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Journal articles on the topic 'Human DNA repair and recombination pathways'

Author: Grafiati

Published: 14 March 2023

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1

Zhao, Lei, Chengyu Bao, Yuxuan Shang, et al. "The Determinant of DNA Repair Pathway Choices in Ionising Radiation-Induced DNA Double-Strand Breaks." BioMed Research International 2020 (August 25, 2020): 1–12. http://dx.doi.org/10.1155/2020/4834965.

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Ionising radiation- (IR-) induced DNA double-strand breaks (DSBs) are considered to be the deleterious DNA lesions that pose a serious threat to genomic stability. The major DNA repair pathways, including classical nonhomologous end joining, homologous recombination, single-strand annealing, and alternative end joining, play critical roles in countering and eliciting IR-induced DSBs to ensure genome integrity. If the IR-induced DNA DSBs are not repaired correctly, the residual or incorrectly repaired DSBs can result in genomic instability that is associated with certain human diseases. Althoug

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2

Jalan, Manisha, Juber Patel, Kyrie S. Olsen, et al. "Abstract 5688: RNA-mediated DNA repair: A novel repair pathway in homologous recombination-deficient cancers." Cancer Research 82, no. 12_Supplement (2022): 5688. http://dx.doi.org/10.1158/1538-7445.am2022-5688.

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Abstract Genome instability has long been considered the primary driver of most cancer types. A double strand break (DSB) in DNA can have deleterious consequences for a cell, which if not repaired faithfully, can lead to mutations and chromosomal rearrangements, or even cell death. DSBs can be processed by several DNA repair pathways, of which homologous recombination (HR) is the preferred method due to its error-free nature. HR uses an intact homologous DNA sequence as a template for recovering the information lost at the break site. A significant proportion of all cancers, especially triple-

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3

Kennedy, Richard D., and Alan D. D'Andrea. "DNA Repair Pathways in Clinical Practice: Lessons From Pediatric Cancer Susceptibility Syndromes." Journal of Clinical Oncology 24, no. 23 (2006): 3799–808. http://dx.doi.org/10.1200/jco.2005.05.4171.

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Human cancers exhibit genomic instability and an increased mutation rate due to underlying defects in DNA repair. Cancer cells are often defective in one of six major DNA repair pathways, namely: mismatch repair, base excision repair, nucleotide excision repair, homologous recombination, nonhomologous endjoining and translesion synthesis. The specific DNA repair pathway affected is predictive of the kinds of mutations, the tumor drug sensitivity, and the treatment outcome. The study of rare inherited DNA repair disorders, such as Fanconi anemia, has yielded new insights to drug sensitivity and

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4

Guo, Yingying, Linda L. Breeden, Helmut Zarbl, Bradley D. Preston, and David L. Eaton. "Expression of a Human Cytochrome P450 in Yeast Permits Analysis of Pathways for Response to and Repair of Aflatoxin-Induced DNA Damage." Molecular and Cellular Biology 25, no. 14 (2005): 5823–33. http://dx.doi.org/10.1128/mcb.25.14.5823-5833.2005.

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ABSTRACT Aflatoxin B1 (AFB1) is a human hepatotoxin and hepatocarcinogen produced by the mold Aspergillus flavus. In humans, AFB1 is primarily bioactivated by cytochrome P450 1A2 (CYP1A2) and 3A4 to a genotoxic epoxide that forms N7-guanine DNA adducts. A series of yeast haploid mutants defective in DNA repair and cell cycle checkpoints were transformed with human CYP1A2 to investigate how these DNA adducts are repaired. Cell survival and mutagenesis following aflatoxin B1 treatment was assayed in strains defective in nucleotide excision repair (NER) (rad14), postreplication repair (PRR) (rad6

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5

Wang, Xuejie, Yang Dong, Xiaocong Zhao, et al. "Rtt105 promotes high-fidelity DNA replication and repair by regulating the single-stranded DNA-binding factor RPA." Proceedings of the National Academy of Sciences 118, no. 25 (2021): e2106393118. http://dx.doi.org/10.1073/pnas.2106393118.

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Single-stranded DNA (ssDNA) covered with the heterotrimeric Replication Protein A (RPA) complex is a central intermediate of DNA replication and repair. How RPA is regulated to ensure the fidelity of DNA replication and repair remains poorly understood. Yeast Rtt105 is an RPA-interacting protein required for RPA nuclear import and efficient ssDNA binding. Here, we describe an important role of Rtt105 in high-fidelity DNA replication and recombination and demonstrate that these functions of Rtt105 primarily depend on its regulation of RPA. The deletion of RTT105 causes elevated spontaneous DNA

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Giot, Loïc, Roland Chanet, Michel Simon, Céline Facca та Gérard Faye. "Involvement of the Yeast DNA Polymerase δ in DNA Repair in Vivo". Genetics 146, № 4 (1997): 1239–51. http://dx.doi.org/10.1093/genetics/146.4.1239.

