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

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Published: 4 June 2021

Last updated: 4 February 2022

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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.

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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

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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.

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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

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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.

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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

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

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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

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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.

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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

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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.

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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

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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.

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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

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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.

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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

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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.

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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,

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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.

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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

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Dutto, Ilaria, Claudia Scalera, Micol Tillhon, et al. "Mutations in CREBBP and EP300 genes affect DNA repair of oxidative damage in Rubinstein-Taybi syndrome cells." Carcinogenesis 41, no. 3 (2019): 257–66. http://dx.doi.org/10.1093/carcin/bgz149.

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Abstract Rubinstein-Taybi syndrome (RSTS) is an autosomal-dominant disorder characterized by intellectual disability, skeletal abnormalities, growth deficiency and an increased risk of tumors. RSTS is predominantly caused by mutations in CREBBP or EP300 genes encoding for CBP and p300 proteins, two lysine acetyl-transferases (KAT) playing a key role in transcription, cell proliferation and DNA repair. However, the efficiency of these processes in RSTS cells is still largely unknown. Here, we have investigated whether pathways involved in the maintenance of genome stability are affected in lymp

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Nieborowska-Skorska, Margaret, Artur Slupianek, Tomasz Stoklosa, Tomasz Poplawski, Kimberly Cramer, and Tomasz Skorski. "BCR/ABL Kinase Elevates ROS-Mediated Oxidative DNA Damage in CML Stem/Progenitor Cells and Affects the Efficiency and Fidelity of DNA Repair To Induce Genetic Instability." Blood 110, no. 11 (2007): 34. http://dx.doi.org/10.1182/blood.v110.11.34.34.

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Abstract BCR/ABL kinase transforms hematopoietic stem cells (HSCs) to induce chronic myelogenous leukemia in chronic phase (CML-CP), which eventually evolves into fatal blast crisis (CML-BC). CML is a stem cell-derived but a progenitor-driven disease. In CML-CP leukemia stem (LSCs) and progenitor (LPCs) cells reside in CD34+CD38− and CD34+CD38+ populations, respectively, whereas in CML-BC LSCs are found also in CD34+CD38+ population. BCR/ABL kinase stimulates genomic instability causing imatinib-resistant point mutations and chromosomal aberrations associated with progression to CML-BC. Genomi

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Tomanicek, Stephen J., Ronny C. Hughes, Joseph D. Ng, and Leighton Coates. "Structure of the endonuclease IV homologue fromThermotoga maritimain the presence of active-site divalent metal ions." Acta Crystallographica Section F Structural Biology and Crystallization Communications 66, no. 9 (2010): 1003–12. http://dx.doi.org/10.1107/s1744309110028575.

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The most frequent lesion in DNA is at apurinic/apyrimidinic (AP) sites resulting from DNA-base losses. These AP-site lesions can stall DNA replication and lead to genome instability if left unrepaired. The AP endonucleases are an important class of enzymes that are involved in the repair of AP-site intermediates during damage-general DNA base-excision repair pathways. These enzymes hydrolytically cleave the 5′-phosphodiester bond at an AP site to generate a free 3′-hydroxyl group and a 5′-terminal sugar phosphate using their AP nuclease activity. Specifically,Thermotoga maritimaendonuclease IV

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von Kobbe, Cayetano, Jeanine A. Harrigan, Alfred May, et al. "Central Role for the Werner Syndrome Protein/Poly(ADP-Ribose) Polymerase 1 Complex in the Poly(ADP-Ribosyl)ation Pathway after DNA Damage." Molecular and Cellular Biology 23, no. 23 (2003): 8601–13. http://dx.doi.org/10.1128/mcb.23.23.8601-8613.2003.

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ABSTRACT A defect in the Werner syndrome protein (WRN) leads to the premature aging disease Werner syndrome (WS). Hallmark features of cells derived from WS patients include genomic instability and hypersensitivity to certain DNA-damaging agents. WRN contains a highly conserved region, the RecQ conserved domain, that plays a central role in protein interactions. We searched for proteins that bound to this region, and the most prominent direct interaction was with poly(ADP-ribose) polymerase 1 (PARP-1), a nuclear enzyme that protects the genome by responding to DNA damage and facilitating DNA r

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Szalat, Raphael, Matija Dreze, Mehmet Kemal Samur, et al. "Nucleotide Excision Repair (NER) Is Frequently Impaired and Affects Outcome in Multiple Myeloma (MM)." Blood 124, no. 21 (2014): 2055. http://dx.doi.org/10.1182/blood.v124.21.2055.2055.

