Relevant bibliographies by topics / DNA damage; Excision repair; Genome instability

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'DNA damage; Excision repair; Genome instability'

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

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'DNA damage; Excision repair; Genome instability.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "DNA damage; Excision repair; Genome instability"

1

Doudican, Nicole A., Binwei Song, Gerald S. Shadel, and Paul W. Doetsch. "Oxidative DNA Damage Causes Mitochondrial Genomic Instability in Saccharomyces cerevisiae." Molecular and Cellular Biology 25, no. 12 (2005): 5196–204. http://dx.doi.org/10.1128/mcb.25.12.5196-5204.2005.

Full text
Abstract:
ABSTRACT Mitochondria contain their own genome, the integrity of which is required for normal cellular energy metabolism. Reactive oxygen species (ROS) produced by normal mitochondrial respiration can damage cellular macromolecules, including mitochondrial DNA (mtDNA), and have been implicated in degenerative diseases, cancer, and aging. We developed strategies to elevate mitochondrial oxidative stress by exposure to antimycin and H2O2 or utilizing mutants lacking mitochondrial superoxide dismutase (sod2Δ). Experiments were conducted with strains compromised in mitochondrial base excision repa
APA, Harvard, Vancouver, ISO, and other styles
2

Tadokoro, Takashi, Mahesh Ramamoorthy, Venkateswarlu Popuri, et al. "Human RECQL5 participates in the removal of endogenous DNA damage." Molecular Biology of the Cell 23, no. 21 (2012): 4273–85. http://dx.doi.org/10.1091/mbc.e12-02-0110.

Full text
Abstract:
Human RECQL5 is a member of the RecQ helicase family, which maintains genome stability via participation in many DNA metabolic processes, including DNA repair. Human cells lacking RECQL5 display chromosomal instability. We find that cells depleted of RECQL5 are sensitive to oxidative stress, accumulate endogenous DNA damage, and increase the cellular poly(ADP-ribosyl)ate response. In contrast to the RECQ helicase family members WRN, BLM, and RECQL4, RECQL5 accumulates at laser-induced single-strand breaks in normal human cells. RECQL5 depletion affects the levels of PARP-1 and XRCC1, and our c
APA, Harvard, Vancouver, ISO, and other styles
3

Kraithong, Thanyalak, Silas Hartley, David Jeruzalmi, and Danaya Pakotiprapha. "A Peek Inside the Machines of Bacterial Nucleotide Excision Repair." International Journal of Molecular Sciences 22, no. 2 (2021): 952. http://dx.doi.org/10.3390/ijms22020952.

Full text
Abstract:
Double stranded DNA (dsDNA), the repository of genetic information in bacteria, archaea and eukaryotes, exhibits a surprising instability in the intracellular environment; this fragility is exacerbated by exogenous agents, such as ultraviolet radiation. To protect themselves against the severe consequences of DNA damage, cells have evolved at least six distinct DNA repair pathways. Here, we review recent key findings of studies aimed at understanding one of these pathways: bacterial nucleotide excision repair (NER). This pathway operates in two modes: a global genome repair (GGR) pathway and a
APA, Harvard, Vancouver, ISO, and other styles
4

Kang, Tae-Hong. "Circadian Rhythm of NER and ATR Pathways." Biomolecules 11, no. 5 (2021): 715. http://dx.doi.org/10.3390/biom11050715.

Full text
Abstract:
Genomic integrity is constantly insulted by solar ultraviolet (UV) radiation. Adaptative cellular mechanisms called DNA damage responses comprising DNA repair, cell cycle checkpoint, and apoptosis, are believed to be evolved to limit genomic instability according to the photoperiod during a day. As seen in many other key cellular metabolisms, genome surveillance mechanisms against genotoxic UV radiation are under the control of circadian clock systems, thereby exhibiting daily oscillations in their catalytic activities. Indeed, it has been demonstrated that nucleotide excision repair (NER), th
APA, Harvard, Vancouver, ISO, and other styles
5

Tummala, Hemanth, Arran D. Dokal, Amanda Walne, et al. "Genome instability is a consequence of transcription deficiency in patients with bone marrow failure harboring biallelic ERCC6L2 variants." Proceedings of the National Academy of Sciences 115, no. 30 (2018): 7777–82. http://dx.doi.org/10.1073/pnas.1803275115.