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The POL3 encoded catalytic subunit of DNA polymerase δ possesses a highly conserved C-terminal cysteine-rich domain in Saccharomyces cerevisiae. Mutations in some of its cysteine codons display a lethal phenotype, which demonstrates an essential function of this domain. The thermosensitive mutant pol3-13, in which a serine replaces a cysteine of this domain, exhibits a range of defects in DNA repair, such as hypersensitivity to different DNA-damaging agents and deficiency for induced mutagenesis and for recombination. These phenotypes are observed at 24°, a temperature at which DNA replication

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7

Priest, Shelby J., Marco A. Coelho, Verónica Mixão, et al. "Factors enforcing the species boundary between the human pathogens Cryptococcus neoformans and Cryptococcus deneoformans." PLOS Genetics 17, no. 1 (2021): e1008871. http://dx.doi.org/10.1371/journal.pgen.1008871.

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Hybridization has resulted in the origin and variation in extant species, and hybrids continue to arise despite pre- and post-zygotic barriers that limit their formation and evolutionary success. One important system that maintains species boundaries in prokaryotes and eukaryotes is the mismatch repair pathway, which blocks recombination between divergent DNA sequences. Previous studies illuminated the role of the mismatch repair component Msh2 in blocking genetic recombination between divergent DNA during meiosis. Loss of Msh2 results in increased interspecific genetic recombination in bacter

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8

Costantino, Lorenzo, Sotirios K. Sotiriou, Juha K. Rantala, et al. "Break-Induced Replication Repair of Damaged Forks Induces Genomic Duplications in Human Cells." Science 343, no. 6166 (2013): 88–91. http://dx.doi.org/10.1126/science.1243211.

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In budding yeast, one-ended DNA double-strand breaks (DSBs) and damaged replication forks are repaired by break-induced replication (BIR), a homologous recombination pathway that requires the Pol32 subunit of DNA polymerase delta. DNA replication stress is prevalent in cancer, but BIR has not been characterized in mammals. In a cyclin E overexpression model of DNA replication stress, POLD3, the human ortholog of POL32, was required for cell cycle progression and processive DNA synthesis. Segmental genomic duplications induced by cyclin E overexpression were also dependent on POLD3, as were BIR

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9

De Falco, Mariarosaria, and Mariarita De Felice. "Take a Break to Repair: A Dip in the World of Double-Strand Break Repair Mechanisms Pointing the Gaze on Archaea." International Journal of Molecular Sciences 22, no. 24 (2021): 13296. http://dx.doi.org/10.3390/ijms222413296.

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All organisms have evolved many DNA repair pathways to counteract the different types of DNA damages. The detection of DNA damage leads to distinct cellular responses that bring about cell cycle arrest and the induction of DNA repair mechanisms. In particular, DNA double-strand breaks (DSBs) are extremely toxic for cell survival, that is why cells use specific mechanisms of DNA repair in order to maintain genome stability. The choice among the repair pathways is mainly linked to the cell cycle phases. Indeed, if it occurs in an inappropriate cellular context, it may cause genome rearrangements

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10

Symington, Lorraine S. "Role of RAD52 Epistasis Group Genes in Homologous Recombination and Double-Strand Break Repair." Microbiology and Molecular Biology Reviews 66, no. 4 (2002): 630–70. http://dx.doi.org/10.1128/mmbr.66.4.630-670.2002.

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SUMMARY The process of homologous recombination is a major DNA repair pathway that operates on DNA double-strand breaks, and possibly other kinds of DNA lesions, to promote error-free repair. Central to the process of homologous recombination are the RAD52 group genes (RAD50, RAD51, RAD52, RAD54, RDH54/TID1, RAD55, RAD57, RAD59, MRE11, and XRS2), most of which were identified by their requirement for the repair of ionizing-radiation-induced DNA damage in Saccharomyces cerevisiae. The Rad52 group proteins are highly conserved among eukaryotes, and Rad51, Mre11, and Rad50 are also conserved in p

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11

Dahal, Sumedha, and Sathees C. Raghavan. "Mitochondrial genome stability in human: understanding the role of DNA repair pathways." Biochemical Journal 478, no. 6 (2021): 1179–97. http://dx.doi.org/10.1042/bcj20200920.

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Mitochondria are semiautonomous organelles in eukaryotic cells and possess their own genome that replicates independently. Mitochondria play a major role in oxidative phosphorylation due to which its genome is frequently exposed to oxidative stress. Factors including ionizing radiation, radiomimetic drugs and replication fork stalling can also result in different types of mutations in mitochondrial DNA (mtDNA) leading to genome fragility. Mitochondria from myopathies, dystonia, cancer patient samples show frequent mtDNA mutations such as point mutations, insertions and large-scale deletions th

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12

Jensen, Ryan B., and Eli Rothenberg. "Preserving genome integrity in human cells via DNA double-strand break repair." Molecular Biology of the Cell 31, no. 9 (2020): 859–65. http://dx.doi.org/10.1091/mbc.e18-10-0668.

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The efficient maintenance of genome integrity in the face of cellular stress is vital to protect against human diseases such as cancer. DNA replication, chromatin dynamics, cellular signaling, nuclear architecture, cell cycle checkpoints, and other cellular activities contribute to the delicate spatiotemporal control that cells utilize to regulate and maintain genome stability. This perspective will highlight DNA double-strand break (DSB) repair pathways in human cells, how DNA repair failures can lead to human disease, and how PARP inhibitors have emerged as a novel clinical therapy to treat

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13

Samstein, Robert. "Influence of DNA damage repair defects on tumor immunogenicity." Journal of Immunology 204, no. 1_Supplement (2020): 242.11. http://dx.doi.org/10.4049/jimmunol.204.supp.242.11.