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Abstract Introduction Multiple Myeloma (MM) is a heterogeneous disease characterized by genomic instability and eventual poor outcome. Aberrations in DNA repair-related pathways have been considered to explain the instability. Nucleotide excision repair (NER) is an important pathway involved in the removal of bulky adducts and DNA crosslinks induced by various genotoxins. Little is known about the relationship between NER in MM biology and patient outcomes. Here we assess the role of NER in MM. Methods We evaluated NER efficiency in a panel of MM cell lines (n=18), with a functional assay base

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Lin, Yunfu, Mei Leng, Ma Wan, and John H. Wilson. "Convergent Transcription through a Long CAG Tract Destabilizes Repeats and Induces Apoptosis." Molecular and Cellular Biology 30, no. 18 (2010): 4435–51. http://dx.doi.org/10.1128/mcb.00332-10.

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ABSTRACT Short repetitive sequences are common in the human genome, and many fall within transcription units. We have previously shown that transcription through CAG repeat tracts destabilizes them in a way that depends on transcription-coupled nucleotide excision repair and mismatch repair. Recent observations that antisense transcription accompanies sense transcription in many human genes led us to test the effects of antisense transcription on triplet repeat instability in human cells. Here, we report that simultaneous sense and antisense transcription (convergent transcription) initiated f

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Chung, Tae-Hoon, Rafael Fonseca, and Wee-Joo Chng. "A Novel Measure of Chromosome Instability Is An Independent Prognostic Factor in Multiple Myeloma." Blood 118, no. 21 (2011): 1824. http://dx.doi.org/10.1182/blood.v118.21.1824.1824.

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Abstract Abstract 1824 Introduction. Chromosomal abnormalities are prevalent in multiple myeloma (MM) and have been useful in delineating disease subtypes and prognosis groups. Globally, a dichotomous developmental pathway based on ploidy status seems to exist. The accumulation of chromosomal abnormalities in MM often gives rise to complex copy number profiles which are difficult to be captured due to the limitations of karyotyping in a relatively non-proliferative tumor. It is therefore unclear if genomic complexity as a reflection of chromosomal instability (CIN) is of biological and clinica

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Szalat, Raphaël, Mehmet Kemal Samur, Alice Cleynen, et al. "Dysregulated Nucleotide Excision Repair (NER) Is a New Target in Multiple Myeloma." Blood 126, no. 23 (2015): 4187. http://dx.doi.org/10.1182/blood.v126.23.4187.4187.

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Abstract Nucleotide excision repair (NER) is involved in the removal of bulky adducts and DNA crosslinks induced by various genotoxins including alkylating agents. In cancer, somatic mutations, genes' up-regulation, and epigenetic silencing of NER may lead to abnormal DNA damage responses. Little is known about the role of NER in biology of multiple myeloma (MM), a heterogeneous disease characterized by genomic instability which is often treated by alkylating agents. In our genome sequencing data we did not observe recurrent mutation in NER although non silent mutations affected 13 genes invol

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Liao, Chengcheng, Srikanth Talluri, Subodh Kumar, et al. "Base Excision Repair and Homologous Recombination Pathway Intermediates Drive Genomic Instability and Evolution in Myeloma." Blood 136, Supplement 1 (2020): 27–28. http://dx.doi.org/10.1182/blood-2020-141042.

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Multiple myeloma (MM) cells demonstrate significant genomic instability with acquisition of new genomic events over time. In an effort to decipher the pathways utilized by MM cells to genomically evolve and to acquire proliferative advantage as well as develop drug resistance, we have investigated role of various pathway intermediates. Based on our prior results showing elevated homologous recombination (HR) contributing to genomic instability and development of drug resistance, we have further studied RAD51, the key HR gene. Also based on the dysfunctional base excision repair (BER) that can

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Kumar, Subodh, Leutz Buon, Srikanth Talluri, et al. "PDZ Binding Kinase (PBK) - a Novel Gene Driving Genomic Evolution in Multiple Myeloma." Blood 132, Supplement 1 (2018): 4474. http://dx.doi.org/10.1182/blood-2018-99-119186.

