Relevant bibliographies by topics / Genome damage

Academic literature on the topic 'Genome damage'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Genome damage"

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Proshkina, Ekaterina, Mikhail Shaposhnikov, and Alexey Moskalev. "Genome-Protecting Compounds as Potential Geroprotectors." International Journal of Molecular Sciences 21, no. 12 (June 24, 2020): 4484. http://dx.doi.org/10.3390/ijms21124484.

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Throughout life, organisms are exposed to various exogenous and endogenous factors that cause DNA damages and somatic mutations provoking genomic instability. At a young age, compensatory mechanisms of genome protection are activated to prevent phenotypic and functional changes. However, the increasing stress and age-related deterioration in the functioning of these mechanisms result in damage accumulation, overcoming the functional threshold. This leads to aging and the development of age-related diseases. There are several ways to counteract these changes: (1) prevention of DNA damage through stimulation of antioxidant and detoxification systems, as well as transition metal chelation; (2) regulation of DNA methylation, chromatin structure, non-coding RNA activity and prevention of nuclear architecture alterations; (3) improving DNA damage response and repair; (4) selective removal of damaged non-functional and senescent cells. In the article, we have reviewed data about the effects of various trace elements, vitamins, polyphenols, terpenes, and other phytochemicals, as well as a number of synthetic pharmacological substances in these ways. Most of the compounds demonstrate the geroprotective potential and increase the lifespan in model organisms. However, their genome-protecting effects are non-selective and often are conditioned by hormesis. Consequently, the development of selective drugs targeting genome protection is an advanced direction.
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Henkel, Ralf R., and Daniel R. Franken. "Sperm DNA Fragmentation: Origin and Impact on Human Reproduction." Journal of Reproductive and Stem Cell Biotechnology 2, no. 2 (December 2011): 88–108. http://dx.doi.org/10.1177/205891581100200204.

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Sperm DNA can be damaged due to a multitude of different noxae, which include disease, and occupational and environmental factors. Depending on the magnitude of the damage, such lesions may be repaired by the oocyte or the embryo. If this is not possible, a permanent damage can be manifested leading to mutations of the male genome. In cases where the oocyte or the embryo does not counter these damages to the male genome in terms of repair or an early abortion, sperm DNA damage and fragmentation can be a cause of numerous diseases including childhood cancer.
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LIU, Wei-Feng, Shan-Shan YU, Guan-Jun CHEN, and Yue-Zhong LI. "DNA Damage Checkpoint, Damage Repair, and Genome Stability." Acta Genetica Sinica 33, no. 5 (May 2006): 381–90. http://dx.doi.org/10.1016/s0379-4172(06)60064-4.

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Alhegaili, Alaa S., Yunhee Ji, Nicolas Sylvius, Matthew J. Blades, Mahsa Karbaschi, Helen G. Tempest, George D. D. Jones, and Marcus S. Cooke. "Genome-Wide Adductomics Analysis Reveals Heterogeneity in the Induction and Loss of Cyclobutane Thymine Dimers across Both the Nuclear and Mitochondrial Genomes." International Journal of Molecular Sciences 20, no. 20 (October 15, 2019): 5112. http://dx.doi.org/10.3390/ijms20205112.

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The distribution of DNA damage and repair is considered to occur heterogeneously across the genome. However, commonly available techniques, such as the alkaline comet assay or HPLC-MS/MS, measure global genome levels of DNA damage, and do not reflect potentially significant events occurring at the gene/sequence-specific level, in the nuclear or mitochondrial genomes. We developed a method, which comprises a combination of Damaged DNA Immunoprecipitation and next generation sequencing (DDIP-seq), to assess the induction and repair of DNA damage induced by 0.1 J/cm2 solar-simulated radiation at the sequence-specific level, across both the entire nuclear and mitochondrial genomes. DDIP-seq generated a genome-wide, high-resolution map of cyclobutane thymine dimer (T<>T) location and intensity. In addition to being a straightforward approach, our results demonstrated a clear differential distribution of T<>T induction and loss, across both the nuclear and mitochondrial genomes. For nuclear DNA, this differential distribution existed at both the sequence and chromosome level. Levels of T<>T were much higher in the mitochondrial DNA, compared to nuclear DNA, and decreased with time, confirmed by qPCR, despite no reported mechanisms for their repair in this organelle. These data indicate the existence of regions of sensitivity and resistance to damage formation, together with regions that are fully repaired, and those for which > 90% of damage remains, after 24 h. This approach offers a simple, yet more detailed approach to studying cellular DNA damage and repair, which will aid our understanding of the link between DNA damage and disease.
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Ferrand, Juliette, Beatrice Rondinelli, and Sophie E. Polo. "Histone Variants: Guardians of Genome Integrity." Cells 9, no. 11 (November 5, 2020): 2424. http://dx.doi.org/10.3390/cells9112424.

