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nucleotide excision repair

Teresa Morales-Ruiz, Álvaro C Romero-Valenzuela, Vanessa M Vázquez-Grande, Teresa Roldán-Arjona, Rafael R Ariza, Dolores Córdoba-Cañero
Base excision repair (BER) is a major defense pathway against spontaneous DNA damage. This multistep process is initiated by DNA glycosylases that recognise and excise the damaged base, and proceeds by the concerted action of additional proteins that perform incision of the abasic site, gap filling and ligation. BER has been extensively studied in bacteria, yeasts and animals. Although knowledge of this pathway in land plants is increasing, there are no reports detecting BER in algae. We describe here an experimental in vitro system allowing the specific analysis of BER in the model alga Chlamydomonas reinhardtii...
March 5, 2018: DNA Repair
Zhen-Jian Zhuo, Wei Liu, Jiao Zhang, Jinhong Zhu, Ruizhong Zhang, Jue Tang, Tianyou Yang, Yan Zou, Jing He, Huimin Xia
Variations in nucleotide excision repair pathway genes may predispose to initiation of cancers. However, polymorphisms of ERCC1/XPF genes and neuroblastoma risk have not been investigated before. To evaluate the relevance of polymorphisms of ERCC1/XPF genes in influencing neuroblastoma susceptibility, we genotyped four polymorphisms in ERCC1/XPF genes using a Chinese population of 393 cases and 812 controls. The results showed that ERCC1 rs2298881 and rs11615 predisposed to enhanced neuroblastoma risk [CA vs...
March 7, 2018: EBioMedicine
Luz I Valenzuela-García, Víctor M Ayala-García, Ana G Regalado-García, Peter Setlow, Mario Pedraza-Reyes
The absence of base excision repair (BER) proteins involved in processing ROS-promoted genetic insults activates a DNA damage scanning (DisA)-dependent checkpoint event in outgrowing Bacillus subtilis spores. Here, we report that genetic disabling of transcription-coupled repair (TCR) or nucleotide excision repair (NER) pathways severely affected outgrowth of ΔdisA spores, and much more so than the effects of these mutations on log phase growth. This defect delayed the first division of spore's nucleoid suggesting that unrepaired lesions affected transcription and/or replication during outgrowth...
March 13, 2018: MicrobiologyOpen
Alex Pines, Madelon Dijk, Matthew Makowski, Elisabeth M Meulenbroek, Mischa G Vrouwe, Yana van der Weegen, Marijke Baltissen, Pim J French, Martin E van Royen, Martijn S Luijsterburg, Leon H Mullenders, Michiel Vermeulen, Wim Vermeulen, Navraj S Pannu, Haico van Attikum
Transcription-blocking DNA lesions are removed by transcription-coupled nucleotide excision repair (TC-NER) to preserve cell viability. TC-NER is triggered by the stalling of RNA polymerase II at DNA lesions, leading to the recruitment of TC-NER-specific factors such as the CSA-DDB1-CUL4A-RBX1 cullin-RING ubiquitin ligase complex (CRLCSA ). Despite its vital role in TC-NER, little is known about the regulation of the CRLCSA complex during TC-NER. Using conventional and cross-linking immunoprecipitations coupled to mass spectrometry, we uncover a stable interaction between CSA and the TRiC chaperonin...
March 12, 2018: Nature Communications
Peng Han, Hongliang Liu, Qiong Shi, Zhensheng Liu, Jesse D Troy, Walter T Lee, Jose P Zevallos, Guojun Li, Erich M Sturgis, Qingyi Wei
Squamous cell carcinoma of head and neck (SCCHN) is one of the most common malignancies worldwide, and nucleotide excision repair (NER) is involved in SCCHN susceptibility. In this analysis of 349 newly diagnosed SCCHN patients and 295 cancer-free controls, we investigated whether expression levels of eight core NER proteins were associated with risk of SCCHN. We quantified NER protein expression levels in cultured peripheral lymphocytes using a reverse-phase protein microarray. Compared with the controls, SCCHN patients had statistically significantly lower expression levels of ERCC3 and XPA (P = 0...
