Rozprawy doktorskie na temat „Genome damage”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 50 najlepszych rozpraw doktorskich naukowych na temat „Genome damage”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
Banerjee, Ujjwal Kumar. "3-D Genome organization of DNA damage repair". Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ121.
Pełny tekst źródłaOur genome is constantly under attack by endogenous and exogenous factors which challenge its integrity and lead to different types of damages. Double strand breaks (DSBs) constitute the most deleterious type of damage since they maylead to loss of genetic information, translocations and cell death. All the repair processes happen in the context of a highly organized and compartmentalized chromatin. Chromatin can be divided into an open transcriptionally active compartment (euchromatin) and a compacted transcriptionally inactive compartment (heterochromatin). These different degrees of compaction play important roles in regulating the DNA damage response. The goal of my first project was to understand the influence of 3D genome organization on DNA repair. I used two complementary approaches to induce and map DSBs in the mouse genome. My results have shown that enrichment of the DNA damage repair factor γH2AX occurs at distinct loci in the mouse embryonic stem cell genome and that the damage persists in the heterochromatin compartment while the euchromatin compartment is protected from DNA damage. For my second project, I mapped the genomic footprint of 53BP1, a factor involved in DSBs repair, in asynchronous and G1 arrested U2OS cells to identify novel 53BP1 binding sites. My results have identified novel 53BP1 binding domains which cover broad regions of the genome and occur in mid to late replicating regions of the genome
Alrumaihi, Faris Abdulrahman I. "Assessment of UVR-induced DNA damage and repair in nuclear genome versus mitochondrial genome". Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37614.
Pełny tekst źródłaManning, Francis C. R. "The persistence of carcinogen damage in specific regions of the genome". Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.277377.
Pełny tekst źródłaAlpi, Arno. "DNA damage checkpoint pathways and the maintenance of genome stability in C. elegans". Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-24487.
Pełny tekst źródłaKasparek, Torben Rudolf. "Identification and characterisation of determinants of genome stability in response to a double-strand break". Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:78e0a145-22c8-4abd-a746-e18c1939f5c9.
Pełny tekst źródłaDurant, Stephen Thomas. "The role of DNA mismatch repair in cellular responses to DNA damage and drug resistance". Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312133.
Pełny tekst źródłaFrigola, Rissech Joan 1991. "Determinants of the local mutation rate variability along the genome". Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/669530.
Pełny tekst źródłaLa velocitat a la que les mutacions s’acumulen al llarg del genoma no és uniforme sinó que depèn de diversos factors. Alguns dels més coneguts són l’empaquetament de la cromatina, el moment de replicació o la transcripció. La majoria d’aquests factors creen variacions mutacionals que abarquen grans àrees del genoma, incloent varies megabases. En els últims anys, però, també s’ha identificat variabilitat en el ritme en que s’acumulen les mutacions a escala molt més petita, en regions de poques bases. Aquesta tesi es centra en l’estudi de dos d’aquestes variacions locals en el ritme en que les mutacions tenen lloc. Primer, hem descrit una reducció en el número de mutacions somàtiques en els exons causades per errors de la AND polimerasa, que hem atribuït a una major eficàcia del mecanisme encarregat aquest tipus d’errors en els exons. En segon lloc, hem estudiat com les lesions en el DNA causades per la llum ultraviolada es generen i són reparades als llocs d’unió dels factors de transcripció i hem determinat fins a quin punt cada un d’aquests processos permeten explicar l’inesperat número de mutacions en aquestes regions. La presència d’aquestes variacions locals la velocitat a la que les mutacions s’acumulen al llarg del genoma posen de manifest la dificultat de modelar correctament aquest procés, un procediment central en molts estudis evolutius i de genòmica del càncer.
Blance, Stephen J. "DNA repair and recombination in Streptomyces coelicolor". Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367139.
Pełny tekst źródłaFinneran, Bryan P. "Developing and Testing an ELISA Biosensor for Measuring UV-Induced Viral Genome and Protein Damage". The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1593640837647181.
Pełny tekst źródłaBhattacharjee, Sonali. "The role of Fml1 and its partner proteins Mhf1 and Mhf2 in promoting genome stability". Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711640.
Pełny tekst źródłaMacpherson, Annie. "Metabolic dysfunction and impairments in the DNA Damage Response : dissecting a pathomechanistic link between Microcephalic Primordial Dwarfisms and cancer cachexia". Thesis, University of Sussex, 2017. http://sro.sussex.ac.uk/id/eprint/71421/.
