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Dissertations / Theses on the topic 'Base excision'

Author: Grafiati

Published: 7 June 2025

Last updated: 16 July 2025

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1

Prasad, Amalthiya. "Base Excision Repair in Chromatin." ScholarWorks @ UVM, 2008. http://library.uvm.edu/dspace/bitstream/123456789/180/1/amalthiyprasadfinal.pdf.

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2

Tait, Phillip Stuart. "Regulation of base excision repair." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504608.

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3

Sleeth, Kate Michelle. "DNA ligases in base excision repair." Thesis, University of Reading, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428317.

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4

Fletcher, Sally C. "Regulation of the base excision repair pathway." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:e3db2385-f9aa-4289-9547-3e37cbeddec9.

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Maintenance of genomic stability is paramount for survival of an organism; failure to repair DNA damage ultimately leads to the accumulation of genetically unstable cells and the onset of different human diseases including cancer. DNA single strand breaks and base oxidation/alkylation are among the most frequent types of DNA damage occurring spontaneously in cells. Base excision repair (BER), which copes with the majority of these lesions, is therefore a fundamental DNA repair system. Accordingly, it is important to understand how BER is regulated, and particularly, how and if BER is affected

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5

Odell, Ian. "Modulation of Base Excision Repair by Nucleosomes." ScholarWorks @ UVM, 2010. http://scholarworks.uvm.edu/graddis/170.

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DNA in eukaryotes is packaged into nucleosomes, which present steric impediments to many of the factors and enzymes that act on DNA, including DNA repair enzymes. Within the nucleosome, DNA remains vulnerable to oxidative damage that can result from normal cellular metabolism, ionizing radiation, and various chemical agents. Oxidatively damaged DNA is repaired in a stepwise fashion via the base excision repair (BER) pathway. Other DNA repair pathways, including Nucleotide Excision Repair (NER), Mismatch Repair (MMR), Homologous Recombination (HR), and Non-homologous End-Joining (NHEJ) are all

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6

Sokhansanj, Bahrad Ali. "Mathematical models of human DNA base excision repair /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.

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7

Jiang, Zhongliang. "Epigenetic Instability Induced by DNA Base Lesion via DNA Base Excision Repair." FIU Digital Commons, 2017. https://digitalcommons.fiu.edu/etd/3566.

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DNA damage can cause genome instability, which may lead to human cancer. The most common form of DNA damage is DNA base damage, which is efficiently repaired by DNA base excision repair (BER). Thus BER is the major DNA repair pathway that maintains the stability of the genome. On the other hand, BER mediates DNA demethylation that can occur on the promoter region of important tumor suppressor genes such as Breast Cancer 1 (BRCA1) gene that is also involved in prevention and development of cancer. In this study, employing cell-based and in vitro biochemical approaches along with bisulfite DNA s

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8

Akbari, Mansour. "Human Base Excision Repair for Preservation of Genomic Stability." Doctoral thesis, Norwegian University of Science and Technology, Department of Cancer Research and Molecular Medicine, 2006. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-1807.

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9

Scott, A. D. "The excision repair of base damage in Saccharomyces cerevisiae." Thesis, Swansea University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.638781.

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In <I>Saccharomyces cerevisiae RAD7 </I>and <I>RAD16</I> are required for nucleotide excision repair (NER) of CPDs in nontranscribed regions of the genome. An inducible component to NER in yeast is examined in this thesis. Excision of CPDs and a minor UV induced lesion characterised by sensitivity to endonuclease III (EIIISS), is enhanced following a prior UV irradiation. No enhancement of repair is detected in either the <I>rad7Δ</I> or the <I>rad16Δ</I> mutant. Since repair of EIIISS in transcriptionally silent DNA is independent of <I>RAD7 </I>and <I>RAD16</I>, these two genes may have two

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10

Thomson, Hellen Frances. "Biochemical characterisation of base excision repair enzymes in Neisseria meningitidis." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435770.

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11

Zhao, Qiyuan. "Investigating enzyme communication during base excision repair in Escherichia coli." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29844.