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Abstract As in all cancers, genomic instability leads to ongoing acquisition of new genetic changes in multiple myeloma (MM). This adaptability underlies the development of drug resistance and progression in MM. This genomic instability is driven by cellular processes, mainly related with DNA repair and perturbed by functional changes in limited number of genes. Since kinases play a critical role in the regulation of biological processes, including DNA damage/repair signaling and are relatively easy to screen for inhibitors, we investigated for novel genes involved in the acquisition of new ge

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Sunaga, Masanobu, Tsukasa Oda, Eiko Yamane та ін. "DNA Polymerases Pol θ/Pol η Involved in Error-Prone DNA Repair Are Highly Expressed in Multiple Myeloma and Upregulated By DNA Damage". Blood 134, Supplement_1 (2019): 4364. http://dx.doi.org/10.1182/blood-2019-125163.

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Background: DNA polymerases (DNA pols) are essential enzymes for DNA replication. In mammalian cells, DNA pols are divided into four families: A (Pol θ, Pol γ, and Pol ν), B (Pol α, Pol δ, Pol ε, and Pol ζ), X (Pol β, Pol λ, Pol μ, and TDT), and Y (Pol η, Pol ι, Pol κ, and REV1). These DNA pols are required for both genome duplication and protecting cells from DNA damage induced by endogenous and exogenous agents, such as ROS, UV, and chemotherapeutic drugs. For example, Pol β, Pol λ, and Pol ι participate in base excision repair. Contrastingly, Pol ζ, REV1, Pol η, Pol ι, and Pol κ can replica

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Karran, P., and M. Bignami. "DNA damage tolerance, mismatch repair and genome instability." BioEssays 16, no. 11 (1994): 833–39. http://dx.doi.org/10.1002/bies.950161110.

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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 (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 immunologica

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Bowater, Richard P., Rhona H. Borts, and Malcolm F. White. "DNA Damage: from Causes to Cures." Biochemical Society Transactions 37, no. 3 (2009): 479–81. http://dx.doi.org/10.1042/bst0370479.

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In order to maintain genome integrity, it is essential that any DNA damage is repaired. This is achieved in diverse ways in all cells to ensure cellular survival. There is a large repertoire of proteins that remove and repair DNA damage. However, sometimes these processes do not function correctly, leading to genome instability. Studies of DNA repair and genome instability and their causes and cures were showcased in the 2008 Biochemical Society Annual Symposium. The present article provides a summary of the talks given and the subsequent papers in this issue of Biochemical Society Transaction

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Duan, Mingrui, Jenna Ulibarri, Ke Jian Liu, and Peng Mao. "Role of Nucleotide Excision Repair in Cisplatin Resistance." International Journal of Molecular Sciences 21, no. 23 (2020): 9248. http://dx.doi.org/10.3390/ijms21239248.

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Cisplatin is a chemotherapeutic drug used for the treatment of a number of cancers. The efficacy of cisplatin relies on its binding to DNA and the induction of cytotoxic DNA damage to kill cancer cells. Cisplatin-based therapy is best known for curing testicular cancer; however, treatment of other solid tumors with cisplatin has not been as successful. Pre-clinical and clinical studies have revealed nucleotide excision repair (NER) as a major resistance mechanism against cisplatin in tumor cells. NER is a versatile DNA repair system targeting a wide range of helix-distorting DNA damage. The NE

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Kaplan, Alanna R., and Peter M. Glazer. "Impact of hypoxia on DNA repair and genome integrity." Mutagenesis 35, no. 1 (2019): 61–68. http://dx.doi.org/10.1093/mutage/gez019.