Pełny tekst źródłaYu, Wei [Verfasser], M. Cristina [Akademischer Betreuer] Cardoso i Barbara [Akademischer Betreuer] Drossel. "Genome-wide analysis of DNA damage and repair / Wei Yu. Betreuer: M. Cristina Cardoso ; Barbara Drossel". Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2015. http://d-nb.info/1110980728/34.
Pełny tekst źródłaWalker, Sarah A. "Investigating the role of the ATR-dependent DNA damage response in the aetiology of microcephalic primordial dwarfism disorders". Thesis, University of Sussex, 2012. http://sro.sussex.ac.uk/id/eprint/43346/.
Pełny tekst źródłaPowell, James Rees. "Measuring DNA damage and associated epigenetic changes genome-wide in cells following exposure to platinum analogue chemotherapeutic drugs". Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/65976/.
Pełny tekst źródłaDuro, Eris. "Identification of MMS22 as a regulator of DNA repair". Thesis, University of Dundee, 2010. https://discovery.dundee.ac.uk/en/studentTheses/7b553aeb-8f92-492e-b16f-c4c96d36fb01.
Pełny tekst źródłaHumphryes, Neil. "Global genome nucleotide excision repair factors and the ubiquitin-proteasome system regulate the DNA damage response in Saccharomyces cerevisiae". Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/55468/.
Pełny tekst źródłaLashgari, Anahita. "Investigating the function of histone H2A.Z in the human genome and mechanisms of chromatin incorporation". Thèse, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/9886.
Pełny tekst źródłaRésumé : La régulation de la transcription est un mécanisme crucial pour le bon développement et fonctionnement des cellules eucaryotes. Chez les eucaryotes, l'ADN est organisé dans une structure dynamique de nucléoprotéines appelée chromatine. La structure de la chromatine forme une barrière qui contrôle l'accès des facteurs de transcription à leurs sites de fixation sur l’ADN. Plusieurs mécanismes ont été acquis au cours de l'évolution pour moduler la dynamique de la chromatine afin de réguler de manière adéquate l'expression des gènes. Un des mécanismes les plus intriguant qui module la structure de la chromatine est le remplacement des histones canoniques par des variants d'histones. Il est effectué par des complex de remodelage de la chromatine. Parmi les variants d'histones, H2A.Z est un régulateur essentiel de la transcription des gènes. H2A.Z est enrichi aux régions régulatrices des gènes, mais des niveaux significatifs de ce variant d'histone peuvent aussi être observés au cœur des gènes. Le rôle de H2A.Z localisé a lèintérieur gènes n'est, pour l'instant, pas bien compris. Des résultats récents suggèrent que le recrutement actif de H2A.Z dans les gènes est requis pour induire leur répression. En opposition à ces résultats, nous montrons que l'inhibition globale de la transcription conduit à l'accumulation de H2A.Z aux sites d'initiation de la transcription, mais aussi au cœur des gènes. Nos résultats indiquent que l'accumulation de H2A.Z dans les gènes réprimés serait une conséquence de l'absence de transcription plutôt qu'un mécanisme actif requit pour établir la répression. La seconde partie de mon doctorat a été dédiée à l'étude du rôle de BRD8 (une sous-unité du complexe p400/Tip60) dans la signalisation contrôlée par p53. Nous avons trouvé que la déplétion de BRD8 conduit à l'induction de p21 et à l'arrêt concomitant du cycle cellulaire en phase G1/S. Nous montrons aussi que le circuit transcriptionnel de p53 est activé dans les cellules déplétées en BRD8. Cela résulte en l'induction de p21, mais aussi de gènes proapoptotiques, ce qui conduit la cellule en apoptose. De manière marquante, la voie de réponse aux dommages de l'ADN est induite suite à la déplétion de BRD8, ce qui est observée par l'apparition de foci de dommages à l'ADN révélés par immunocoloration de γ-H2AX. De plus, l'acétylation de H4K16 est réduite dans les cellules déplétées en BRD8, suggérant que BRD8 pourrait avoir un rôle dans le recrutement et/ou la stabilisation du complexe p400/Tip60 dans la chromatine, et pourrait donc faciliter la réparation de l'ADN. En accord avec le fait que la réponse aux dommages de l'ADN soit activée, nous trouvons que dans les cellules déplétées en BRD8, CHK2 est activé mais étonnamment le niveau de la protéine CHK1 était fortement diminué. Ensemble, nos résultats suggèrent que BRD8 est impliqué non seulement dans la répression des gènes régulés par p53, mais aussi dans la réponse aux dommages de l'ADN. Finalement, dans la dernière partie de mon doctorat j'ai étudié le mécanisme qui pouvait être responsable du recrutement du complexe p400 au niveau de la chromatine. Nous avons montré que le variant d'histone H2A.Z est essentiel pour le recrutement de p53 et de p400 au site distal de fixation de p53 sur le promoteur de p21. De plus, en utilisant des cellules MEF DKO pour p300/CBP, nous avons montré que la déplétion de p300/CBP conduit à une diminution sévère du recrutement de p400 au promoteur de p21. En conclusion, mes études permettent de mieux comprendre les mécanismes moléculaires impliqués dans la régulation de la chromatine par l'histone H2A.Z et le complexe de remodelage de la chromatine p400.