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Mismatch uracil DNA Glycosylase (MUG) from Escherichia coli is an initiating enzyme in the base excision repair (BER) pathway and is responsible for the removal of 3,N4-ethenocytosine and uracil from DNA during the stationary phase of E.coli cell growth. As with other DNA glycosylases, the abasic product is potentially more harmful than the initial lesion. MUG is widely regarded as a 'single turnover' enzyme because it still remains tightly bound to its abasic product after cleavage, thus impeding its catalytic turnover. This may be a general protective mechanism to protect the abasic BER inte

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12

Pachkowski, Brian Francis Swenberg James A. "Functional studies of accessory factors associated with base excision repair." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1717.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.<br>Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Environmental Sciences and Engineering." Discipline: Environmental Sciences and Engineering; Department/School: Public Health.

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13

Beaver, Jill M. "Trinucleotide Repeat Instability is Modulated by DNA Base Lesions and DNA Base Excision Repair." FIU Digital Commons, 2016. http://digitalcommons.fiu.edu/etd/3056.

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Trinucleotide repeat (TNR) expansions are the cause of over 40 human neurodegenerative diseases, and are linked to DNA damage and base excision repair (BER). We explored the role of DNA damage and BER in modulating TNR instability through analysis of DNA structures, BER protein activities, and reconstitution of repair using human BER proteins and synthesized DNA containing various types of damage. We show that DNA damage and BER can modulate TNR expansions by promoting removal of a TNR hairpin through coordinated activities of BER proteins and cofactors. We found that during repair in a TNR ha

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14

Carter, Alan Neil. "The role of base excision repair in regulating endotoxin induced inflammation." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-base-excision-repair-in-regulating-endotoxin-induced-inflammation(35c4d11f-c691-4d15-8cba-732cd5a4db27).html.

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Endotoxins a component of the outer membrane of the cell wall of gram negative bacteria, stimulate the innate immune system to elicit an inflammatory response in mammals. Deletion of base excision repair (BER) genes has been reported to decrease the immune response to endotoxin in mouse models. It is currently unknown whether this role is limited to a few select proteins or a result of the general function of the BER pathway. The aim of this study was to identify if the loss of other BER proteins would trigger a similar response by measuring the levels of inflammatory cytokines produced and ce

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15

Dulic, Anna. "Studies on protein : protein interactions in mammalian DNA base-excision repair." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404820.

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16

Chaim, Isaac Alexander. "Functional DNA repair capacity assays : a focus on base excision repair." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104221.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2016.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>The integrity of our DNA is challenged by roughly 100,000 lesions per cell on a daily basis. Failure to cope with DNA damage can lead to cancer, immunodeficiency and degenerative disease. Quantitating and understanding an individual's DNA repair capacity may enable us to predict and prevent disease in a personalized manner. Base Excision Repair (BER) is known for the recognition and repair of endogenous and exogen

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17

Cooper, Sarah Louise Pamela. "Base excision repair of radiation-induced DNA damage in mammalian cells." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:2c4b3d1e-67c3-4da5-8967-3080b1ebf27a.

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A specific feature of ionising radiation is the formation of clustered DNA damage, where two or more lesions form within one to two helical turns of the DNA induced by a single radiation track. The complexity of ionising radiation-induced DNA damage increases with increasing ionisation density and it has been shown that complex DNA damage has reduced efficiency of repairability. In mammalian cells, base excision repair (BER) is the predominant pathway for the repair of non-DSB clustered DNA lesions and is split into two sub-pathways known as short patch (SP) BER and long patch (LP) BER. SP-BER

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18

Onyango, David O. "Base excision repair apurinic/apyrimidinic endonucleases in apicomplexan parasite Toxoplasma gondii." Thesis, Indiana University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3610136.

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<p> Toxoplasma gondii is an obligate intracellular parasite of the phylum Apicomplexa. Toxoplasma infection is a serious threat to immunocompromised individuals such as AIDS patients and organ transplant recipients. Side effects associated with current drug treatment calls for identification of new drug targets. DNA repair is essential for cell viability and proliferation. In addition to reactive oxygen species produced as a byproduct of their own metabolism, intracellular parasites also have to manage oxidative stress generated as a defense mechanism by the host immune response. Most of the o

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19

Xu, Meng. "Oxidative DNA Damage Modulates Trinucleotide Repeat Instability Via DNA Base Excision Repair." FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1576.