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Abstract Hypoxia is a hallmark of the tumour microenvironment with profound effects on tumour biology, influencing cancer progression, the development of metastasis and patient outcome. Hypoxia also contributes to genomic instability and mutation frequency by inhibiting DNA repair pathways. This review summarises the diverse mechanisms by which hypoxia affects DNA repair, including suppression of homology-directed repair, mismatch repair and base excision repair. We also discuss the effects of hypoxia mimetics and agents that induce hypoxia on DNA repair, and we highlight areas of potential cl

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Zhu, Chenxu, Lining Lu, Jun Zhang, et al. "Tautomerization-dependent recognition and excision of oxidation damage in base-excision DNA repair." Proceedings of the National Academy of Sciences 113, no. 28 (2016): 7792–97. http://dx.doi.org/10.1073/pnas.1604591113.

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NEIL1 (Nei-like 1) is a DNA repair glycosylase guarding the mammalian genome against oxidized DNA bases. As the first enzymes in the base-excision repair pathway, glycosylases must recognize the cognate substrates and catalyze their excision. Here we present crystal structures of human NEIL1 bound to a range of duplex DNA. Together with computational and biochemical analyses, our results suggest that NEIL1 promotes tautomerization of thymine glycol (Tg)—a preferred substrate—for optimal binding in its active site. Moreover, this tautomerization event also facilitates NEIL1-catalyzed Tg excisio

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Rastogi, Rajesh P., Richa, Ashok Kumar, Madhu B. Tyagi, and Rajeshwar P. Sinha. "Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair." Journal of Nucleic Acids 2010 (2010): 1–32. http://dx.doi.org/10.4061/2010/592980.

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DNA is one of the prime molecules, and its stability is of utmost importance for proper functioning and existence of all living systems. Genotoxic chemicals and radiations exert adverse effects on genome stability. Ultraviolet radiation (UVR) (mainly UV-B: 280–315 nm) is one of the powerful agents that can alter the normal state of life by inducing a variety of mutagenic and cytotoxic DNA lesions such as cyclobutane-pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar valence isomers as well as DNA strand breaks by interfering the genome integrity. To counteract these lesions,

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Jiang, Guochun, and Aziz Sancar. "Recruitment of DNA Damage Checkpoint Proteins to Damage in Transcribed and Nontranscribed Sequences." Molecular and Cellular Biology 26, no. 1 (2006): 39–49. http://dx.doi.org/10.1128/mcb.26.1.39-49.2006.

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ABSTRACT We developed a chromatin immunoprecipitation method for analyzing the binding of repair and checkpoint proteins to DNA base lesions in any region of the human genome. Using this method, we investigated the recruitment of DNA damage checkpoint proteins RPA, Rad9, and ATR to base damage induced by UV and acetoxyacetylaminofluorene in transcribed and nontranscribed regions in wild-type and excision repair-deficient human cells in G1 and S phases of the cell cycle. We find that all 3 damage sensors tested assemble at the site or in the vicinity of damage in the absence of DNA replication

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Vaughn, Courtney M., Christopher P. Selby, Yanyan Yang, David S. Hsu, and Aziz Sancar. "Genome-wide single-nucleotide resolution of oxaliplatin–DNA adduct repair in drug-sensitive and -resistant colorectal cancer cell lines." Journal of Biological Chemistry 295, no. 22 (2020): 7584–94. http://dx.doi.org/10.1074/jbc.ra120.013347.

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Platinum-based chemotherapies, including oxaliplatin, are a mainstay in the management of solid tumors and induce cell death by forming intrastrand dinucleotide DNA adducts. Despite their common use, they are highly toxic, and approximately half of cancer patients have tumors that are either intrinsically resistant or develop resistance. Previous studies suggest that this resistance is mediated by variations in DNA repair levels or net drug influx. Here, we aimed to better define the roles of nucleotide excision repair and DNA damage in platinum chemotherapy resistance by profiling DNA damage

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Terabayashi, Takeshi, and Katsuhiro Hanada. "Genome instability syndromes caused by impaired DNA repair and aberrant DNA damage responses." Cell Biology and Toxicology 34, no. 5 (2018): 337–50. http://dx.doi.org/10.1007/s10565-018-9429-x.

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Li, Chongping, and Joseph Tin Yum Wong. "DNA Damage Response Pathways in Dinoflagellates." Microorganisms 7, no. 7 (2019): 191. http://dx.doi.org/10.3390/microorganisms7070191.