March 12, 2018: Molecular Carcinogenesis
Kalyani Khanra, Indranil Choudhuri, Nandan Bhattacharyya
Background: DNA polymerase β (pol β) is a key enzyme of base excision repair pathway. It is a 1-kb gene consisting of 14 exons. Its catalytic part lies between exon 8 and exon 14. Exon 12 has a role in deoxyribonucleotide triphosphate selection for nucleotide transferase activity. Methods: Genomic DNA was isolated from ovarian carcinoma samples. Single strand conformation polymorphism method was used to detect mutation in genomic DNA. Results: Twenty-four patients of the 152 pair of tumor samples (15...
March 10, 2018: Iranian Biomedical Journal
Kang-Yi Su, Liang-In Lin, Steven D Goodman, Rong-Syuan Yen, Cho-Yuan Wu, Wei-Chen Chang, Ya-Chien Yang, Wern-Cherng Cheng, Woei-Horng Fang
Deamination of adenine can occur spontaneously under physiological conditions to generate the highly mutagenic lesion, deoxyinosine (hypoxanthine deoxyribonucleotide, dI). In DNA, dI preferably pairs with cytosine rather than thymine and results in A:T to G:C transition mutations after DNA replication. The deamination of adenine is enhanced by ROS from exposure of DNA to ionizing radiation, UV light, nitrous acid, or heat. In Escherichia coli, dI repair is initiated by endonuclease V (endo V; nfi gene product) nicking but a complete repair mechanism has yet to be elucidated...
February 17, 2018: DNA Repair
Masoud Najafi, Mohsen Cheki, Saeed Rezapoor, Ghazale Geraily, Elahe Motevaseli, Carla Carnovale, Emilio Clementi, Alireza Shirazi
The diabetes drug metformin can mitigate the genotoxic effects of cytotoxic agents and has been proposed to prevent or even cure certain cancers. Metformin reduces DNA damage by mechanisms that are only incompletely understood. Metformin scavenges free radicals, including reactive oxygen species and nitric oxide, which are produced by genotoxicants such as ionizing or non-ionizing radiation, heavy metals, and chemotherapeutic agents. The drug may also increase the activities of antioxidant enzymes and inhibit NADPH oxidase, cyclooxygenase-2, and inducible nitric oxide synthase, thereby limiting macrophage recruitment and inflammatory responses...
March 2018: Mutation Research
Shalaka Chitale, Holger Richly
The integrity of the genome is maintained by specific DNA repair pathways. The main pathway removing DNA lesions induced by exposure to UV light is nucleotide excision repair (NER). The DNA damage response at chromatin is accompanied by the recruitment of DNA repair factors to the lesion site and the deposition of specific histone marks. The function of these histone marks in NER stays for the most part elusive. We have recently reported that the methyltransferase MMSET catalyzes the dimethylation of histone H4 at lysine 20 (H4K20me2) at the lesion site...
February 26, 2018: Nucleus
Helge Leander B Jensen, Meryl S Lillenes, Alberto Rabano, Clara-Cecilie Günther, Tahira Riaz, Shewit T Kalayou, Ingun D Ulstein, Thomas Bøhmer, Tone Tønjum
Age-related changes are increased in patients with Alzheimer's disease (AD), including oxidative stress and DNA damage. We propose that genotoxic stress and DNA repair responses influence neurodegeneration in the pathogenesis of AD. Here, we focus on nucleotide excision repair (NER). Real-time qPCR and mass spectrometry were employed to determine the expression levels of selected NER components. The mRNA levels of the genes encoding the NER proteins RAD23B, RPA1, ERCC1, PCNA and LIG3 as well as the NER-interacting base excision repair protein MPG in blood and brain tissue from four brain regions in patients with AD or mild cognitive impairment and healthy controls (HC), were assessed...