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Trinucleotide repeat (TNR) expansion is the cause of more than 40 types of human neurodegenerative diseases such as Huntington’s disease. Recent studies have linked TNR expansion with oxidative DNA damage and base excision repair (BER). In this research, we provided the first evidence that oxidative DNA damage can induce CAG repeat deletion/contraction via BER. We found that BER of an oxidized DNA base lesion, 8-oxoguanine in a CAG repeat tract, resulted in the formation of a CTG hairpin at the template strand. DNA polymerase β (pol b) then skipped over the hairpin creating a 5’-flap that was

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20

Nichols, Joseph A. "In vitro binding of base excision repair glycosylases to poly(adp-ribose)." Online access for everyone, 2008. http://www.dissertations.wsu.edu/Thesis/Summer2008/j_nichols_071008.pdf.

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21

Woodhouse, Bethany Clare. "The role of poly(ADP-ribose) polymerase-1 in base excision repair." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670110.

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22

Zhou, Jing. "Roles of DNA Base Excision Repair in Maintaining the Integrity of DNA Methylation." FIU Digital Commons, 2013. http://digitalcommons.fiu.edu/etd/1024.

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DNA methylation and demethylation are involved in regulation of gene expression. CpG clusters have been identified as hotspots of oxidative damages and mutagenesis. DNA base excision repair can remove oxidative DNA damage on CpG clusters and mediate an active DNA demethylation pathway. In this study, we examined the molecular mechanisms underlying interactions among DNA methylation, demethylation and BER. Our results demonstrated that a single 5-methylcytosine did not exhibit a significant effect on BER. Surprisingly we found that the abasic site completely inhibited the activity of thymine DN

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23

Cho, Kosai. "ALC1/CHD1L, a chromatin-remodeling enzyme, is required for efficient base excision repair." Kyoto University, 2018. http://hdl.handle.net/2433/232078.

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24

Menoni, Hervé. "La réparation par excision de base d’une lésion oxydative sur des matrices nucléosomales." Lyon, École normale supérieure (sciences), 2008. http://www.theses.fr/2008ENSL0487.

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Les bases de l'ADN, support du patrimoine génétique de tout être vivant, peuvent à tout moment subir des oxydations. La principale lésion oxydative, la 8-oxoG, doit être retirée du génome par la voie d'excision de base pour contrer ses effets mutagéniques. La glycolase OGG1 qui initie la réparation de cette lésion chez les eucaryotes doit agir dans un contexte chromatinien. Le premier niveau d'organisation de cette stucture complexe de l'ADN peut inhiber ou rester transparente suivant les processus mis en jeu. Nous montrons que la réparation par excision de base d'une 8-oxoG est fortement inhi

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25

Oka, Hayato. "DNA damage response protein ASCIZ links base excision repair with immunoglobulin gene conversion." Kyoto University, 2010. http://hdl.handle.net/2433/120923.

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26

Yoshimura, Michio. "Vertebrate POLQ and POLβ cooperate in base excision repair of oxidative DNA damage". Kyoto University, 2007. http://hdl.handle.net/2433/135652.

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27

Neishabury, Maryam. "Contributions of nucleotide and base excision repair to the repair of DNA oxidative base damage in Saccharomyces cerevisiae." Thesis, Swansea University, 1998. https://cronfa.swan.ac.uk/Record/cronfa42904.

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In order to further investigate the contribution of NER to the repair of oxidative base lesions in <I>Saccharomyces cerevisiae</I>, a series of mutant strains were constructed that were deficient in NER, or in both NER and BER by disruption of the <I>RAD14</I> gene via transformation in the wile type and <I>OGG1 </I>deficient strains respectively. In addition, another set of mutants was created by transforming the cells with a high copy number plasmid that over-expresses the <I>OGG1</I> gene. The frequency of spontaneous forward mutation to canavanine resistance (Can<SUP>R</SUP>) was determine

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28

Hanssen-Bauer, Audun. "X-ray repair cross-complementing protein 1 associated multiprotein complexes in base excision repair." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for kreftforskning og molekylær medisin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-16986.