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Abstract In recent years, immune checkpoint inhibitors (ICI) have dramatically altered the treatment landscape for patients with advanced stage and metastatic cancers. Durable benefit, however, is limited to subsets of histologies and patients, highlighting the importance of identifying predictive biomarkers to select for patients who may benefit. DNA damage repair and response (DDR) deficiency including mismatch repair deficiency and resulting increased tumor neoantigens have been associated with improved response. We hypothesize that a similar concept may extend to other defects in DDR pathw

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14

Bukowska, Barbara, and Boleslaw T. Karwowski. "The Clustered DNA Lesions – Types, Pathways of Repair and Relevance to Human Health." Current Medicinal Chemistry 25, no. 23 (2018): 2722–35. http://dx.doi.org/10.2174/0929867325666180226110502.

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The clustered DNA lesions are a characteristic feature of ionizing radiation and are defined as two or more damage sites formed within 20 bps after the passage of a single radiation track. The clustered DNA lesions are divided into two major groups: double-stranded breaks (DSBs) and non-DSB clusters also known as Oxidatively-induced Clustered DNA Lesions (OCDLs), which could involve either two opposing strands or the same strand. As irradiation is gaining greater interest in cancer treatment as well as in imaging techniques, the detailed knowledge of its genotoxicity and the mechanisms of repa

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15

Skaar, Eric P., Matthew P. Lazio, and H. Steven Seifert. "Roles of the recJ and recN Genes in Homologous Recombination and DNA Repair Pathways of Neisseria gonorrhoeae." Journal of Bacteriology 184, no. 4 (2002): 919–27. http://dx.doi.org/10.1128/jb.184.4.919-927.2002.

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ABSTRACT The paradigm of homologous recombination comes from Escherichia coli, where the genes involved have been segregated into pathways. In the human pathogen Neisseria gonorrhoeae (the gonococcus), the pathways of homologous recombination are being delineated. To investigate the roles of the gonococcal recN and recJ genes in the recombination-based processes of the gonococcus, these genes were inactivated in the N. gonorrhoeae strain FA1090. We report that both recN and recJ loss-of-function mutants show decreased DNA repair ability. In addition, the recJ mutant was decreased in pilus-depe

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16

Hartlerode, Andrea J., and Ralph Scully. "Mechanisms of double-strand break repair in somatic mammalian cells." Biochemical Journal 423, no. 2 (2009): 157–68. http://dx.doi.org/10.1042/bj20090942.

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DNA chromosomal DSBs (double-strand breaks) are potentially hazardous DNA lesions, and their accurate repair is essential for the successful maintenance and propagation of genetic information. Two major pathways have evolved to repair DSBs: HR (homologous recombination) and NHEJ (non-homologous end-joining). Depending on the context in which the break is encountered, HR and NHEJ may either compete or co-operate to fix DSBs in eukaryotic cells. Defects in either pathway are strongly associated with human disease, including immunodeficiency and cancer predisposition. Here we review the current k

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17

Pan-Hammarström, Qiang, Anne-Marie Jones, Aleksi Lähdesmäki, et al. "Impact of DNA ligase IV on nonhomologous end joining pathways during class switch recombination in human cells." Journal of Experimental Medicine 201, no. 2 (2005): 189–94. http://dx.doi.org/10.1084/jem.20040772.

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Class switch recombination (CSR) is a region-specific, transcriptionally regulated, nonhomologous recombinational process that is initiated by activation-induced cytidine deaminase (AID). The initial lesions in the switch (S) regions are subsequently processed and resolved, leading to recombination of the two targeted S regions. The mechanisms by which repair and ligation of the broken DNA ends occurs is still elusive. Recently, a small number of patients lacking DNA ligase IV, a critical component of the nonhomologous end joining (NHEJ) machinery, have been identified. We show that these pati

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18

Luo, Wei, Ting Guo, Guangyu Li, et al. "Variants in Homologous Recombination Genes EXO1 and RAD51 Related with Premature Ovarian Insufficiency." Journal of Clinical Endocrinology & Metabolism 105, no. 10 (2020): e3566-e3574. http://dx.doi.org/10.1210/clinem/dgaa505.

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Abstract Context Premature ovarian insufficiency (POI) is characterized by cessation of menstruation before 40 years of age and elevated serum level of FSH (&gt;25 IU/L). Recent studies have found a few causative genes responsible for POI enriched in meiotic recombination and DNA damage repair pathways. Objective To investigate the role of variations in homologous recombination genes played in POI pathogenesis. Methods The whole exome sequencing was performed in 50 POI patients with primary amenorrhea. Functional characterizations of the novel variants were carried out in budding yeast and

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19

Jalan, Manisha, Kyrie S. Olsen, and Simon N. Powell. "Emerging Roles of RAD52 in Genome Maintenance." Cancers 11, no. 7 (2019): 1038. http://dx.doi.org/10.3390/cancers11071038.