Hiller, Björn. "The role of RNase H2 in genome maintenance and autoimmune disease". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-193520.
Pełny tekst źródłaAdamson, Brittany Susan. "A Genome-Wide Study of Homologous Recombination in Mammalian Cells Identifies RBMX, a Novel Component of the DNA Damage Response". Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10723.
Pełny tekst źródłaGuillemette, Shawna S. "Investigating Tumor Suppressors in the DNA Damage Response: Caretakers of the Genome and Biomarkers to Predict Therapeutic Response: A Dissertation". eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/712.
Pełny tekst źródłaLawson, Jonathan Luke Done. "Genome-wide microscopy screening identifies links across processes including a conserved connection between DNA damage control and the microtubule cytoskeleton". Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/253007.
Pełny tekst źródłaGuillemette, Shawna S. "Investigating Tumor Suppressors in the DNA Damage Response: Caretakers of the Genome and Biomarkers to Predict Therapeutic Response: A Dissertation". eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/712.
Pełny tekst źródłaBianchi, Joy J. "Origin of somatic mutations in lymphoid cancers : role of the V(D)J recombinase Breakage-fusion-bridge events trigger complex genome rearrangements and amplifications in developmentally arrested T cell lymphomas End donation errors at antigen receptor loci trigger genome-wide instability in ATM-deficient T cell lymphomas". Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB057.
Pełny tekst źródłaLymphoid cancers frequently harbor chromosomal aberrations. Abnormal V(D)J recombinase (i.e RAG endonuclease) activity is thought to promote genomic instability in lymphocytes, while DNA damage response (DDR) factors such as Ataxia-telangiectasia mutated (ATM) and p53 have been shown to suppress aberrant chromosomal rearrangements and lymphomagenesis. During my thesis, to test the relative contribution of these factors in shaping the pattern of somatic mutations in lymphoma genome, I performed whole genome and transcriptome sequencing of several genetically modified mouse lymphoma models in which the activities of RAG and DDR were perturbed. In a first study, I have identified specific recurrent genomic lesions caused by off-target RAG activity and, more surprisingly, a unique pattern of aberrant rearrangements occurring in the absence of RAG. I provided evidence that, in the absence of RAG, Breakage-Fusion-Bridge triggers instability and amplification of a genomic region of several megabases leading to the overexpression of multiple known and putative cancer genes. Importantly, I also showed that this region is found amplified in a subset of human leukemia. Using additional animal models in which blocked T cell differentiation due to the absence of RAG was rescued by the expression of a transgenic T cell receptor, I could demonstrate that both developmental stage and RAG activity determine T cell lymphoma genome landscapes and mediate malignant transformation through distinct oncogenic paths. In addition, I have established the first genome-wide analysis of ATM-deficient T-cell lymphomas and identified a high number of aberrations localized at antigen receptor loci and ectopic locations in these tumors. My results suggest that, in the absence of ATM, aberrantly resolved RAG-induced DNA breaks at antigen receptor loci trigger massive complex rearrangements spreading to ectopic locations and affecting cancer genes. Overall, my studies provide new insights into the mechanisms of somatic mutations arising in lymphoid cancers in the context of aberrant V(D)J recombination and DDR
Boyko, Oleksandr, i University of Lethbridge Faculty of Arts and Science. "The versatile role of homologous recombination in plant cell : repair of DNA damage, stress-directed genome evolution and foreign DNA integration". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/724.
Pełny tekst źródłaxxi, 246 leaves : ill. ; 29 cm. --
Kaku, Taijin. "RD1 region in mycobacterial genome is involved in the induction of necrosis in infected RAW264 cells via mitochondrial membrane damage and ATP depletion". Kyoto University, 2007. http://hdl.handle.net/2433/135912.
Pełny tekst źródłaLyraki, Rodanthi. "Molecular mechanisms underlying Retinitis pigmentosa type 2". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31254.
Pełny tekst źródłaPowers, Kyle Thomas. "Structure and function of the disordered regions within translesion synthesis DNA polymerases". Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6625.
Pełny tekst źródłaMeisenberg, Cornelia. "The role of ubiquitylation in regulating apurinic/apyrimidinic endonuclease 1". Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:9a6582d4-6fc0-48c9-9c13-6c99e23e66e9.
Pełny tekst źródłaWalz, Paul S. "Influence of pathogenic bacterial determinants on genome stability of exposed intestinal cells and of distal liver and spleen cells". Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biology, c2011, 2011. http://hdl.handle.net/10133/3405.
Pełny tekst źródłaxiv, 132 leaves : ill. (chiefly col.) ; 29 cm
Kosicki, Michal Konrad. "Cas9-induced on-target genomic damage". Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289911.
Pełny tekst źródłaDamasceno, Jeziel Dener. "Caracterização molecular do envolvimento das proteínas LmHus1 e LmRad9 em mecanismos de reconhecimento e reparo de DNA no parasito Leishmania major". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-04042013-114550/.
Pełny tekst źródłaGenome stability is a essential condition for survival and proper functioning of living organisms. However, a broad range of elements may lead to DNA damage. For instance, about 104 DNA lesions may be inflicted upon any given mammalian cell everyday. In order to maintain the genome integrity and circumvent the deleterious effects of these lesions, a molecular machinery composed of proteins specialized in detecting and repairing DNA damage has been selected in evolution. Defects of the proteins that constitute such machineries may result not only in a high mutation rate, but also in breaks in the DNA structure that can mediate gene amplification as observed in cancer cells. In an apparent opposition to such requirement for stability as an essential condition to life, the protozoan Leishmania presents a highly malleable genome and explores genome amplification as a survival and adaptation tool. Despite of the fact that the Leishmania genome plasticity can be easily demonstrated, the precise mechanisms that coordinate the molecular machineries involved in the detection and signaling of DNA damage, and in the regulation of gene amplification is still largely unknown. In order to contribute to a better understanding of these processes, we identified and studied the Leishmania major proteins that are homologues of those proteins that compose the 9-1-1 complex (Rad9-Hus1-Rad1). The proteins LmHus1 and LmRad9 present a high structural divergence when compared to its homologues from other eukaryotes and no obvious homologue of Rad1 was identified in the parasite genome. Phylogeny analysis indicated that LmHus1 and LmRad9 are closely related to heterotrimeric complexes involved in the detection of DNA damage. In accordance to that, our experiments demonstrated that altered levels of these proteins interfere with the parasite ability to deal with genotoxic stress. Moreover, LmHus1 was localized to the parasite nucleus and is a required protein for normal parasite proliferation. Besides, we showed that decreased levels of LmHus1 compromise cell cycle regulation and the maintenance of telomeres. LmRad9 was also shown to be localized to the cell nucleus and its overexpression led to growth defects and affected the L. major response to genotoxic stress. We also observed that LmHus1 and LmRad9 interact with each other to for a protein complex that is responsive to DNA damage in vivo, which strongly suggested that the 9-1-1 complex was conserved in L. major. The structural peculiarities of these proteins indicate that the possible L. major 9-1-1 complex has a different architecture when compared to the complex found in higher eukaryotes. In addition to that, other proteins, such as LmRpa1, also present a marked structural divergence. Altogether, these findings suggest that the DNA damage signaling pathway involving the 9-1-1 complex and LmRpa1 in L. major, may present a peculiar mode of action. These observations may contribute to a better understanding not only of the evolution of the signaling pathway mediated by the 9-1-1 complex in eukaryotes, but also of the molecular basis of the genome plasticity and the gene amplification phenomenon.