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XRCC1 assoierte multiproteinkomplekser i base eksisjonsreparasjon Arvestoffet (DNA) degraderes konstant av ytre faktorer, som stråling og kjemikalier, og indre faktorer, som produkter av metabolismen. Slik degradering ødelegger informasjonen som ligger i DNA, og kan derfor være toksisk for cellene og mutagent under replikasjon. Sannsynligheten for mutasjon er likevel ekstremt lav fordi DNAets integritet opprettholdes ved en lang rekke reparasjonsmekanismer. Disse involverer mange enzymer, struktur- og regulatoriske proteiner, med overlappende roller. Feil eller mangelfull reparasjon er drivkr

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29

Guo, Yin. "Biochemical Characterization of DNA Glycosylases from Mycobacterium Tuberculosis." ScholarWorks @ UVM, 2010. http://scholarworks.uvm.edu/graddis/96.

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The DNA glycosylases function in the first step of the base excision repair (BER) process, that is responsible for removing base lesions resulting from oxidation, alkylation or deamination. The DNA glycosylases that recognize oxidative base damage fall into two general families: the Fpg/Nei family and the Nth superfamily. Based on protein sequence alignments, we identified four putative Fpg/Nei family members as well as a putative Nth protein in Mycobacterium tuberculosis H37Rv, the causative agent of tuberculosis. While Fpg proteins are widely distributed among the bacteria and plants,

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30

Bennett, L. "Epigenetic mechanisms involved in the cellular response to DNA damage processed by Base Excision Repair." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3012159/.

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Chromatin remodelling is required for access to occluded sequences of DNA by proteins involved in important biological processes, including DNA replication and transcription. There is an increasing amount of evidence for chromatin remodelling during DNA repair, although this has been mostly focused towards DNA double strand break and nucleotide excision repair. At this time there is little evidence for chromatin remodelling in base excision repair (BER). BER is a highly conserved DNA repair pathway which processes spontaneous endogenous DNA base damages generated by oxidative metabolism, but a

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31

Mayhead, Natalie. "Modulation of the base excision repair (BER) pathway in the treatment of glioblastoma with radiotherapy." Thesis, University of Surrey, 2018. http://epubs.surrey.ac.uk/849272/.

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Glioblastoma is an aggressive brain cancer with a median survival rate of 14.6 months post diagnosis. Treatments for glioblastoma include surgery, radiotherapy, and chemotherapy with the alkylating agent temozolomide (TMZ). In 50% of patients, TMZ treatment is ineffective due to the reparative action of the protein O6- MeG DNA methyltransferase (MGMT). The base excision repair (BER) pathway repairs the most common lesions caused by TMZ. This work reports the characterization of several glioblastoma cell lines in terms of their repair status and sensitivity to traditional therapy of X-ray irrad

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32

Mavajian, Zahra. "Investigation of DNA Base Excision Repair in MTH1 Depleted T-cell Acute Lymphoblastic Leukemia cells." Thesis, KTH, Skolan för kemi, bioteknologi och hälsa (CBH), 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-230172.

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Genomic alterations may initiate cancer development as the consequence of endogenous or exogenous DNA damaging factors. Defects in DNA repair mechanisms may also facilitate cancer progression as well as accumulation of mutations which favor cancer cell survival. However, DNA repair pathways in cancer cells can be considered as their Achilles heel which are possible targets in order to compromise their survival. For instance, it has been demonstrated recently that inhibition of a protein called MTH1 via RNA interference (RNAi) or chemical inhibitors can stop tumor growth and triggers cell death

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33

Burgess, Heather Elizabeth. "Epigenetic and transcriptional regulation by the base excision repair protein thymine DNA glycosylase during development." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708334.

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34

Grippon, Ayse Seden. "Protein complexes in base excision repair : biochemical and kinetic analysis of mismatch uracil DNA glycosylase." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/5666.

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Mismatch uracil DNA glycosylase (MUG) is an E. coli enzyme involved in the repair of ethenocytosine and uracil through the base excision repair pathway. MUG is known to bind the abasic site tightly. This may act to protect the abasic lesion, but the question then is how is the site handed over to the AP Endonuclease? Much has been made of the increase in turnover of some DNA glycosylases by AP endonucleases, but it is not clear whether this occurs via an active displacement mechanism or by passive diffusion. We are addressing these questions by studying the kinetics of MUG interactions with it

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35

Faria, Caio Matheus Prates Batalha. "Estudo do papel de mTOR na regulação da atividade de reparo do DNA mitocondrial humano." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-08052018-151734/.

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mTOR (mammalian target of rapamycin) é uma proteína com papel central no crescimento, na proliferação e na manutenção das células, que participa da formação de dois complexos, mTORC1 e mTORC2. Diversos estudos associam menor atividade de mTOR, em especial o complexo 1, com efeitos protetores contra o envelhecimento e mesmo aumento da expectativa de vida máxima. Alterações no DNA têm sido propostas desde cedo na história dos estudos bioquímicos sobre o envelhecimento como um fator causar da perda de função dos organismos com a idade. Muitos estudos já foram realizados tentando analisar diversos

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36

Pereira, Carolina Parga Martins. "Estudo das atividades de reparo de DNA por excisão de bases em extratos mitocondriais de cérebros de indivíduos normais e acometidos pela doença de Alzheimer." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-30092014-084746/.

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O envelhecimento da população mundial no último século elevou significativamente o número de casos da doença de Alzheimer (DA), bem como os custos para os sistemas de saúde pública. Apesar de avanços significativos no entendimento da fisiopatologia da doença, pouco se sabe a respeito dos mecanismos moleculares que desencadeiam a perda de memória e a morte neuronal. Resultados recentes sugerem que o acúmulo de bases oxidadas no DNA mitocondrial e alterações nas vias que removem essas lesões desempenham um papel importante na morte neuronal observada em DA. A maioria das lesões em DNA induzidas

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37

Lia, Debora. "Role of alphaOGG1 in the Maintenance of Mitochondrial Physiology." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS125/document.

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Les mitochondries sont des structures uniques dans la cellule mammifère. Ces organites portent leur propre génome (ADN mitochondrial, ADNmt) qui se compose d'une petite molécule qui codifie pour 13 polypeptides de la chaîne de transport d'électrons (ETC), 22 ARNt et 2 gènes d'ARNr pour sa propre synthèse protéique. Le MTDNA est proposé pour être plus susceptible au stress oxydatif que le génome nucléaire (ADNn) parce que non seulement il manque d'histones protectrices, mais aussi en raison de sa proximité avec les complexes ETC qui sont les principaux producteurs de ROS dans les cellules de ma

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38

Bulgar, Alina D. "New Insights into Molecular Mechanisms of Fludarabine." Cleveland State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1228966107.

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39

Steenkamp, Anzaan. "Establishing the comet assay to determine the effects of different perturbations on DNA repair capacity / by Anzaan Steenkamp." Thesis, North-West University, 2011. http://hdl.handle.net/10394/4628.

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Single cell gel electrophoresis (SCGE), more commonly known as the Comet assay, is an uncomplicated, affordable and versatile method for investigating DNA damage and repair. Existing comet–assay based methods were modified and applied in this study in order to examine the effects of different perturbations on the DNA repair capacity of different samples. Mitochondrial functioning has a vast effect on overall cell physiology and does not simply involve the production of energy in the form of ATP that sustains common biological processes, but is also associated with important cellular occurrence

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40

Wang, Yan. "Effects of glucocorticoid receptor binding on base excision repair at deoxyuridine in the glucocorticoid response element." Online access for everyone, 2006. http://www.dissertations.wsu.edu/Thesis/Summer2006/y%5Fwang%5F072106.pdf.

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41

Kartalou, Maria 1972. "The role of base excision repair proteins in the cellular responses to the anticancer drug cisplatin." Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/73346.

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42

Sawant, Akshada S. "The Role of Base Excision Repair and Mismatch Repair Proteins in the Processing of Cisplatin Interstrand Cross-Links." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1404407224.

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43

Guo, Chunguang. "Ugene, a Newly Identified Protein that is Commonly Over-Expressed in Cancer, and that Binds to Uracil DNA-Glycosylase." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1217422102.

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44

Stevens, Rachel L. "Characterization of Novel Extracellular and Intracellular Modifiers of Apurinic/Apyrimidinic Endonuclease 1." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1275417842.