February 21, 2018: Neuroscience Letters
John A Burns, Moinuddin A Chowdhury, Laura Cartularo, Christian Berens, David A Scicchitano
Simple sequence repeats (SSRs) are found throughout the genome, and under some conditions can change in length over time. Germline and somatic expansions of trinucleotide repeats are associated with a series of severely disabling illnesses, including Huntington's disease. The underlying mechanisms that effect SSR expansions and contractions have been experimentally elusive, but models suggesting a role for DNA repair have been proposed, in particular the involvement of transcription-coupled nucleotide excision repair (TCNER) that removes transcription-blocking DNA damage from the transcribed strand of actively expressed genes...
February 21, 2018: Nucleic Acids Research
Larissa Alexsandra da Silva Neto Trajano, Luiz Philippe da Silva Sergio, Ana Carolina Stumbo, Andre Luiz Mencalha, Adenilson de Souza da Fonseca
Exposure of cells to genotoxic agents causes modifications in DNA, resulting to alterations in the genome. To reduce genomic instability, cells have DNA damage responses in which DNA repair proteins remove these lesions. Excessive free radicals cause DNA damages, repaired by base excision repair and nucleotide excision repair pathways. When non-oxidative lesions occur, genomic stability is maintained through checkpoints in which the cell cycle stops and DNA repair occurs. Telomere shortening is related to the development of various diseases, such as cancer...
February 10, 2018: Journal of Photochemistry and Photobiology. B, Biology
Marie-Catherine Drigeard Desgarnier, Patrick J Rochette
Absorption of solar ultraviolet (UV) radiation by DNA leads to the formation of the highly mutagenic cyclobutane pyrimidine dimer (CPD). The mutagenicity of CPD is caused, in part, by the fact that their recognition and repair by the nucleotide excision repair (NER) pathway is challenging and slow. It has been previously shown that a pre-stimulation with genotoxic agents improve NER efficiency of CPD, indicating a potential adaptive response of this repair pathway. We have pre-treated human dermal fibroblasts with repeated subletal low doses of UVB (chronic low-dose of UVB; CLUV) to determine whether it could enhance NER capacity to repair CPD...
March 2018: DNA Repair
Yongqing Liu, Chunwen Yue, Juan Li, Jing Wu, Shikang Wang, Deqing Sun, Yanxia Guo, Zhaomin Lin, Denglu Zhang, Rongmei Wang
Retigeric acid B (RAB), a natural compound isolated from lichen, has been demonstrated to inhibit cell growth and promote apoptosis in prostate cancer (PCa) cells. The present study evaluated the function of RAB combined with clinical chemotherapeutic drugs in PCa cell lines by MTT assay, reverse transcription quantitative polymerase chain reaction and western blot analysis, and identified that RAB at low doses produced significant synergistic cytotoxicity in combination with cisplatin (CDDP); however, no marked synergism between RAB and the other chemotherapeutics was observed...
March 2018: Oncology Letters
Liang Sang, Zhi Lv, Li-Ping Sun, Qian Xu, Yuan Yuan
AIM: To investigate the interactions of the DNA repair gene excision repair cross complementing group 5 (ERCC5) and the metabolic gene glutathione S-transferase pi 1 (GSTP1) and their effects on atrophic gastritis (AG) and gastric cancer (GC) risk. METHODS: Seven ERCC5 single nucleotide polymorphisms (SNPs) (rs1047768, rs2094258, rs2228959, rs4150291, rs4150383, rs751402, and rs873601) and GSTP1 SNP rs1695 were detected using the Sequenom MassARRAY platform in 450 GC patients, 634 AG cases, and 621 healthy control subjects in a Chinese population...
February 7, 2018: World Journal of Gastroenterology: WJG
Yunes Panahi, Amir Fattahi, Hamid Reza Nejabati, Sina Abroon, Zeinab Latifi, Abolfazl Akbarzadeh, Tohid Ghasemnejad
Sulfur mustard (SM) is an alkylating agent that causes severe damages to the skin, eyes, and the respiratory system. DNA alkylation is one of the most critical lesions that could lead to monoadducts and cross-links, as well as DNA strand breaks. In response to these adducts, cells initiate a series of reactions to recruit specific DNA repair pathways. The main DNA repair pathways in human cells, which could be involved in the DNA SM-induced DNA damages, are base excision repair (BER), nucleotide excision repair (NER), homologous recombination (HR) and non-homologous end joining (NHEJ)...
February 2, 2018: Environmental Toxicology and Pharmacology
Alessandra Allione, Barbara Pardini, Clara Viberti, Marco Oderda, Marco Allasia, Paolo Gontero, Paolo Vineis, Carlotta Sacerdote, Giuseppe Matullo
BACKGROUND: Bladder cancer (BC) is one of the most aggressive malignancies of the urinary tract, with the highest lifetime treatment costs per patient of all cancers, due to the high rate of recurrences requiring continuous surveillance. An early diagnosis is essential to improve survival of patients with BC. Noninvasive and sensitive molecular biomarkers are needed to improve current strategies for the detection and monitoring of BC. Previous studies suggested that elevated DNA damage levels and suboptimal nucleotide excision DNA repair (NER) may be associated with BC...
February 6, 2018: Urologic Oncology
Luiz Philippe S Sergio, Leda M F Lucinda, Maycon M Reboredo, Flavia de Paoli, Lídia M C Fonseca, Bruno V Pinheiro, Andre L Mencalha, Adenilson S Fonseca
Purpose/Aim of the study: Patients suffering from chronic obstructive pulmonary disease (COPD) in association with acute respiratory distress syndrome (ARDS) present oxidative stress in lung cells, with production of free radicals and DNA lesions in pulmonary and adjacent cells. Once the DNA molecule is damaged, a set of enzymatic mechanisms are trigged to preserve genetic code integrity and cellular homeostasis. These enzymatic mechanisms include the base and the nucleotide excision repair pathways, as well as telomere regulation...
February 8, 2018: Experimental Lung Research
Janin Lehmann, Steffen Schubert, Christina Seebode, Antje Apel, Andreas Ohlenbusch, Steffen Emmert
The two endonucleases XPF and XPG are essentially involved in nucleotide excision repair (NER) and interstrand crosslink (ICL) repair. Defects in these two proteins result in severe diseases like xeroderma pigmentosum (XP). We applied our newly CRISPR/Cas9 generated human XPF knockout cell line with complete loss of XPF and primary fibroblasts from an XP-G patient (XP20BE) to analyze until now uncharacterized spontaneous mRNA splice variants of these two endonucleases. Functional analyses of these variants were performed using luciferase-based reporter gene assays...
January 2, 2018: Oncotarget
Ewelina Zarakowska, Jolanta Czerwinska, Agnieszka Tupalska, Matt J Yousefzadeh, Siobhán Q Gregg, Claudette M St Croix, Laura J Niedernhofer, Marek Foksinski, Daniel Gackowski, Anna Szpila, Marta Starczak, Barbara Tudek, Ryszard Olinski
5-Hydroxymethylcytosine and 5-formylcytosine are stable DNA base modifications generated from 5-methylcytosine by the ten-eleven translocation protein family that function as epigenetic markers. 5-Hydroxymethyluracil may also be generated from thymine by ten-eleven translocation enzymes. Here, we asked if these epigenetic changes accumulate in senescent cells, since they are thought to be inversely correlated with proliferation. Testing this in ERCC1-XPF-deficient cells and mice also enabled discovery if these DNA base changes are repaired by nucleotide excision repair...
February 3, 2018: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
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