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Dinoflagellates are a general group of phytoplankton, ubiquitous in aquatic environments. Most dinoflagellates are non-obligate autotrophs, subjected to potential physical and chemical DNA-damaging agents, including UV irradiation, in the euphotic zone. Delay of cell cycles by irradiation, as part of DNA damage responses (DDRs), could potentially lead to growth inhibition, contributing to major errors in the estimation of primary productivity and interpretations of photo-inhibition. Their liquid crystalline chromosomes (LCCs) have large amount of abnormal bases, restricted placement of coding

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Selby, Christopher P., Laura A. Lindsey-Boltz, Yanyan Yang, and Aziz Sancar. "Mycobacteria excise DNA damage in 12- or 13-nucleotide-long oligomers by prokaryotic-type dual incisions and performs transcription-coupled repair." Journal of Biological Chemistry 295, no. 50 (2020): 17374–80. http://dx.doi.org/10.1074/jbc.ac120.016325.

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In nucleotide excision repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genome by concerted dual incisions bracketing the lesion, followed by gap filling and ligation. So far, two dual-incision patterns have been discovered: the prokaryotic type, which removes the damage in 11–13-nucleotide-long oligomers, and the eukaryotic type, which removes the damage in 24–32-nucleotide-long oligomers. However, a recent study reported that the UvrC protein of Mycobacterium tuberculosis removes damage in a manner analogous to yeast and humans in a 25-mer oligo

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Adar, Sheera, Jinchuan Hu, Jason D. Lieb, and Aziz Sancar. "Genome-wide kinetics of DNA excision repair in relation to chromatin state and mutagenesis." Proceedings of the National Academy of Sciences 113, no. 15 (2016): E2124—E2133. http://dx.doi.org/10.1073/pnas.1603388113.

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We recently developed a high-resolution genome-wide assay for mapping DNA excision repair named eXcision Repair-sequencing (XR-seq) and have now used XR-seq to determine which regions of the genome are subject to repair very soon after UV exposure and which regions are repaired later. Over a time course, we measured repair of the UV-induced damage of cyclobutane pyrimidine dimers (CPDs) (at 1, 4, 8, 16, 24, and 48 h) and (6-4)pyrimidine-pyrimidone photoproducts [(6-4)PPs] (at 5 and 20 min and 1, 2, and 4 h) in normal human skin fibroblasts. Each type of damage has distinct repair kinetics. The

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Tang, Ming, Huangqi Tang, Bo Tu, and Wei-Guo Zhu. "SIRT7: a sentinel of genome stability." Open Biology 11, no. 6 (2021): 210047. http://dx.doi.org/10.1098/rsob.210047.

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SIRT7 is a class III histone deacetylase that belongs to the sirtuin family. The past two decades have seen numerous breakthroughs in terms of understanding SIRT7 biological function. We now know that this enzyme is involved in diverse cellular processes, ranging from gene regulation to genome stability, ageing and tumorigenesis. Genomic instability is one hallmark of cancer and ageing; it occurs as a result of excessive DNA damage. To counteract such instability, cells have evolved a sophisticated regulated DNA damage response mechanism that restores normal gene function. SIRT7 seems to have

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Kang, Josephine, and Martin J. Blaser. "UvrD Helicase Suppresses Recombination and DNA Damage-Induced Deletions." Journal of Bacteriology 188, no. 15 (2006): 5450–59. http://dx.doi.org/10.1128/jb.00275-06.

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ABSTRACT UvrD, a highly conserved helicase involved in mismatch repair, nucleotide excision repair (NER), and recombinational repair, plays a critical role in maintaining genomic stability and facilitating DNA lesion repair in many prokaryotic species. In this report, we focus on the UvrD homolog in Helicobacter pylori, a genetically diverse organism that lacks many known DNA repair proteins, including those involved in mismatch repair and recombinational repair, and that is noted for high levels of inter- and intragenomic recombination and mutation. H. pylori contains numerous DNA repeats in

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Hoogstraten, D., S. Bergink, J. M. Y. Ng, et al. "Versatile DNA damage detection by the global genome nucleotide excision repair protein XPC." Journal of Cell Science 121, no. 17 (2008): 2850–59. http://dx.doi.org/10.1242/jcs.031708.