Ozols, Agris. "Low-dose studies of genomic instability-mechanisms and targets". Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271260.
Pełny tekst źródłaPerl, Abbey Leigh. "Leveraging Small Molecule Activators of Protein Phosphatase 2A (PP2A) toElucidate PP2As Role in Regulating DNA Replication and Apoptosis". Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1574418174603893.
Pełny tekst źródłaCosta, Natalia Layane Badaró. "Improved procedures to assess plant protoplast viability: evidencing cytological and genomic damages". Universidade Federal de Viçosa, 2017. http://www.locus.ufv.br/handle/123456789/11949.
Pełny tekst źródłaMade available in DSpace on 2017-10-09T14:46:30Z (GMT). No. of bitstreams: 1 texto completo.pdf: 4569752 bytes, checksum: 7423d0749a49ab3a18033fe827e2181d (MD5) Previous issue date: 2017-07-21
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Fundação de Amparo a Pesquisa do Estado de Minas Gerais
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Em todas as aplicações, o teste de viabilidade e necessario para medir a taxa de protoplastos viáveis, possibiltando decidir os procedimentos de isolamento e purificação mais adequados e verificar se ha celulas suficientes para as etapas subsequentes. A microscopia de fluorescência geralmente é empregada para o teste de viabilidade. No entanto, alguns problemas têm sido apontados: longo tempo necessário para contar um número relativamente pequeno de protoplastos, aglomerados de células que impedem a observação dos protoplastos e percepção visual da fluorescência subjetiva ao observador. Este estudo teve como objetivo estabelecer procedimentos para teste de viabilidade adaptado para citometria de fluxo (FCM), MuseTM cell analyzer (Muse) e Ensaio cometa (CA). Para isso, Capsicum annuum foi escolhido devido a natureza morfogênica recalcitrante dos protoplastos. Após o isolamento e a purificação, as aplicações permitiram avaliar um grande número de protoplastos (FCM e MUSE) e núcleos dos protoplastos (CA) em um curto período de tempo. A partir das adaptações nos procedimentos, foram evidenciados diferentes tipos e níveis de danos citológicos (FCM e Muse) e genômicos (Muse e CA), possibilitando discriminar e mensurar os protoplastos viãveis. Considerando os resultados, este estudo introduz procedimentos quantitativos melhorados para o teste de viabilidade. Alem disso, visando a regeneração de plântulas, diferentes métodos podem ser aplicados para avaliar a viabilidade de protoplastos, definindo os procedimentos de isolamento e purificação mais adequados. Corraborando para este propósito, foram mostrados guias para FCM, Muse e CA visando a padronizaçao dos testes de viabilidade em protoplastos de plantas.
Plant protoplasts are valuable in biotechnology, enabling the plantlet regeneration until the gene function determination. In all applications, viability test is required to measure the rate of viable protoplasts, allowing to decide on the most adequate isolation and purification procedures and to verify whether there are sufficient cells for subsequent steps. Fluorescence microscopy is usually employed for viability test. However, some problems have been pointed out: long time required to count a relatively small number of protoplasts, cell clumps preventing their observation, and the subjective visual perception of the fluorescence by observer. This study aimed to establish procedures for viability test adapted for flow cytometry (FCM), MuseTM cell analyzer (Muse) and Comet Assay (CA). For this, Capsicum annuum was chosen due to recalcitrant morphogenic nature of its protoplasts. After isolation and purification, the applications allowed assessing large numbers of protoplasts (FCM and MUSE) and protoplasts nuclei (CA) in a short time period. From the adjusted procedures, different types and levels of cytological (FCM and Muse) and genomic damages (Muse and CA) were evidenced, allowing to discriminate and measure the viable protoplasts. Considering the results, this study introduces improved quantitative procedures for viability test. Besides of these and aiming the plantlet regeneration, different methods can be applied to assess the protoplast viability, defining the more adequate isolation and purification procedures. Contributing with this purpose, guides were showed for FCM, Muse and CA to standardization of viability tests in plant protoplasts
Yamazaki, Hiroyuki. "APOBEC3B promotes genomic instability in myeloma cells". Kyoto University, 2020. http://hdl.handle.net/2433/259004.
Pełny tekst źródłaChau, P. Y. Pauline. "Mechanism of genomic instability in Prelamin A based premature ageing". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557352.