Full text
Abstract:
Biallelic variants in the ERCC excision repair 6 like 2 gene (ERCC6L2) are known to cause bone marrow failure (BMF) due to defects in DNA repair and mitochondrial function. Here, we report on eight cases of BMF from five families harboring biallelic variants in ERCC6L2, two of whom present with myelodysplasia. We confirm that ERCC6L2 patients’ lymphoblastoid cell lines (LCLs) are hypersensitive to DNA-damaging agents that specifically activate the transcription coupled nucleotide excision repair (TCNER) pathway. Interestingly, patients’ LCLs are also hypersensitive to transcription inhibitors
APA, Harvard, Vancouver, ISO, and other styles
6

Savina, Nataliya V., Nataliya V. Nikitchenko, Tatyana D. Kuzhir, Alexander I. Rolevich, Sergei A. Krasny, and Roza I. Goncharova. "The Cellular Response to Oxidatively Induced DNA Damage and Polymorphism of Some DNA Repair Genes Associated with Clinicopathological Features of Bladder Cancer." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/5710403.

Full text
Abstract:
Genome instability and impaired DNA repair are hallmarks of carcinogenesis. The study was aimed at evaluating the DNA damage response in H2O2-treated lymphocytes using the alkaline comet assay in bladder cancer (BC) patients as compared to clinically healthy controls, elderly persons, and individuals with chronic inflammations. Polymorphism in DNA repair genes involved in nucleotide excision repair (NER) and base excision repair (BER) was studied using the PCR-RFLP method in the Belarusian population to elucidate the possible association of their variations with both bladder cancer risk and cl
APA, Harvard, Vancouver, ISO, and other styles
7

Zhao, Shengyuan, Megha Thakur, Alex W. Klattenhoff, and Dawit Kidane. "Aberrant DNA Polymerase Beta Enhances H. pylori Infection Induced Genomic Instability and Gastric Carcinogenesis in Mice." Cancers 11, no. 6 (2019): 843. http://dx.doi.org/10.3390/cancers11060843.

Full text
Abstract:
H. pylori is a significant risk factor of gastric cancer that induces chronic inflammation and oxidative DNA damage to promote gastric carcinoma. Base excision repair (BER) is required to maintain the genome integrity and prevent oxidative DNA damage. Mutation in DNA polymerase beta (Pol β) impacts BER efficiency and has been reported in approximately 30–40% of gastric carcinoma tumors. In this study, we examined whether reduced BER capacity associated with mutation in the POLB gene, along with increased DNA damage generated by H. pylori infection, accelerates gastric cancer development. By in
APA, Harvard, Vancouver, ISO, and other styles
8

Fanale, Daniele, Viviana Bazan, Stefano Caruso, et al. "Hypoxia and Human Genome Stability: Downregulation of BRCA2 Expression in Breast Cancer Cell Lines." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/746858.

Full text
Abstract:
Previously, it has been reported that hypoxia causes increased mutagenesis and alteration in DNA repair mechanisms. In 2005, an interesting study showed that hypoxia-induced decreases in BRCA1 expression and the consequent suppression of homologous recombination may lead to genetic instability. However, nothing is yet known about the involvement of BRCA2 in hypoxic conditions in breast cancer. Initially, a cell proliferation assay allowed us to hypothesize that hypoxia could negatively regulate the breast cancer cell growth in short term in vitro studies. Subsequently, we analyzed gene express
APA, Harvard, Vancouver, ISO, and other styles
9

Lovejoy, Courtney A., Kimberli Lock, Ashwini Yenamandra, and David Cortez. "DDB1 Maintains Genome Integrity through Regulation of Cdt1." Molecular and Cellular Biology 26, no. 21 (2006): 7977–90. http://dx.doi.org/10.1128/mcb.00819-06.