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Hoogstraten, D., S. Bergink, V. H. M. Verbiest, et al. "Versatile DNA damage detection by the global genome nucleotide excision repair protein XPC." Journal of Cell Science 121, no. 17 (2008): 2972. http://dx.doi.org/10.1242/jcs.03502.

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Hoogstraten, D., S. Bergink, J. M. Y. Ng, et al. "Versatile DNA damage detection by the global genome nucleotide excision repair protein XPC." Journal of Cell Science 121, no. 23 (2008): 3991. http://dx.doi.org/10.1242/jcs.03503.

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Borsos, Barbara N., Hajnalka Majoros, and Tibor Pankotai. "Emerging Roles of Post-Translational Modifications in Nucleotide Excision Repair." Cells 9, no. 6 (2020): 1466. http://dx.doi.org/10.3390/cells9061466.

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Nucleotide excision repair (NER) is a versatile DNA repair pathway which can be activated in response to a broad spectrum of UV-induced DNA damage, such as bulky adducts, including cyclobutane-pyrimidine dimers (CPDs) and 6–4 photoproducts (6–4PPs). Based on the genomic position of the lesion, two sub-pathways can be defined: (I) global genomic NER (GG-NER), involved in the ablation of damage throughout the whole genome regardless of the transcription activity of the damaged DNA locus, and (II) transcription-coupled NER (TC-NER), activated at DNA regions where RNAPII-mediated transcription tak

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Faridounnia, Maryam, Gert Folkers, and Rolf Boelens. "Function and Interactions of ERCC1-XPF in DNA Damage Response." Molecules 23, no. 12 (2018): 3205. http://dx.doi.org/10.3390/molecules23123205.

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Numerous proteins are involved in the multiple pathways of the DNA damage response network and play a key role to protect the genome from the wide variety of damages that can occur to DNA. An example of this is the structure-specific endonuclease ERCC1-XPF. This heterodimeric complex is in particular involved in nucleotide excision repair (NER), but also in double strand break repair and interstrand cross-link repair pathways. Here we review the function of ERCC1-XPF in various DNA repair pathways and discuss human disorders associated with ERCC1-XPF deficiency. We also overview our molecular

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Farkash, Evan A., and Eline T. Luning Prak. "DNA Damage and L1 Retrotransposition." Journal of Biomedicine and Biotechnology 2006 (2006): 1–8. http://dx.doi.org/10.1155/jbb/2006/37285.

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Barbara McClintock was the first to suggest that transposons are a source of genome instability and that genotoxic stress assisted in their mobilization. The generation of double-stranded DNA breaks (DSBs) is a severe form of genotoxic stress that threatens the integrity of the genome, activates cell cycle checkpoints, and, in some cases, causes cell death. Applying McClintock's stress hypothesis to humans, are L1 retrotransposons, the most active autonomous mobile elements in the modern day human genome, mobilized by DSBs? Here, evidence that transposable elements, particularly retrotransposo

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Ghosh, Soma, and Tapas Saha. "Central Role of Ubiquitination in Genome Maintenance: DNA Replication and Damage Repair." ISRN Molecular Biology 2012 (February 8, 2012): 1–9. http://dx.doi.org/10.5402/2012/146748.

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Faithful transmission of genetic information through generations ensures genomic stability and integrity. However, genetic alterations occur every now and then during the course of genome duplication. In order to repair these genetic defects and lesions, nature has devised several repair pathways which function promptly to prevent the cell from accumulating permanent mutations. These repair mechanisms seem to be significantly impacted by posttranslational modifications of proteins like phosphorylation and ubiquitination. Protein ubiquitination is emerging as a critical regulatory mechanism of

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Crooke, Philip S., and Fritz F. Parl. "A Mathematical Model for DNA Damage and Repair." Journal of Nucleic Acids 2010 (2010): 1–7. http://dx.doi.org/10.4061/2010/352603.

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In cells, DNA repair has to keep up with DNA damage to maintain the integrity of the genome and prevent mutagenesis and carcinogenesis. While the importance of both DNA damage and repair is clear, the impact of imbalances between both processes has not been studied. In this paper, we created a combined mathematical model for the formation of DNA adducts from oxidative estrogen metabolism followed by base excision repair (BER) of these adducts. The model encompasses a set of differential equations representing the sequence of enzymatic reactions in both damage and repair pathways. By combining

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Kidane, Dawit. "Molecular Mechanisms of H. pylori-Induced DNA Double-Strand Breaks." International Journal of Molecular Sciences 19, no. 10 (2018): 2891. http://dx.doi.org/10.3390/ijms19102891.