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Chromatin integrity is key for cell homeostasis and for preventing pathological development. Alterations in core chromatin components, histone proteins, recently came into the spotlight through the discovery of their driving role in cancer. Building on these findings, in this review, we discuss how histone variants and their associated chaperones safeguard genome stability and protect against tumorigenesis. Accumulating evidence supports the contribution of histone variants and their chaperones to the maintenance of chromosomal integrity and to various steps of the DNA damage response, including damaged chromatin dynamics, DNA damage repair, and damage-dependent transcription regulation. We present our current knowledge on these topics and review recent advances in deciphering how alterations in histone variant sequence, expression, and deposition into chromatin fuel oncogenic transformation by impacting cell proliferation and cell fate transitions. We also highlight open questions and upcoming challenges in this rapidly growing field.
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Thomas, Mark, Gaetan Burgio, David J. Adams, and Vivek Iyer. "Collateral damage and CRISPR genome editing." PLOS Genetics 15, no. 3 (March 14, 2019): e1007994. http://dx.doi.org/10.1371/journal.pgen.1007994.

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Petruseva, I. O., A. N. Evdokimov, and O. I. Lavrik. "Molecular Mechanism of Global Genome Nucleotide Excision Repair." Acta Naturae 6, no. 1 (March 15, 2014): 23–34. http://dx.doi.org/10.32607/20758251-2014-6-1-23-34.

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Nucleotide excision repair (NER) is a multistep process that recognizes and eliminates a wide spectrum of damage causing significant distortions in the DNA structure, such as UV-induced damage and bulky chemical adducts. The consequences of defective NER are apparent in the clinical symptoms of individuals affected by three disorders associated with reduced NER capacities: xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). These disorders have in common increased sensitivity to UV irradiation, greatly elevated cancer incidence (XP), and multi-system immunological and neurological disorders. The eucaryotic NER system eliminates DNA damage by the excision of 24-32 nt single-strand oligonucleotides from a damaged strand, followed by restoration of an intact double helix by DNA repair synthesis and DNA ligation. About 30 core polypeptides are involved in the entire repair process. NER consists of two pathways distinct in initial damage sensor proteins: transcription-coupled repair (TC-NER) and global genome repair (GG-NER). The article reviews current knowledge on the molecular mechanisms underlying damage recognition and its elimination from mammalian DNA.
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Trakhtenberg, I. M., Y. I. Gubsky, E. L. Levitsky, and I. F. Belenichev. "Biochemical mechanisms of free-radical damage to the nuclear genome by cadmium." Ukrainian Biochemical Journal 90, no. 3 (June 25, 2018): 5–16. http://dx.doi.org/10.15407/ubj90.03.005.

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Collura, Ada, Joel Blaisonneau, Giuseppe Baldacci, and Stefania Francesconi. "The Fission Yeast Crb2/Chk1 Pathway Coordinates the DNA Damage and Spindle Checkpoint in Response to Replication Stress Induced by Topoisomerase I Inhibitor." Molecular and Cellular Biology 25, no. 17 (September 1, 2005): 7889–99. http://dx.doi.org/10.1128/mcb.25.17.7889-7899.2005.

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ABSTRACT Living organisms experience constant threats that challenge their genome stability. The DNA damage checkpoint pathway coordinates cell cycle progression with DNA repair when DNA is damaged, thus ensuring faithful transmission of the genome. The spindle assembly checkpoint inhibits chromosome segregation until all chromosomes are properly attached to the spindle, ensuring accurate partition of the genetic material. Both the DNA damage and spindle checkpoint pathways participate in genome integrity. However, no clear connection between these two pathways has been described. Here, we analyze mutants in the BRCT domains of fission yeast Crb2, which mediates Chk1 activation, and provide evidence for a novel function of the Chk1 pathway. When the Crb2 mutants experience damaged replication forks upon inhibition of the religation activity of topoisomerase I, the Chk1 DNA damage pathway induces sustained activation of the spindle checkpoint, which in turn delays metaphase-to-anaphase transition in a Mad2-dependent fashion. This new pathway enhances cell survival and genome stability when cells undergo replicative stress in the absence of a proficient G2/M DNA damage checkpoint.
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Hu, Jinchuan, Jason D. Lieb, Aziz Sancar, and Sheera Adar. "Cisplatin DNA damage and repair maps of the human genome at single-nucleotide resolution." Proceedings of the National Academy of Sciences 113, no. 41 (September 29, 2016): 11507–12. http://dx.doi.org/10.1073/pnas.1614430113.

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Cisplatin is a major anticancer drug that kills cancer cells by damaging their DNA. Cancer cells cope with the drug by removal of the damages with nucleotide excision repair. We have developed methods to measure cisplatin adduct formation and its repair at single-nucleotide resolution. “Damage-seq” relies on the replication-blocking properties of the bulky base lesions to precisely map their location. “XR-seq” independently maps the removal of these damages by capturing and sequencing the excised oligomer released during repair. The damage and repair maps we generated reveal that damage distribution is essentially uniform and is dictated mostly by the underlying sequence. In contrast, cisplatin repair is heterogeneous in the genome and is affected by multiple factors including transcription and chromatin states. Thus, the overall effect of damages in the genome is primarily driven not by damage formation but by the repair efficiency. The combination of the Damage-seq and XR-seq methods has the potential for developing novel cancer therapeutic strategies.
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Dissertations / Theses on the topic "Genome damage"

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Banerjee, Ujjwal Kumar. "3-D Genome organization of DNA damage repair." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ121.

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Notre génome est constamment attaqué par des facteurs endogènes et exogènes qui menacent son intégrité et conduisent à différents types de dommages. Les cassures double brins (CDBs) font partie des dommages les plus nuisibles car elles peuvent entraîner la perte d'information génétique, des translocations chromosomiques et la mort cellulaire. Tous les processus de réparation se déroulent dans le cadre d'une chromatine hautement organisée et compartimentée. Cette chromatine peut être divisée en un compartiment ouvert transcriptionnellement actif (euchromatine) et un compartiment compacté transcriptionnellement inactif (hétérochromatine). Ces différents degrés de compaction jouent un rôle dans la régulation de la réponse aux dommages à l’ADN. L'objectif de mon premier projet était de comprendre l'influence de l'organisation 3D du génome sur la réparation de l'ADN. Pour cela, j’ai utilisé deux approches complémentaires dans le but d’induire et de cartographier les CDBs dans le génome de souris. Mes résultats ont mis en évidence un enrichissement de γH2AX, facteur de réparation des dommages à l’ADN, sur différentes régions du génome de cellules souches embryonnaires de souris, et ont également montré que les dommages persistent dans l’hétérochromatine, contrairement à l’euchromatine qui est protégée des dommages. Pour mon deuxième projet, j'ai cartographié l'empreinte génomique de 53BP1, facteur impliqué dans la réparation des CDBs, dans des cellules U2OS asynchrones et des cellules bloquées en G1 afin d’identifier de nouveaux sites de liaison de 53BP1. Mes résultats ont permis d’identifier de nouveaux domaines de liaison de 53BP1 couvrant de larges régions du génome, et ont montré que ces domaines de liaison apparaissent dans des régions de réplication moyenne et tardive
Our 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
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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.

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DNA is a key molecular-target for the deleterious effects of ultraviolet radiation (UVR). Cells contain two types of DNA: nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) and UVR induces various types of damage in the both DNAs, notably CPDs and 8-oxodG. The aim of this thesis is to examine UVR induced DNA damage formation and repair in nDNA and mtDNA and to determine which is the most important genomic target with respect to cell killing in vitro using HaCaT calls as models of human skin. The cell viability data showed that UVB induces significant cell death, which increased over 48 h. SSR-exposure also showed significant levels of cell death after 24 h but with evidence of significant survival after 48 h. Alkaline modified comet assay data showed that CPDs and 8-oxodG were significantly produced in HaCaT cells exposed to UVB and SSR, with CPDs being formed in a greater yields and there being no significant repair of CPDs over 48 h post-exposure to UVB. However, HaCaT cells irradiated with SSR showed significant repair of both CPD and 8-oxodG over 48 h. QPCR data showed that UVB and SSR induced similar profiles of damage in both nDNA and mtDNA; despite the induced damage levels being higher with UVB. The data also showed that nDNA is the main target for UVR in HaCaT cells exposed to UVB and SSR. The UVB-induced QPCR-detectable DNA damage in nDNA and mtDNA was not fully repaired, with a significant level of DNA damage remaining at 48 h, however, there was significant repair of the induced-damage in nDNA post-exposure to SSR (correlating with survival/re-growth), whereas the damage to mtDNA was not fully repaired. The greater lethality of UVB is probably due to more the damage induced and poorer repair (notably of CPD) in nuclear DNA following UVB exposure. Whereas the proficient repair of SSR-induced CPD in nDNA probably dictates survival following SSR exposure – as there was still a notable level of residual damage in mtDNA post-SSR exposure. However, nDNA is the main target for UVR causing DNA damage and may lead to mutations, which increase the risk of skin cancer development.
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Manning, 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.

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Alpi, 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.

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Kasparek, 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.

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Chromosomal rearrangements can lead to loss of heterozygosity (LOH) and oncogene activation, both of which represent possible causative events in cancer development. Such outcomes can result from the misrepair of DNA damage arising from a variety of events including DNA double-strand breaks (DSBs), collapsed replication forks, and dysfunctional telomeres. In response to a DSB, chromosomal stability is principally maintained through the two major DNA repair pathways; non- homologous DNA end-joining (NHEJ) and homologous recombination (HR). The objective of this thesis was to identify novel factors functioning in prevention of chromosomal instability in response to a DSB in Schizosaccharomyces pombe. To achieve this, a central aim was to identify the genes mutated in a number of radiation-sensitive mutants in fission yeast, previously isolated by the laboratory. These include the ‘loh’ mutants loh-2, loh-5, loh-6 and loh-7, which were found to harbour mutations in known DNA repair genes rad3, rad17, and rad57. Further, a pan-genomic screen for novel HR repair factors was carried out. The Bioneer Version 2 deletion-library, consisting of 3308 haploid deletion strains, was screened for strains displaying hypersensitivity to the DNA damaging agents MMS, bleomycin and camptothecin. This screen yielded 209 hits which were further characterised, utilising a set of non-essential Ch16 minichromosomes . The minichromosome Ch16-LMYAU harbours an HO endonuclease recognition sequence and a centromere-distal ade6-M216 heteroallele. Following break-induction, failed repair of the DSB leads to loss of the ade6 allele, indicated by pink sectoring on low adenine plates. 39 sectoring hits were identified and further characterised to quantify levels of gene conversion via HR in response to a DSB, utilising Ch16-RMYAH. As a result of this study, a group of novel genes functioning in HR repair were identified. Finally, one of these hits, putative RNA metabolism protein Nrl1, was subjected to further characterisation, associating this protein with DNA damage repair for the first time. The work presented here, documents the approaches taken to successfully identify novel DNA repair factors in fission yeast.
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Durant, 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.

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Frigola, 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.

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The rate at which mutations accumulate along the genome is not uniform but influenced by factors such as chromatin compactness, replication time or transcription. Most of these factors create mutational biases that encompass large areas of the genomes, including several megabases. In recent years, though, local mutational asymmetries spanning just a few base pairs have also been identified. This thesis focuses on the study of two of these local mutational asymmetries. First, we describe a reduction in the number of exonic somatic mutations caused by DNA polymerase mismatches, which we attribute to a higher efficacy of the mismatch repair mechanism in these locations. Second we study the UV induced DNA damage formation and repair at transcription factor binding sites and assess the relative contribution of these two factors to the unexpected number of mutations of these areas across transcription factors families. The presence of these local mutation rate variations illustrates the difficulty of properly modeling the mutation rate, an important procedure in many cancer genomics and evolutionary studies.
La 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.
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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.

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Finneran, 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.

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Bhattacharjee, 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.

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Books on the topic "Genome damage"

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Aging of the genome: The dual role of the DNA in life and death. Oxford ; New York: Oxford University Press, 2007.

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Yosef, Shiloh, and SpringerLink (Online service), eds. The DNA Damage Response: Implications on Cancer Formation and Treatment. Dordrecht: Springer Netherlands, 2009.

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Genes and the environment. London: Taylor & Francis, 1999.

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Achary, V. Mohan Murali, Anca Macovei, Kaoru Okamoto Yoshiyama, and Ayako N. Sakamoto, eds. Maintenance of Genome Integrity: DNA Damage Sensing, Signaling, Repair and Replication in Plants. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-820-7.

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Vijg, Jan. Aging of the Genome: The Dual Role of DNA in Life and Death. Oxford University Press, USA, 2007.

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Vijg, Jan. Aging of the Genome: The Dual Role of DNA in Life and Death. Oxford University Press, USA, 2007.

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Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Pathophysiological changes of ageing and their relevance to anaesthesia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0002.