Full text
Abstract:
ABSTRACT DDB1, a component of a Cul4A ubiquitin ligase complex, promotes nucleotide excision repair (NER) and regulates DNA replication. We have investigated the role of human DDB1 in maintaining genome stability. DDB1-depleted cells accumulate DNA double-strand breaks in widely dispersed regions throughout the genome and have activated ATM and ATR cell cycle checkpoints. Depletion of Cul4A yields similar phenotypes, indicating that an E3 ligase function of DDB1 is important for genome maintenance. In contrast, depletion of DDB2, XPA, or XPC does not cause activation of DNA damage checkpoints,
APA, Harvard, Vancouver, ISO, and other styles
10

Hyka-Nouspikel, Nevila, Kimon Lemonidis, Wei-Ting Lu, and Thierry Nouspikel. "Circulating human B lymphocytes are deficient in nucleotide excision repair and accumulate mutations upon proliferation." Blood 117, no. 23 (2011): 6277–86. http://dx.doi.org/10.1182/blood-2010-12-326637.

Full text
Abstract:
Abstract Faithful repair of DNA lesions is a crucial task that dividing cells must actively perform to maintain genome integrity. Strikingly, nucleotide excision repair (NER), the most versatile DNA repair system, is specifically down-regulated in terminally differentiated cells. This prompted us to examine whether NER attenuation might be a common feature of all G0-arrested cells, and in particular of those that retain the capacity to reenter cell cycle and might thus convert unrepaired DNA lesions into mutations, a prerequisite for malignant transformation. Here we report that quiescent prim
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "DNA damage; Excision repair; Genome instability"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Szalat, Raphaël. "Rôle des voies de réparation des dommages de l'ADN dans l'instabilité génomique observée au cours du myélome multiple." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCC094.

Full text
Abstract:
Le myélome multiple (MM) est une hémopathie maligne caractérisée par la prolifération clonale de plasmocytes. Le MM est cliniquement et moléculairement hétérogène et comprend différents sous-groupes avec des pronostics différents. Divers événements génomiques, notamment des translocations récurrentes impliquant le gène des immunoglobulines (Ig) avec différents partenaires, des anomalies chromosomiques et de nombreuses mutations contribuent à l'hétérogénéité de la maladie. Si les translocations impliquant le Ig gene sont supposées survenir durant la maturation des lymphocytes B, les mécanismes
APA, Harvard, Vancouver, ISO, and other styles
3

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

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
4

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

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
6

Humphryes, 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/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Meisenberg, 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.

Full text
Abstract:
Apurinic/apyrimidinic endonuclease 1 (APE1) is a key DNA repair factor involved in the DNA base excision repair (BER) pathway that is required for the maintenance of genome stability. In this pathway, APE1 cleaves DNA at an abasic site to generate a DNA single strand break, allowing for repair completion by a DNA polymerase and a DNA ligase. High levels of APE1 have been observed in multiple cancer types however it is not understood if this contributes to cancer onset and development. What is known is that these cancers tend to display increased resistance to DNA damaging treatments and APE1 i
APA, Harvard, Vancouver, ISO, and other styles
8

Damasceno, 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/.

Full text
Abstract:
A estabilidade genômica é condição essencial à sobrevivência e ao funcionamento dos organismos vivos. No entanto, várias situações podem provocar danos no DNA. Por exemplo, cerca de 104 lesões podem ocorrer no material genético de uma célula de mamífero a cada dia. No intuito de preservar a integridade genômica e contornar os efeitos deletérios destas modificações, uma maquinaria constituída de proteínas especializadas em reconhecer e reparar estes danos foi selecionada ao longo do curso evolutivo. Defeitos em proteínas destas maquinarias causam instabilidade genômica e pode resultar em elevad
APA, Harvard, Vancouver, ISO, and other styles
9

Thakur, Roshan Singh. "Role of Mycobacterium Tuberculosis RecG Helicase in DNA Repair, Recombination and in Remodelling of Stalled Replication Forks." Thesis, 2015. http://etd.iisc.ernet.in/2005/3535.

Full text
Abstract:
Tuberculosis, caused by the infection with Mycobacterium tuberculosis remained as a major global health challenge with one third of world population being infected by this pathogen. M. tuberculosis can persist for decades in infected individuals in the latent state as an asymptomatic disease and can emerge to cause active disease at a later stage. Thus, pathways and the mechanisms that are involved in the maintenance of genome integrity appear to be important for M. tuberculosis survival, persistence and pathogenesis. Helicases are ubiquitous enzymes known to play a key role in DNA replicatio
APA, Harvard, Vancouver, ISO, and other styles
10

Ayyar, Sandeep. "The Molecular Mechanism of Break Induced Replication." 2013. http://hdl.handle.net/1805/3225.