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Infections contribute to carcinogenesis through inflammation-related mechanisms. H. pylori infection is a significant risk factor for gastric carcinogenesis. However, the molecular mechanism by which H. pylori infection contributes to carcinogenesis has not been fully elucidated. H. pylori-associated chronic inflammation is linked to genomic instability via reactive oxygen and nitrogen species (RONS). In this article, we summarize the current knowledge of H. pylori-induced double strand breaks (DSBs). Furthermore, we provide mechanistic insight into how processing of oxidative DNA damage via b

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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 (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 distri

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Daniel, Laurianne, Elena Cerutti, Lise-Marie Donnio, et al. "Mechanistic insights in transcription-coupled nucleotide excision repair of ribosomal DNA." Proceedings of the National Academy of Sciences 115, no. 29 (2018): E6770—E6779. http://dx.doi.org/10.1073/pnas.1716581115.

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Nucleotide excision repair (NER) guarantees genome integrity against UV light-induced DNA damage. After UV irradiation, cells have to cope with a general transcriptional block. To ensure UV lesions repair specifically on transcribed genes, NER is coupled with transcription in an extremely organized pathway known as transcription-coupled repair. In highly metabolic cells, more than 60% of total cellular transcription results from RNA polymerase I activity. Repair of the mammalian transcribed ribosomal DNA has been scarcely studied. UV lesions severely block RNA polymerase I activity and the ful

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Ataian, Yeganeh, and Jocelyn E. Krebs. "Five repair pathways in one context: chromatin modification during DNA repairThis paper is one of a selection of papers published in this Special Issue, entitled 27th International West Coast Chromatin and Chromosome Conference, and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 84, no. 4 (2006): 490–94. http://dx.doi.org/10.1139/o06-075.

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The eukaryotic cell is faced with more than 10 000 various kinds of DNA lesions per day. Failure to repair such lesions can lead to mutations, genomic instability, or cell death. Therefore, cells have developed 5 major repair pathways in which different kinds of DNA damage can be detected and repaired: homologous recombination, nonhomologous end joining, nucleotide excision repair, base excision repair, and mismatch repair. However, the efficient repair of DNA damage is complicated by the fact that the genomic DNA is packaged through histone and nonhistone proteins into chromatin, a highly con

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Tran, Oanh TN, Serkalem Tadesse, Christopher Chu, and Dawit Kidane. "Overexpression of NEIL3 associated with altered genome and poor survival in selected types of human cancer." Tumor Biology 42, no. 5 (2020): 101042832091840. http://dx.doi.org/10.1177/1010428320918404.

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Base excision repair, which is initiated by the DNA N-glycosylase proteins, is the frontline for repairing potentially mutagenic DNA base damage. Several base excision repair genes are deregulated in cancer and affect cellular outcomes to chemotherapy and carcinogenesis. Endonuclease VIII-like 3 (NEIL3) is a DNA glycosylase protein that is involved in oxidative and interstrand crosslink DNA damage repair. Our previous work has showed that NEIL3 is required to maintain replication fork integrity. It is unknown whether NEIL3 overexpression could contribute to cancer phenotypes, and its prognosti

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Olipitz, Werner, Nicole Scheer, Franz Quehenberger, et al. "Base Excision Repair Deficiency in Acute Myeloid Leukemia." Blood 114, no. 22 (2009): 1106. http://dx.doi.org/10.1182/blood.v114.22.1106.1106.

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Abstract Abstract 1106 Poster Board I-128 Base excision repair (BER) is the main DNA repair mechanism for single DNA base lesions resulting from oxidative stress, chemical damage or ionizing radiation. We investigated BER in acute myeloid leukemia (AML), a disorder characterized by widespread genomic instability. AML cell lines were treated with H2O2 and DNA damage induction and repair were monitored using the alkaline comet assay. Significantly reduced single strand break (SSB) formation - representing BER intermediates - was observed in 5/10 cell lines. Significantly reduced SSB formation wa

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