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The molecular basis of ageing is reviewed. This includes the concept of a summation of DNA damage over a lifetime causing genome instability. Epigenetic alterations, telomeric shortening, and the possibility of their modification are discussed. Oxidative and mitochondrial DNA damage and the resulting dysfunction leading to senescence are briefly described. Systemic problems and resultant behavioural adaptation may mask the decline in functional reserve and cause some of the difficulties in identifying its presence in ill elderly patients. Specific organ system changes are then described in some detail. These include the major concerns with the cardiovascular, respiratory, renal, hepatic, neurologic, endocrine, and musculoskeletal systems. The effect of ageing on the special senses of vision and hearing are covered, with emphasis on issues of informed consent.
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Clement, Jan, and Piet Maes. Hantaviral infections. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0188_update_001.

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Hantavirus disease is a viral zoonosis, caused by inhalation of infectious aerosolized excreta from chronically infected rodents, which are both the reservoir and the vector of different hantavirus species. Hantavirus infections manifest mainly as haemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, which traditionally but incorrectly were thought to be caused by exclusively Old World hantaviruses and New World hantaviruses, respectively.Hantavirus diseases are characterized by non-specific flu-like symptoms, followed by a sometimes lethal capillary leak syndrome, haemorrhage, and rarely by shock. Infection is accompanied by augmented release of pro-inflammatory cytokines which indirectly causes organ damage. Diagnosis can be made by serology or plaque reduction neutralization tests, detection of viral proteins by Western blot assay, or detection of hantavirus genome by reverse transcription-polymerase chain reaction. Treatment is mainly supportive.Together with leptospirosis, haemorrhagic fever with renal syndrome is the only form of acute kidney injury against which vaccines are in use, but a World Health Organization-licensed vaccine is still lacking.
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Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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Catherine, Rice-Evans, and Burdon R. H, eds. Free radical damage and its control. Amsterdam: Elsevier, 1994.

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Book chapters on the topic "Genome damage"

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Rasmussen, Lene Juel, and Keshav K. Singh. "Oxidative Damage and Repair in the Mitochondrial Genome." In Oxidative Damage to Nucleic Acids, 109–22. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72974-9_9.

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Evans, M. D., and M. S. Cooke. "Oxidative Damage to DNA in Non-Malignant Disease: Biomarker or Biohazard?" In Genome and Disease, 53–66. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000092500.

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Eppink, Berina, Jeroen Essers, and Roland Kanaar. "Interplay and Quality Control of DNA Damage Repair Mechanisms." In Genome Organization and Function in the Cell Nucleus, 395–415. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527639991.ch16.

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Richard, Derek J., and Kum Kum Khanna. "Single-Stranded DNA Binding Proteins Involved in Genome Maintenance." In The DNA Damage Response: Implications on Cancer Formation and Treatment, 349–66. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2561-6_16.

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Golato, T., and D. M. Wilson III. "Chapter 30. DNA Damage and the Maintenance of Nuclear Genome Integrity in Aging and Associated Phenotypes." In DNA Damage, DNA Repair and Disease, 388–425. Cambridge: Royal Society of Chemistry, 2020. http://dx.doi.org/10.1039/9781839162541-00388.

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Mao, Peng, and John J. Wyrick. "Genome-Wide Mapping of UV-Induced DNA Damage with CPD-Seq." In The Nucleus, 79–94. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0763-3_7.

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Mitra, J., H. Wang, M. Kodavati, S. Mitra, and M. L. Hegde. "Chapter 13. Emerging Roles of Non-canonical RNA Binding Proteins in the Repair of Genome Damage Linked to Human Pathologies." In DNA Damage, DNA Repair and Disease, 301–22. Cambridge: Royal Society of Chemistry, 2020. http://dx.doi.org/10.1039/9781839160769-00301.

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Sakai, Wataru, and Kaoru Sugasawa. "DNA Damage Recognition and Repair in Mammalian Global Genome Nucleotide Excision Repair." In DNA Replication, Recombination, and Repair, 155–74. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55873-6_7.

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Rechkunova, N. I., and O. I. Lavrik. "Nucleotide Excision Repair in Higher Eukaryotes: Mechanism of Primary Damage Recognition in Global Genome Repair." In Subcellular Biochemistry, 251–77. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3471-7_13.

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Ravi, Dashnamoorthy, and Alexander James Roy Bishop. "Identification of Genes Required for Damage Survival Using a Cell-Based RNAi Screen Against the Drosophila Genome." In Methods in Molecular Biology, 9–26. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-998-3_2.

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Conference papers on the topic "Genome damage"

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"Lesion recognition and cleavage of damage-containing G-quadruplexes by DNA glycosylases." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-357.

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"DNA damage to nervous tissue due to lead intoxication combined with glucose loading." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-338.

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Green, Abby M., Sebastien Landry, James P. Evans, Sophia Shalhout, Ashok S. Bhagwat, and Matthew D. Weitzman. "Abstract 3016: APOBEC3 enzymes induce damage to the cellular genome during DNA replication." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3016.

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Gilbertson, Matthew, Radhika Patel, Karin C. Nitiss, and John L. Nitiss. "Abstract 3580: Topoisomerase II mediated DNA damage generates unique classes of genome rearrangements." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3580.

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Weaver, Alice N., Tiffiny S. Cooper, Hoa Q. Trummell, James A. Bonner, Eben L. Rosenthal, and Eddy S. Yang. "Abstract A1-63: Characterizing the DNA damage repair defect in HPV-positive oropharyngeal squamous cell carcinoma." In Abstracts: AACR Special Conference: Translation of the Cancer Genome; February 7-9, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.transcagen-a1-63.

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Alhegaili, Alaa, George D. Jones, and Marcus S. Cooke. "Abstract LB-163: Genome-wide analysis of DNA damage and repair reveals differential sites and rates of repair, together with differential sensitivities to damage." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-163.

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Lu, Wei-ting, Lykourgos-Panagiotis Zalmas, Thomas Webber, Nnennaya Kanu, and Charles Swanton. "Abstract 2567: TRACERx: Intra-tumor subclonal driver mutation results in defective DNA damage response (DDR) and genome instability." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2567.

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Lu, Wei-ting, Lykourgos-Panagiotis Zalmas, Thomas Webber, Nnennaya Kanu, and Charles Swanton. "Abstract 2567: TRACERx: Intra-tumor subclonal driver mutation results in defective DNA damage response (DDR) and genome instability." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2567.

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Gout, J., L. Perkhofer, M. Morawe, F. Arnold, E. Roger, M. Müller, T. Seufferlein, Frappart PO, and A. Kleger. "PARP inhibitor resistance induces massive genome alterations responsible of the acquisition of multidrug resistance in DNA damage repair-deficient pancreatic cancer." In DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716148.

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Daly, G., C. M. Francis, V. M. Pastukh, D. Absher, R. J. Langley, and M. N. Gillespie. "Rapid Redistribution of Oxidative Base Damage in DNA Regulatory Sequences Accompanies Transcriptional Modulation by Hypoxia in the Human Endothelial Cell Genome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4191.

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Reports on the topic "Genome damage"

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Dynan, William S. Links between persistent DNA damage, genome instability, and aging. Office of Scientific and Technical Information (OSTI), November 2016. http://dx.doi.org/10.2172/1332061.

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Stewart, Robert D. Kinetic Modeling of Damage Repair, Genome Instability, and Neoplastic Transformation. Office of Scientific and Technical Information (OSTI), March 2007. http://dx.doi.org/10.2172/900981.

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Dynan, William S. Final report- Links between persistent DNA damage, genome instability, and aging. Office of Scientific and Technical Information (OSTI), November 2016. http://dx.doi.org/10.2172/1333814.

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Mordes, Daniel, Heather L. Ball, Mark Ehrhardt, Daniel Mordes, and David Cortez. Maintenance of Genome Stability and Breast Cancer: Molecular Analysis of DNA Damage-Activated Kinases. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada494969.

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Ball, Heather L., Mark Ehrhardt, Daniel Mordes, and David Cortez. Maintenance of Genome Stability and Breast Cancer: Molecular Analysis of DNA Damage-Activated Kinases. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada470345.

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Abagyan, Ruben, and Jianghong An. Genome-Wide Identification and 3D Modeling of Proteins involved in DNA Damage Recognition and Repair (Final Report). Office of Scientific and Technical Information (OSTI), August 2005. http://dx.doi.org/10.2172/893896.

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Ruben A. Abagyan, PhD. Genome-Wide Identification and 3D Modeling of Proteins involved in DNA Damage Recognition and Repair (Final Report). Office of Scientific and Technical Information (OSTI), April 2004. http://dx.doi.org/10.2172/823103.

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Green, Brian M. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-Replication. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436928.

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Green, Brian M., and Joachim J. Li. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-replication. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada467931.

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Green, Brian. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-replication. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada482750.

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