RecN, an SOS induced structural maintenance of chromosome-like (SMC-like) protein. In the absence of RecN, the proximity between both sister chromatids is lost and this has a deleterious effect on cell viability. By tagging the chromosome with fluorescent proteins, we have revealed that RecN can also mediated a progressive regression of two previously segregated sister chromatids and this is coordinated with a whole nucleoid compaction. Further studies showed that this genome compaction is orderly and is not the result of a random compaction in response to DNA damage.Interestingly, inhibiting TopoIV in a recN mutant fully restores viability and sister chromatid cohesion suggesting that RecN’s action is mainly structural. Preserving cohesion through precatenanes is sufficient to favor repair and cell viability even in the absence of RecN.An RNA-seq experiment in a WT strain and a recN mutant revealed that the whole SOS response is downregulated in a recN mutant. This suggests that RecN may have an effect on the induction of the SOS response and thus RecA filament formation. This is in good agreement with the change in RecA-mcherry foci formation we observed. In the WT strain, the RecA-mcherry foci are defined as described in previous work. However, in the recN, the RecA-mcherry foci seemed to form bundle like structures. These RecA bundles were previsously described by Lesterlin et al. in the particular case of a DSB occurring on a chromatid that has already been segregated from its homolog. This could mean that in the absence of recN, the sister chromatids segregate and RecA forms bundle like structures in order to perform a search for the intact homologous sister chromatid.Altogether, these results reveal that RecN is an essential protein for sister chromatid cohesion upon a genotoxic stress. RecN favors sister chromatid cohesion by preventing their segregation. Through a whole nucleoid rearrangement, RecN mediates sister chromatid regression, favoring DNA repair and cell viability
Davidson, Adam. "Investigating the Role of Interferon Regulatory Factor 3 in Response to Genotoxic Stress." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24928.
Повний текст джерелаLiu, Jia, and 劉佳. "Role of FBXO31 in regulating MAPK-mediated genotoxic stress response and cancer cell survival." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/205657.
Повний текст джерелаpublished_or_final_version
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Al-Asadi, Mazin Gh. "Investigation of dormancy in acute myeloid leukaemia cells and the induction of dormancy in their response to genotoxic stress." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/43320/.
Повний текст джерелаStockwell, Simon Reidar. "The role of threonine 286 phosphorylation on cyclin D1 in sub-cellular localisation and proteolysis in response to genotoxic stress." Thesis, Institute of Cancer Research (University Of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406688.
Повний текст джерелаDuarte, Alexandra. "The interplay between MYCN and the DNA damage response : modulation of MYCN expression, its interactions with components of the DNA damage response and cellular responses to N-myc following genotoxic stress." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9832.
Повний текст джерелаCook, Peter Joseph. "Eya a dual function nuclear factor crucial for regulation of developmental gene expression and prevention of apoptosis in response to genotoxic stress /." Diss., [La Jolla, Calif.] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3344509.
Повний текст джерелаTitle from first page of PDF file (viewed March 13, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Tomkins, C. E. "Cellular responses to genotoxic stress." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362104.
Повний текст джерелаMokrani, Sofiane. "Maintenance de la stabilité chromosomique des cellules souches neurales murines au cours du développement et après un stress génotoxique aiguë ou chronique Impaired brain development and behavior of Xlf null mice linked to chromosome instability-induced premature neurogenesis Higher Chromosome Stability in Mouse Embryonic Neural Stem and Progenitor Cells than in Fibroblasts in Response to Acute or Chronic Genotoxic Stress." Thesis, Institut polytechnique de Paris, 2019. http://www.theses.fr/2019IPPAX010.
Повний текст джерелаPrenatal exposure to ionizing radiation has been associated with many neurodevelopmental disorders due to the DNA damage induced in neural stem and progenitors cells (NSPC). Thus, genetic stability of NSPC is crucial for brain development and homeostasis. Nevertheless, genomic alterations occurring during development in NSPC may have a potential impact on the physiological neuronal diversity. XLF is a component of the NHEJ (Non-Homologous End-Joining) repair pathway. Here, we show that NSPC from Xlf-/- embryos exhibit increased chromosome instability, leading to premature neurogenesis and consequently neurobehavioral disorders. Using cytogenetic approaches, we compared the chromosome stability of mouse embryonic NSPC and fibroblasts (MEF) exposed to acute (γ-irradiation) or chronic (incorporation of tritiated thymidine into DNA) genotoxic stress. Our results demonstrate the higher capacity of NSPC as compared to MEF to maintain their genomic integrity. We evidenced that NSPC have more efficient DNA repair activity than MEF, allowing them to develop an adaptive response to chronic genotoxic stress. This adaptive response involves XLF and acts together with apoptosis and cell cycle checkpoints to preserve the stability of the genome and to eliminate damaged cells. Altogether, our results provide new insights into the robust DNA damage response in NSPC and highlight the importance of Xlf during brain development
Gao, Hong. "Effect of Partial Poly (ADP-ribose) Glycohydrolase Gene Deletion on Cellular Responses to Genotoxic Stress." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/195842.
Повний текст джерелаMoore, Anne Margaret. "Identification and characterisation of novel plant specific regulators of cellular responses to double stranded DNA breaks." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/9504.
Повний текст джерелаFinzel, Pérez Ana [Verfasser]. "Upstream control and downstream responses of p53 are involved in its tumor suppression functions upon genotoxic stress / Ana Finzel Pérez." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1122111193/34.
Повний текст джерелаMarques, Regina Célia Pereira. "Identificação de genes de reparo de DNA em Caulobacter crescentus através da seleção de clones sensíveis a agentes genotóxicos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42132/tde-22092008-130133/.
Повний текст джерелаThis work aimed to identify genes related to DNA damage protection in C. crescentus, by means of screening a Tn5 -mutated library for clones sensitive to UV-B light and MMS. Out of 249 selected clones, we were able to identify mutations in 102 genes, classified in ten different functional categories, including DNA metabolism. In addition to genes already described as playing a role in genome defense to lesions, the results provide new potential functions to several other genes. More detailed investigation indicates also that the mutations in some of these genes may also affect cell stress and cell cycle, being potentially involved in check-point responses. Moreover, mutants for nucleotide excision repair genes were also found to be sensitive to H2O2, indicating that this DNA repair system also acts in DNA oxidative damage. These data are the first establishing a role in genome protection for several genes in C. crescentus, as well as other alpha-proteobacteria.
Hull, Rodney. "Stress response to genotoxic agents and to infection." Thesis, 2012. http://hdl.handle.net/10539/12067.
Повний текст джерелаGrewal, Mandeep Kaur. "ARAP2 is induced in response to genotoxic stress and B cell stimulation." 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=370348&T=F.
Повний текст джерела近藤, 琢磨. "Involvement of pRB-Related p107 Protein in the Inhibition of S-Phase Progression in Response to Genotoxic Stress." Doctoral thesis, 2001. http://hdl.handle.net/2115/32664.
Повний текст джерелаKučerová, Alena. "Role of PML in nucleolar functions." Master's thesis, 2016. http://www.nusl.cz/ntk/nusl-266185.
Повний текст джерелаImrichová, Terezie. "Buněčná odpověď na protinádorové terapie založené na genotoxickém stresu." Doctoral thesis, 2019. http://www.nusl.cz/ntk/nusl-409233.
Повний текст джерелаRoy, Raju. "Exploring the role of low complexity protein sequence in regulating RNA granule dynamics and translation control." Thesis, 2022. https://etd.iisc.ac.in/handle/2005/5975.
Повний текст джерелаKnoblochová, Lucie. "Úloha nádorového supresoru PML v odpovědi na poškození DNA a buněčné senescenci po genotoxickém stresu." Master's thesis, 2015. http://www.nusl.cz/ntk/nusl-267925.
Повний текст джерелаPhan, Ryan. "The BCL6 proto-oncogene regulates responses to genotoxic stress in germinal-center B cells /." 2005. http://digitalcommons.libraries.columbia.edu/dissertations/AAI3182977/.
Повний текст джерелаDepartment: Cellular, Molecular and Biophysical Studies. Includes bibliographical references (leaves 103-107). Proquest Digital Dissertations Online ; Subscription required. Also available via the World Wide Web;