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45

Zhou, Jia. "Dna Glycosylases Remove Oxidized Base Damages From G-Quadruplex Dna Structures." ScholarWorks @ UVM, 2015. http://scholarworks.uvm.edu/graddis/529.

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The G-quadruplex DNA is a four-stranded DNA structure that is highly susceptible to oxidation due to its G-rich sequence and its structure. Oxidative DNA base damages can be mutagenic or lethal to cells if they are left unrepaired. The base excision repair (BER) pathway is the predominant pathway for repair of oxidized DNA bases. DNA glycosylases are the first enzymes in BER and are responsible for removing base lesions from DNA. How DNA glycosylases remove base lesions from duplex and single-stranded DNA has been intensively studied, while how they act on G-quadruplex DNA remains to be explor

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46

Boesch, Pierre. "Caractérisation d'un mécanisme de réparation de l'ADN par excision de base dans les mitochondries des cellules végétales." Université Louis Pasteur (Strasbourg) (1971-2008), 2005. http://www.theses.fr/2005STR13181.

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Les mitochondries de plantes possèdent leur propre ADN (mtDNA) et sont une source majeur de production d’espèces réactives de l’oxigène. De part leur grande proximité avec la chaîne de transport d’électrons l’ADNmt a de grande chance d’être oxidé. La 8-oxo-guanine (8oxoG) et l’uracile sont les lésions oxidatives les plus étudiées et sont réparées par le voie de réparation par excision de base (BER). Cette voie est le seul mécanisme de réparation de l’ADN retrouvée avec certitude dans les mitochondries. La réparation de l’ADN dans les mitochondries des plantes n’ayant pas encore été étudiée not

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47

Górniak, Joanna Paulina. "Age-related epigenetic changes at base excision repair genes and their modulation by dietary restriction in mice." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2932.

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Accumulation of damage in DNA is a characteristic feature of ageing which may result from a decline in DNA repair efficiency. Base excision repair (BER) is the primary mechanism used to repair small-scale DNA damage such as that caused by oxidation. I hypothesised that epigenetic events contribute to the ageing process through deregulation of BER gene expression and that these adverse effects of ageing may be modulated by dietary restriction (DR). To test these hypotheses, I quantified DNA methylation and histone post-translational modifications at BER-gene (Ogg1 and Apex) promoters, together

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48

Charles, Richard John Lalith. "FACT, réparation par excision de bases et fixation du facteur de transcription NF-kB sur la chromatine." Thesis, Grenoble, 2012. http://www.theses.fr/2012GRENV034/document.

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Abstract:

FACT est une protéine clé, qui joue de multiples rôles, y compris dans la transcription et la réparation de l'ADN endommagé. Néanmoins, comment FACT participe à la réparation et à la transcription de la chromatine n'est pas élucidé. Dans ce travail nous avons tout d'abord étudié le rôle de FACT dans le processus de réparation par excision de base (BER). Nous avons utilisé des nucléosomes reconstitués avec de l'ADN à uracile incorporé au hasard. Nous avons trouvé que l'enzyme UDG est capable d'enlever les uraciles localisés du côté de la solution et pas les uraciles se trouvant en face de l'oct

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49

Dangeti, Venkata Srinivas Mohan Nimai. "Processing of Cisplatin Interstrand crosslinks (ICLs) by DNA repair proteins." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1352833172.

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50

Budworth, Helen Louise. "Role of Base and nucleotide excision repair pathways in processing of clustered DNA lesions induced by ionising radiation." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:357d0c93-77bf-4097-85a7-05fa0dca740a.

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Abstract:

Ionising radiation (IR) induces a wide spectrum of lesions in DNA, including double- and single-strand breaks, abasic (AP) sites and a variety of base lesions. IR-induced damage to DNA can range from simple, isolated lesions to clustered DNA damage in which multiple lesions are formed, usually within a single helical turn of the DNA. Individual lesions within a cluster are recognised by repair enzymes of the base excision repair (BER) pathway, however, clustered DNA damage may be recognised as a bulky lesion and be processed by nucleotide excision repair (NER). Additionally, the presence of ot

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