Pełny tekst źródłaChau, P. Y. Pauline, i 周珮然. "Mechanism of genomic instability in Prelamin A based premature ageing". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557352.
Pełny tekst źródłaLi, Han. "Impact of KU80 in genomic stability, cancer and aging: a dissertation /". San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1324370271&sid=2&Fmt=2&clientId=70986&RQT=309&VName=PQD.
Pełny tekst źródłaBankoglu, Ezgi Eylül [Verfasser], i Helga [Gutachter] Stopper. "Oxidative status and genomic damage in an obesity model / Ezgi Eylül Bankoglu. Gutachter: Helga Stopper". Würzburg : Universität Würzburg, 2016. http://d-nb.info/1112466339/34.
Pełny tekst źródłaNandi, Saikat. "Deciphering the molecular mechanism by which Fml1 promotes and constrains homologous recombination". Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.561123.
Pełny tekst źródłaChen, Hong, i 陳紅. "A study of male accessory sex glands in protecting: the genomic integrity of sperm in the golden hamster(Mesocricetus auratus)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31245195.
Pełny tekst źródłaRajaraman, Gnana Oli [Verfasser], i Helga [Akademischer Betreuer] Stopper. "Oxidative stress : role in genomic damage and disease = Oxidativer Stress / Gnana Oli Rajaraman. Betreuer: Helga Stopper". Würzburg : Universitätsbibliothek der Universität Würzburg, 2012. http://d-nb.info/1024851885/34.
Pełny tekst źródłaWang, Zhenxing [Verfasser]. "Early genomic response to X-ray induced DNA damage and transposon regulation in Arabidopsis thaliana / Zhenxing Wang". Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1077211910/34.
Pełny tekst źródłaNyberg, Kara Ann. "Analysis of RAD9 functions: Roles in the checkpoint response, DNA damage processing, and prevention of genomic instability". Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/280312.
Pełny tekst źródłaKinvi-Dossou, Gbèssiho Raphaël. "Étude de la résistance à l’impact et de l’endommagement des composites stratifiés à matrice Elium acrylique : caractérisation expérimentale et modélisation numérique multi-échelle". Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0249/document.
Pełny tekst źródłaIn the race for light materials able of meeting modern environmental challenges, an acrylic resin (Elium) has been developed. Elium is a thermoplastic resin able to replace thermosetting matrices, which are widespread nowadays in the industrial world. The present study aims to evaluate the impact resistance and to understand the failure mechanisms of composite laminates based on acrylic matrix under impact loading. We provide a contribution to the multiscale analysis of the impact resistance of laminated composite.First, the impact resistance and the damage tolerance of the acrylic resin based composites were compared with those of conventional composites. Then, the impact performance of the laminated composites has been enhanced by adding copolymer blocks to the liquid acrylic resin. These copolymers are able to form micelles of nanometer sizes, which lead to the improvement of both the acrylic matrix fracture toughness and the impact resistance. The effects of the impact energy, temperature, and composition in nano-copolymers have also been investigated.In order to provide a numerical tool for the prediction of the impact response of the glass fiber/Acrylic laminates, two strategies have been analyzed. The first one, performed at the macroscopic scale, considers the woven ply of the laminate as homogeneous material, and the second one (at the mesoscopic scale), deals with a realistic geometrical description of the yarns undulation. Both models use cohesive zones at the interface between the adjacent plies, to simulate the delamination. For this purpose, experimental and numerical delamination tests were performed to feed the inter-ply damage model. Mechanical tests for material characterization were also performed on specimens in order to identify the ply-damage model parameters. The Mechanics of Structure Genome (MSG) and a finite element based micromechanics approaches were then conducted to evaluate the effective thermomechanical properties of the yarns and the plain woven composite laminate. The realistic topological and morphological textures of the composite were accounted through Texgen software. These numerical impact simulations were performed using the finite element software ABAQUS/Explicit. Both models were implemented through a user material subroutine VUMAT. The obtained results appear in a good agreement with the experimental data and confirm the relevance of the proposed approach
Awad, Eman Da'as [Verfasser], i Helga [Gutachter] Stopper. "Modulation of insulin-induced genotoxicity in vitro and genomic damage in gestational diabetes / Eman Da'as Awad ; Gutachter: Helga Stopper". Würzburg : Universität Würzburg, 2019. http://d-nb.info/1185983120/34.