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The maintenance of genome integrity is critical for cell survival. Homologous recombination (HR) is considered the major error-free repair pathway in combatting endogenously generated double-stranded lesions in DNA. Nevertheless, a number of alternative repair pathways have been described as protectors of genome stability, especially in HR-deficient cells. One of the factors that appears to have a role in many of these pathways is human RAD52, a DNA repair protein that was previously considered to be dispensable due to a lack of an observable phenotype in knock-out mice. In later studies, RAD5

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20

Bjorkman, Andrea, Likun Du, Annika Lindblom, and Qiang Pan-Hammarstrom. "Altered class switch recombination junctions in patients with deficiency in Mlh1 and Brca1 (109.6)." Journal of Immunology 188, no. 1_Supplement (2012): 109.6. http://dx.doi.org/10.4049/jimmunol.188.supp.109.6.

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Abstract Class switch recombination (CSR) is a B-cell specific process that results in the change of immunoglobulin isotype from IgM to IgA, IgG or IgE. It involves the creation of DNA double strand breaks (DSBs) in switch regions, which are sensed and repaired by DNA damage response proteins and the non-homologous end-joining (NHEJ) pathway. Here we have studied CSR in patients with heterozygous mutations in both the mismatch repair (MMR) gene Mlh1 and the breast cancer susceptibility gene Brca1 and in patients with mutations in either Mlh1 or Brca1 alone. Brca1 is involved in several process

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Sinclair, Alison, Sarah Yarranton, and Celine Schelcher. "DNA-damage response pathways triggered by viral replication." Expert Reviews in Molecular Medicine 8, no. 5 (2006): 1–11. http://dx.doi.org/10.1017/s1462399406010544.

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Many viruses, with distinct replication strategies, activate DNA-damage response pathways, including the lentivirus human immunodeficiency virus (HIV) and the DNA viruses Epstein–Barr virus (EBV), herpes simplex virus 1, adenovirus and SV40. DNA-damage response pathways involving DNA-dependent protein kinase, ataxia-telengiectasia mutated (ATM) and ‘ataxia-telengiectasia and Rad3-related’ (ATR) have all been implicated. This review focuses on the effects of HIV and EBV replication on DNA repair pathways. It has been suggested that activation of cellular DNA repair and recombination enzymes is

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Gusa, Asiya, and Sue Jinks-Robertson. "Mitotic Recombination and Adaptive Genomic Changes in Human Pathogenic Fungi." Genes 10, no. 11 (2019): 901. http://dx.doi.org/10.3390/genes10110901.

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Genome rearrangements and ploidy alterations are important for adaptive change in the pathogenic fungal species Candida and Cryptococcus, which propagate primarily through clonal, asexual reproduction. These changes can occur during mitotic growth and lead to enhanced virulence, drug resistance, and persistence in chronic infections. Examples of microevolution during the course of infection were described in both human infections and mouse models. Recent discoveries defining the role of sexual, parasexual, and unisexual cycles in the evolution of these pathogenic fungi further expanded our und

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Derbyshire, M. K., L. H. Epstein, C. S. Young, P. L. Munz, and R. Fishel. "Nonhomologous recombination in human cells." Molecular and Cellular Biology 14, no. 1 (1994): 156–69. http://dx.doi.org/10.1128/mcb.14.1.156-169.1994.

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Nonhomologous recombination (NHR) is a major pathway for the repair of chromosomal double-strand breaks in the DNA of somatic cells. In this study, a comparison was made between the nonhomologous end joining of transfected adenovirus DNA fragments in vivo and the ability of purified human proteins to catalyze nonhomologous end joining in vitro. Adenovirus DNA fragments were shown to be efficiently joined in human cells regardless of the structure of the ends. Sequence analysis of these junctions revealed that the two participating ends frequently lost nucleotides from the 3' strands at the sit

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Derbyshire, M. K., L. H. Epstein, C. S. Young, P. L. Munz, and R. Fishel. "Nonhomologous recombination in human cells." Molecular and Cellular Biology 14, no. 1 (1994): 156–69. http://dx.doi.org/10.1128/mcb.14.1.156.

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Nonhomologous recombination (NHR) is a major pathway for the repair of chromosomal double-strand breaks in the DNA of somatic cells. In this study, a comparison was made between the nonhomologous end joining of transfected adenovirus DNA fragments in vivo and the ability of purified human proteins to catalyze nonhomologous end joining in vitro. Adenovirus DNA fragments were shown to be efficiently joined in human cells regardless of the structure of the ends. Sequence analysis of these junctions revealed that the two participating ends frequently lost nucleotides from the 3' strands at the sit

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Sugimura, Kazuto, Shin-ichiro Takebayashi, Hiroshi Taguchi, Shunichi Takeda, and Katsuzumi Okumura. "PARP-1 ensures regulation of replication fork progression by homologous recombination on damaged DNA." Journal of Cell Biology 183, no. 7 (2008): 1203–12. http://dx.doi.org/10.1083/jcb.200806068.

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Poly-ADP ribose polymerase 1 (PARP-1) is activated by DNA damage and has been implicated in the repair of single-strand breaks (SSBs). Involvement of PARP-1 in other DNA damage responses remains controversial. In this study, we show that PARP-1 is required for replication fork slowing on damaged DNA. Fork progression in PARP-1−/− DT40 cells is not slowed down even in the presence of DNA damage induced by the topoisomerase I inhibitor camptothecin (CPT). Mammalian cells treated with a PARP inhibitor or PARP-1–specific small interfering RNAs show similar results. The expression of human PARP-1 r

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Heaton, Brook E., Daniel Barkan, Paola Bongiorno, Petros C. Karakousis, and Michael S. Glickman. "Deficiency of Double-Strand DNA Break Repair Does Not Impair Mycobacterium tuberculosis Virulence in Multiple Animal Models of Infection." Infection and Immunity 82, no. 8 (2014): 3177–85. http://dx.doi.org/10.1128/iai.01540-14.

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ABSTRACTMycobacterium tuberculosispersistence within its human host requires mechanisms to resist the effector molecules of host immunity, which exert their bactericidal effects through damaging pathogen proteins, membranes, and DNA. Substantial evidence indicates that bacterial pathogens, includingM. tuberculosis, require DNA repair systems to repair the DNA damage inflicted by the host during infection, but the role of double-strand DNA break (DSB) repair systems is unclear. Double-strand DNA breaks are the most cytotoxic form of DNA damage and must be repaired for chromosome replication to

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Guo, Hongrui, Huan Liu, Hongbin Wu, et al. "Nickel Carcinogenesis Mechanism: DNA Damage." International Journal of Molecular Sciences 20, no. 19 (2019): 4690. http://dx.doi.org/10.3390/ijms20194690.

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Nickel (Ni) is known to be a major carcinogenic heavy metal. Occupational and environmental exposure to Ni has been implicated in human lung and nasal cancers. Currently, the molecular mechanisms of Ni carcinogenicity remain unclear, but studies have shown that Ni-caused DNA damage is an important carcinogenic mechanism. Therefore, we conducted a literature search of DNA damage associated with Ni exposure and summarized known Ni-caused DNA damage effects. In vitro and vivo studies demonstrated that Ni can induce DNA damage through direct DNA binding and reactive oxygen species (ROS) stimulatio

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Zhao, Yucui, and Siyu Chen. "Targeting DNA Double-Strand Break (DSB) Repair to Counteract Tumor Radio-resistance." Current Drug Targets 20, no. 9 (2019): 891–902. http://dx.doi.org/10.2174/1389450120666190222181857.

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During the last decade, advances of radiotherapy (RT) have been made in the clinical practice of cancer treatment. RT exerts its anticancer effect mainly via leading to the DNA Double-Strand Break (DSB), which is one of the most toxic DNA damages. Non-Homologous End Joining (NHEJ) and Homologous Recombination (HR) are two major DSB repair pathways in human cells. It is known that dysregulations of DSB repair elicit a predisposition to cancer and probably result in resistance to cancer therapies including RT. Therefore, targeting the DSB repair presents an attractive strategy to counteract radi

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Tomkinson, Alan E., Tasmin Naila, and Seema Khattri Bhandari. "Altered DNA ligase activity in human disease." Mutagenesis 35, no. 1 (2019): 51–60. http://dx.doi.org/10.1093/mutage/gez026.

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Abstract The joining of interruptions in the phosphodiester backbone of DNA is critical to maintain genome stability. These breaks, which are generated as part of normal DNA transactions, such as DNA replication, V(D)J recombination and meiotic recombination as well as directly by DNA damage or due to DNA damage removal, are ultimately sealed by one of three human DNA ligases. DNA ligases I, III and IV each function in the nucleus whereas DNA ligase III is the sole enzyme in mitochondria. While the identification of specific protein partners and the phenotypes caused either by genetic or chemi

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Hussain, Suleman S., Rahul Majumdar, Grace M. Moore, et al. "Measuring nonhomologous end-joining, homologous recombination and alternative end-joining simultaneously at an endogenous locus in any transfectable human cell." Nucleic Acids Research 49, no. 13 (2021): e74-e74. http://dx.doi.org/10.1093/nar/gkab262.

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Abstract Double strand break (DSB) repair primarily occurs through 3 pathways: non-homologous end-joining (NHEJ), alternative end-joining (Alt-EJ), and homologous recombination (HR). Typical methods to measure pathway usage include integrated cassette reporter assays or visualization of DNA damage induced nuclear foci. It is now well understood that repair of Cas9-induced breaks also involves NHEJ, Alt-EJ, and HR pathways, providing a new format to measure pathway usage. Here, we have developed a simple Cas9-based system with validated repair outcomes that accurately represent each pathway and

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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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Jackson, S. P. "Detecting, signalling and repairing DNA double-strand breaks." Biochemical Society Transactions 29, no. 6 (2001): 655–61. http://dx.doi.org/10.1042/bst0290655.

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DNA double-strand breaks (DSBs) can be generated by a variety of genotoxic agents, including ionizing radiation and radiomimetic chemicals. They can also occur when DNA replication complexes encounter other forms of DNA damage, and are produced as intermediates during certain site-specific recombination processes. It is crucial that cells recognize DSBs and bring about their efficient repair, because a single unrepaired cellular DSB can induce cell death, and defective DSB repair can lead to mutations or the loss of significant segments of chromosomal material. Eukaryotic cells have evolved a

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Hu, Changkun, Taylor Bugbee, Dalton Dacus, Rachel Palinski, and Nicholas Wallace. "Beta human papillomavirus 8 E6 allows colocalization of non-homologous end joining and homologous recombination repair factors." PLOS Pathogens 18, no. 2 (2022): e1010275. http://dx.doi.org/10.1371/journal.ppat.1010275.

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Beta human papillomavirus (β-HPV) are hypothesized to make DNA damage more mutagenic and potentially more carcinogenic. Double strand breaks (DSBs) are the most deleterious DNA lesion. They are typically repaired by homologous recombination (HR) or non-homologous end joining (NHEJ). HR occurs after DNA replication while NHEJ can occur at any point in the cell cycle. HR and NHEJ are not thought to occur in the same cell at the same time. HR is restricted to cells in phases of the cell cycle where homologous templates are available, while NHEJ occurs primarily during G1. β-HPV type 8 protein E6

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Drzewiecka, Małgorzata, Gabriela Barszczewska-Pietraszek, Piotr Czarny, Tomasz Skorski та Tomasz Śliwiński. "Synthetic Lethality Targeting Polθ". Genes 13, № 6 (2022): 1101. http://dx.doi.org/10.3390/genes13061101.

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Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient’s anti-cancer chemotherapy. Among the factors that are targets for the induction of the synthetic lethality effect, those involved in DNA repair seem to be the most relevant. Specifically, when mutation in one of the canonical DNA double-strand break (DSB) repair pathways occurs, which is a frequent event in cancer cells, the alternative pathways may be a promising target for the elimination of abnormal cell

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Choi, Vivian W., Douglas M. McCarty, and R. Jude Samulski. "Host Cell DNA Repair Pathways in Adeno-Associated Viral Genome Processing." Journal of Virology 80, no. 21 (2006): 10346–56. http://dx.doi.org/10.1128/jvi.00841-06.

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ABSTRACT Recentstudies have shown that wild-type and recombinant adeno-associated virus (AAV and rAAV) genomes persist in human tissue predominantly as double-stranded (ds) circular episomes derived from input linear single-stranded virion DNA. Using self-complementary recombinant AAV (scAAV) vectors, we generated intermediates that directly transition to ds circular episomes. The scAAV genome ends are palindromic hairpin-structured terminal repeats, resembling a double-stranded break repair intermediate. Utilizing this substrate, we found cellular DNA recombination and repair factors to be es

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Meng, Yuan, Changwei Liu, Lei Shen, et al. "TRAF6 mediates human DNA2 polyubiquitination and nuclear localization to maintain nuclear genome integrity." Nucleic Acids Research 47, no. 14 (2019): 7564–79. http://dx.doi.org/10.1093/nar/gkz537.

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Abstract The multifunctional human DNA2 (hDNA2) nuclease/helicase is required to process DNA ends for homology-directed recombination repair (HDR) and to counteract replication stress. To participate in these processes, hDNA2 must localize to the nucleus and be recruited to the replication or repair sites. However, because hDNA2 lacks the nuclear localization signal that is found in its yeast homolog, it is unclear how its migration into the nucleus is regulated during replication or in response to DNA damage. Here, we report that the E3 ligase TRAF6 binds to and mediates the K63-linked polyub

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Oakley, Gregory G., Lisa I. Loberg, Jiaqin Yao, et al. "UV-induced Hyperphosphorylation of Replication Protein A Depends on DNA Replication and Expression of ATM Protein." Molecular Biology of the Cell 12, no. 5 (2001): 1199–213. http://dx.doi.org/10.1091/mbc.12.5.1199.

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Exposure to DNA-damaging agents triggers signal transduction pathways that are thought to play a role in maintenance of genomic stability. A key protein in the cellular processes of nucleotide excision repair, DNA recombination, and DNA double-strand break repair is the single-stranded DNA binding protein, RPA. We showed previously that the p34 subunit of RPA becomes hyperphosphorylated as a delayed response (4–8 h) to UV radiation (10–30 J/m2). Here we show that UV-induced RPA-p34 hyperphosphorylation depends on expression of ATM, the product of the gene mutated in the human genetic disorder

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Topp, Monique, Lynne Hartley, Michele Cook, et al. "Targeting therapy based on preclinical analysis of clinical, molecular, and functional characteristics of individual high-grade serous ovarian cancers." Journal of Clinical Oncology 30, no. 15_suppl (2012): 5073. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.5073.

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5073 Background: Recent molecular exploration of high-grade epithelial ovarian cancer (OC) has revealed potential targets for novel therapy based on altered DNA repair function, deregulated pathways and recurrent amplifications (Cancer Genome Atlas Research Network. 2011. Nature 474). Improved pre-clinical models allowing analysis of specific molecular subsets of ovarian cancer are urgently required to test novel treatment strategies. Methods: We have generated a novel xenograft model of human high-grade serous OC (HG-SOC). Histologic, functional and molecular analysis of the novel xenograft c

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O'Rourke, Thomas W., Nicole A. Doudican, Melinda D. Mackereth, Paul W. Doetsch, and Gerald S. Shadel. "Mitochondrial Dysfunction Due to Oxidative Mitochondrial DNA Damage Is Reduced through Cooperative Actions of Diverse Proteins." Molecular and Cellular Biology 22, no. 12 (2002): 4086–93. http://dx.doi.org/10.1128/mcb.22.12.4086-4093.2002.

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ABSTRACT The mitochondrial genome is a significant target of exogenous and endogenous genotoxic agents; however, the determinants that govern this susceptibility and the pathways available to resist mitochondrial DNA (mtDNA) damage are not well characterized. Here we report that oxidative mtDNA damage is elevated in strains lacking Ntg1p, providing the first direct functional evidence that this mitochondrion-localized, base excision repair enzyme functions to protect mtDNA. However, ntg1 null strains did not exhibit a mitochondrial respiration-deficient (petite) phenotype, suggesting that mtDN

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Chiolo, Irene, Marco Saponaro, Anastasia Baryshnikova, Jeong-Hoon Kim, Yeon-Soo Seo, and Giordano Liberi. "The Human F-Box DNA Helicase FBH1 Faces Saccharomyces cerevisiae Srs2 and Postreplication Repair Pathway Roles." Molecular and Cellular Biology 27, no. 21 (2007): 7439–50. http://dx.doi.org/10.1128/mcb.00963-07.

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ABSTRACTTheSaccharomyces cerevisiaeSrs2 UvrD DNA helicase controls genome integrity by preventing unscheduled recombination events. While Srs2 orthologues have been identified in prokaryotic and lower eukaryotic organisms, human orthologues of Srs2 have not been described so far. We found that the human F-box DNA helicase hFBH1 suppresses specific recombination defects ofS. cerevisiae srs2mutants, consistent with the finding that the helicase domain of hFBH1 is highly conserved with that of Srs2. Surprisingly, hFBH1 in the absence ofSRS2also suppresses the DNA damage sensitivity caused by inac

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Stohl, Elizabeth A., and H. Steven Seifert. "Neisseria gonorrhoeae DNA Recombination and Repair Enzymes Protect against Oxidative Damage Caused by Hydrogen Peroxide." Journal of Bacteriology 188, no. 21 (2006): 7645–51. http://dx.doi.org/10.1128/jb.00801-06.

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ABSTRACT The strict human pathogen Neisseria gonorrhoeae is exposed to oxidative damage during infection. N. gonorrhoeae has many defenses that have been demonstrated to counteract oxidative damage. However, recN is the only DNA repair and recombination gene upregulated in response to hydrogen peroxide (H2O2) by microarray analysis and subsequently shown to be important for oxidative damage protection. We therefore tested the importance of RecA and DNA recombination and repair enzymes in conferring resistance to H2O2 damage. recA mutants, as well as RecBCD (recB, recC, and recD) and RecF-like

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Desai, Amar, Yulan Qing, and Stanton L. Gerson. "Characterization of Hematopoietic Stem Cell Function and Sensitivity in the Homologous Recombination Deficient Exonuclease1mut Mouse Model." Blood 118, no. 21 (2011): 1293. http://dx.doi.org/10.1182/blood.v118.21.1293.1293.

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Abstract Abstract 1293 Hematopoietic stem cell (HSC) maintenance is essential for sustained longevity and tissue function. The HSC population has lifelong self-renewing capabilities and gives rise to subsets of multipotent progenitor cells, and in turn a progeny of terminally differentiated mature cells consisting of all subtypes of the myeloid and lymphoid lineages. Long term reconstituting HSCs are necessary to replace these differentiated cells after losses caused by normal degradation or damage accumulation, with failure to replenish these stores being linked to a variety of human pathogen

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Björkman, Andrea, Per Qvist, Likun Du, et al. "Aberrant recombination and repair during immunoglobulin class switching in BRCA1-deficient human B cells." Proceedings of the National Academy of Sciences 112, no. 7 (2015): 2157–62. http://dx.doi.org/10.1073/pnas.1418947112.

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Breast cancer type 1 susceptibility protein (BRCA1) has a multitude of functions that contribute to genome integrity and tumor suppression. Its participation in the repair of DNA double-strand breaks (DSBs) during homologous recombination (HR) is well recognized, whereas its involvement in the second major DSB repair pathway, nonhomologous end-joining (NHEJ), remains controversial. Here we have studied the role of BRCA1 in the repair of DSBs in switch (S) regions during immunoglobulin class switch recombination, a physiological, deletion/recombination process that relies on the classical NHEJ

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Kearsey, Stephen E., Abigail L. Stevenson, Takashi Toda, and Shao-Win Wang. "Fission Yeast Cut8 Is Required for the Repair of DNA Double-Strand Breaks, Ribosomal DNA Maintenance, and Cell Survival in the Absence of Rqh1 Helicase." Molecular and Cellular Biology 27, no. 5 (2006): 1558–67. http://dx.doi.org/10.1128/mcb.01495-06.

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ABSTRACT Schizosaccharomyces pombe Rqh1 is a member of the RecQ DNA helicase family. Members of this protein family are mutated in cancer predisposition diseases, causing Bloom's, Werner, and Rothmund-Thomson syndromes. Rqh1 forms a complex with topoisomerase III and is proposed to process or disrupt aberrant recombination structures that arise during S phase to allow proper chromosome segregation during mitosis. Intriguingly, in the absence of Rqh1, processing of these structures appears to be dependent on Rad3 (human ATR) in a manner that is distinct from its role in checkpoint control. Here

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Yang, Xuejing, Yedan Lu, Fuhong He та ін. "Benzene metabolite hydroquinone promotes DNA homologous recombination repair via the NF-κB pathway". Carcinogenesis 40, № 8 (2019): 1021–30. http://dx.doi.org/10.1093/carcin/bgy157.

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Abstract Benzene, a widespread environmental pollutant, induces DNA double-strand breaks (DSBs) and DNA repair, which may further lead to oncogenic mutations, chromosomal rearrangements and leukemogenesis. However, the molecular mechanisms underlying benzene-induced DNA repair and carcinogenesis remain unclear. The human osteosarcoma cell line (U2OS/DR-GFP), which carries a GFP-based homologous recombination (HR) repair reporter, was treated with hydroquinone, one of the major benzene metabolites, to identify the potential effects of benzene on DSB HR repair. RNA-sequencing was further employe

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Mladenov, Emil, Katja Paul-Konietzko, Veronika Mladenova, Martin Stuschke, and George Iliakis. "Increased Gene Targeting in Hyper-Recombinogenic LymphoBlastoid Cell Lines Leaves Unchanged DSB Processing by Homologous Recombination." International Journal of Molecular Sciences 23, no. 16 (2022): 9180. http://dx.doi.org/10.3390/ijms23169180.

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In the cells of higher eukaryotes, sophisticated mechanisms have evolved to repair DNA double-strand breaks (DSBs). Classical nonhomologous end joining (c-NHEJ), homologous recombination (HR), alternative end joining (alt-EJ) and single-strand annealing (SSA) exploit distinct principles to repair DSBs throughout the cell cycle, resulting in repair outcomes of different fidelity. In addition to their functions in DSB repair, the same repair pathways determine how cells integrate foreign DNA or rearrange their genetic information. As a consequence, random integration of DNA fragments is dominant

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Mukherjee, Shibani, Debapriya Sinha, Souparno Bhattacharya, Kalayarasan Srinivasan, Salim Abdisalaam, and Aroumougame Asaithamby. "Werner Syndrome Protein and DNA Replication." International Journal of Molecular Sciences 19, no. 11 (2018): 3442. http://dx.doi.org/10.3390/ijms19113442.

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Werner Syndrome (WS) is an autosomal recessive disorder characterized by the premature development of aging features. Individuals with WS also have a greater predisposition to rare cancers that are mesenchymal in origin. Werner Syndrome Protein (WRN), the protein mutated in WS, is unique among RecQ family proteins in that it possesses exonuclease and 3′ to 5′ helicase activities. WRN forms dynamic sub-complexes with different factors involved in DNA replication, recombination and repair. WRN binding partners either facilitate its DNA metabolic activities or utilize it to execute their specific

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Sullivan, Meghan R., and Kara A. Bernstein. "RAD-ical New Insights into RAD51 Regulation." Genes 9, no. 12 (2018): 629. http://dx.doi.org/10.3390/genes9120629.

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The accurate repair of DNA is critical for genome stability and cancer prevention. DNA double-strand breaks are one of the most toxic lesions; however, they can be repaired using homologous recombination. Homologous recombination is a high-fidelity DNA repair pathway that uses a homologous template for repair. One central HR step is RAD51 nucleoprotein filament formation on the single-stranded DNA ends, which is a step required for the homology search and strand invasion steps of HR. RAD51 filament formation is tightly controlled by many positive and negative regulators, which are collectively

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Jain, Kanika, Elizabeth A. Wood, and Michael M. Cox. "The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ." PLOS Genetics 17, no. 12 (2021): e1009972. http://dx.doi.org/10.1371/journal.pgen.1009972.

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The RarA protein, homologous to human WRNIP1 and yeast MgsA, is a AAA+ ATPase and one of the most highly conserved DNA repair proteins. With an apparent role in the repair of stalled or collapsed replication forks, the molecular function of this protein family remains obscure. Here, we demonstrate that RarA acts in late stages of recombinational DNA repair of post-replication gaps. A deletion of most of the rarA gene, when paired with a deletion of ruvB or ruvC, produces a growth defect, a strong synergistic increase in sensitivity to DNA damaging agents, cell elongation, and an increase in SO

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Pisani, Francesca, Ettore Napolitano, Luisa Napolitano, and Silvia Onesti. "Molecular and Cellular Functions of the Warsaw Breakage Syndrome DNA Helicase DDX11." Genes 9, no. 11 (2018): 564. http://dx.doi.org/10.3390/genes9110564.

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DDX11/ChlR1 (Chl1 in yeast) is a DNA helicase involved in sister chromatid cohesion and in DNA repair pathways. The protein belongs to the family of the iron–sulphur cluster containing DNA helicases, whose deficiencies have been linked to a number of diseases affecting genome stability. Mutations of human DDX11 are indeed associated with the rare genetic disorder named Warsaw breakage syndrome, showing both chromosomal breakages and chromatid cohesion defects. Moreover, growing evidence of a potential role in oncogenesis further emphasizes the clinical relevance of DDX11. Here, we illustrate t

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