Full text
Abstract:
Indiana University-Purdue University Indianapolis (IUPUI)<br>DNA double strand break (DSB) is one of the most threatening of all types of DNA damages as it leads to a complete breakage of the chromosome. The cell has evolved several mechanisms to repair DSBs, one of which is break-induced replication (BIR). BIR repair of DSBs occurs through invasion of one end of the broken chromosome into a homologous template followed by processive replication of DNA from the donor molecule. BIR is a key cellular process and is implicated in the restart of collapsed replication forks and several chromosomal
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "DNA damage; Excision repair; Genome instability"

1

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sugasawa, Kaoru. "DNA Damage Recognition for Mammalian Global Genome Nucleotide Excision Repair." In DNA Repair. InTech, 2011. http://dx.doi.org/10.5772/23254.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wang, H., M. Lu, B. Dever, S. Shen, and X. C. Le. "DNA Damage, Repair, and Genome Instability (Including Affinity Techniques)." In Comprehensive Sampling and Sample Preparation. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-381373-2.00079-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Aqeel, Amna, Javaria Zafar, Naureen Ehsan, Qurat-Ul-Ain, Mahnoor Tariq, and Abdul Hannan. "Interstrand Crosslink Repair: New Horizons of DNA Damage Repair." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97551.

Full text
Abstract:
Since the dawn of civilization, living organisms are unceasingly exposed to myriads of DNA damaging agents that can temper the ailments and negatively influence the well-being. DNA interstrand crosslinks (ICLs) are spawned by various endogenous and chemotherapeutic agents, thus posing a somber menace to genome solidity and cell endurance. However, the robust techniques of damage repair including Fanconi anemia pathway, translesion synthesis, nucleotide excision and homologous recombination repair faithfully protect the DNA by removing or tolerating damage to ensure the overall survival. Aberrations in such repair mechanisms adverse the pathophysiological states of several hereditary disorders i.e. Fanconi Anemia, xeroderma pigmentosum, cerebro-oculo-facio-skeletal syndrome and cockayne syndrome etc. Although, the recognition of ICL lesions during interphase have opened the new horizons of research in the field of genetics but still the detailed analysis of conditions in which repair should occur is largely elusive.
APA, Harvard, Vancouver, ISO, and other styles
5

Goodenow, Donna, Kiran Lalwani, and Christine Richardson. "DNA Damage and Repair Mechanisms Triggered by Exposure to Bioflavonoids and Natural Compounds." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95453.

Full text
Abstract:
Eukaryotic cells use homologous recombination (HR), classical end-joining (C-NHEJ), and alternative end-joining (Alt-EJ) to repair DNA double-strand breaks (DSBs). Repair pathway choice is controlled by the activation and activity of pathways specific proteins in eukaryotes. Activity may be regulated by cell cycle stage, tissue type, and differentiation status. Bioflavonoids and other environmental agents such as pesticides have been shown to biochemically act as inhibitors of topoisomerase II (Top2). In cells, bioflavonoids directly lead to DNA double-strand breaks through both Top2-dependent and independent mechanisms, as well as induce DNA damage response (DDR) signaling, and promote alternative end-joining and chromosome alterations. This chapter will present differences in expression and activity of proteins in major DNA repair pathways, findings of Top2 inhibition by bioflavonoids and cellular response, discuss how these compounds trigger alternative end-joining, and conclude with implications for genome instability and human disease.
APA, Harvard, Vancouver, ISO, and other styles
6

Glaire, Mark A., and David N. Church. "Genetics and genetic instability in cancer." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0004.

Full text
Abstract:
"The Integrity"of the human genome is under continual threat from endogenous and exogenous mutagens, and as a result of errors introduced during DNA replication. As the lesions generated by these processes, if left uncorrected, may lead to deleterious mutations, cells employ several sophisticated mechanisms to both prevent and repair such genomic damage. Failure of these repair mechanisms, leading to genomic instability, is common in cancer, and has even been suggested to be a universal characteristic of malignancy. This chapter outlines these cellular processes and reviews the both the mechanisms and consequences of their dysregulation in human cancer. It also highlights the emerging evidence suggesting that genomic instability is an important determinant of tumour behaviour. Finally, it discusses the possibility that targeting genomic instability may benefit patients with genomically unstable tumours in the clinic.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'DNA damage; Excision repair; Genome instability' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography