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Relevant bibliographies by topics / Human DNA repair and recombination pathways

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Journal articles

Academic literature on the topic 'Human DNA repair and recombination pathways'

Author: Grafiati

Published: 14 March 2023

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

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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6

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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