Pełny tekst źródłaKirk, Austin J. "The partial development of novel assays for the analysis of distribution and quantification of oxidative damage in genomic DNA". Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288302.
Pełny tekst źródłaRamey, Christopher Joshua. "The role of histone H3/H4 chaperone anti-silencing function1 in maintaining genomic integrity /". Connect to full text via ProQuest. IP filtered, 2006.
Znajdź pełny tekst źródłaTypescript. Includes bibliographical references (leaves 119-130). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Núñez, Ollé Marc 1984. "The Role of cyclin O in the DNA damage response". Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/459302.
Pełny tekst źródłaLa Ciclina O és una nova ciclina que interacciona amb CDK1 i CDK2, i que s’ha demonstrat ser necessària per l’apoptòsi induïda per radiació gamma en una linia cel·lular d’origen linfoide. La radiació gamma indueix la formació de talls de doble cadena (DSBs) al DNA activant la resposta per dany al DNA (DDR) per tal de reduïr-ne les conseqüències citotòxiques i reparar el dany al DNA. L’objectiu d’aquesta tesi ha esta el d’estudiar el paper de la Ciclina O en l’activació de la resposta per dany al DNA i les conseqüències sobre la supervivència cel·lular. Utilitzant cèl·lules deficients en Ciclina O com a model, hem trobat que la Cyclina O limita el processament dels talls de doble cadena necessaris per a la reparació del dany al DNA per recombinació homologa. També hem una deficient activació d’ATM i la fosforil·lació d’alguns substrats d’aquesta proteína en cèl·lules deficients per la Ciclina O. Finalment, hem vist que els complexes de Ciclina O fosforil·len ATM in vitro, un fet que obre una porta a l’estudi de nous mecanismes de regulació de la resposta per dany al DNA mitjançant la Ciclina O.
Bolton, Elisabeth Spring. "Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP". Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/234916.
Pełny tekst źródłaPh.D.
In chronic myelogenous leukemia (CML), activation of BCR-ABL, the product of the bcr-abl chimeric gene, leads to constitutive activation of pathways that increase genomic instability through endogenous production of reactive oxygen species (ROS) that cause oxidative DNA damage and inactivate the function of repair proteins leading to unfaithful DNA repair. If misrepaired, oxidative DNA damage, such as 8-oxoguanine (8-oxoG), may result in point mutations and/or DNA double-strand breaks (DSBs) leading to drug resistance to the BCR-ABL kinase inhibitor imatinib mesylate (IM) and accumulation of chromosomal aberrations associated with malignant CML progression from a benign chronic phase (CP) to a fatal blast phase (BP). To determine which population of CML-CP cells, leukemia stem cells (LSCs) and/or leukemia progenitor cells (LPCs), displays elevated levels of ROS and oxidative DNA damage, and whether these elevated levels of ROS and oxidative DNA damage in CML-CP subpopulations result in the accumulation of genomic instability, we employed the tetracycline-inducible SCLtTA/BCR-ABL transgenic mouse model. We showed that LSCs, including the quiescent subpopulation, but not LPCs, displayed elevated levels of ROS and oxidative DNA damage, perhaps due to deregulated expression of genes involved in ROS metabolism, resulting in genomic instability manifested by both point mutations and genetic alterations. We also examined the effect of IM on ROS, oxidative DNA damage and genomic instability displayed by CML-CP subpopulations, and determined that elevated ROS and oxidative DNA damage were not inhibited by IM in quiescent LSCs, nor was genomic instability and deregulated gene expression prevented. To explore underlying mechanisms, i.e. BCR-ABL expression levels, by which CML-CP cells accumulate genomic instability, we examined the effect of low and high BCR-ABL expression on ROS and oxidative DNA damage in BCR-ABL-transduced human CD34+ cells. We detected elevated ROS and oxidative DNA damage in high BCR-ABL-expressing CD34+ cells compared to low BCR-ABL-expressing cells. Furthermore, BCR-ABL exerted a kinase-dependent effect on ROS-dependent DNA damage. These data support the hypothesis that genomic instability may originate from LSCs, but do not exclude the potential role of LPCs, and may have important clinical implications for CML treatment since additional genetic aberrations that encode primary resistance may protect LSCs, including the quiescent subpopulation, from eradication by tyrosine kinase inhibitors (TKIs), and the continuous accumulation of genetic errors may trigger disease relapse and progression.
Temple University--Theses