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BER pathway

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https://www.readbyqxmd.com/read/28199214/base-excision-repair-of-oxidative-dna-damage-from-mechanism-to-disease
#1
Amy M Whitaker, Matthew A Schaich, Mallory S Smith, Tony S Flynn, Bret D Freudenthal
Reactive oxygen species continuously assault the structure of DNA resulting in oxidation and fragmentation of the nucleobases. Both oxidative DNA damage itself and its repair mediate the progression of many prevalent human maladies. The major pathway tasked with removal of oxidative DNA damage, and hence maintaining genomic integrity, is base excision repair (BER). The aphorism that structure often dictates function has proven true, as numerous recent structural biology studies have aided in clarifying the molecular mechanisms used by key BER enzymes during the repair of damaged DNA...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28181292/tumor-associated-ape1-variant-exhibits-reduced-complementation-efficiency-but-does-not-promote-cancer-cell-phenotypes
#2
Jennifer L Illuzzi, Daniel R McNeill, Paul Bastian, Boris Brenerman, Robert Wersto, Helen R Russell, Fred Bunz, Peter J McKinnon, Kevin G Becker, David M Wilson
Base excision repair (BER) is the major pathway for coping with most forms of endogenous DNA damage, and defects in the process have been associated with carcinogenesis. Apurinic/apyrimidinic endonuclease 1 (APE1) is a central participant in BER, functioning as a critical endonuclease in the processing of noncoding abasic sites in DNA. Evidence has suggested that APE1 missense mutants, as well as altered expression or localization of the protein, can contribute to disease manifestation. We report herein that the tumor-associated APE1 variant, R237C, shows reduced complementation efficiency of the methyl methanesulfonate hypersensitivity and impaired cell growth exhibited by APE1-deficient mouse embryonic fibroblasts...
March 2017: Environmental and Molecular Mutagenesis
https://www.readbyqxmd.com/read/28161249/inhibitors-of-nuclease-and-redox-activity-of-apurinic-apyrimidinic-endonuclease-1-redox-effector-factor-1-ape1-ref-1-%C3%A2
#3
REVIEW
Sergey S Laev, Nariman F Salakhutdinov, Olga I Lavrik
Human apurinic/apyrimidinic endonuclease 1/redox effector factor 1 (APE1/Ref-1) is a multifunctional protein which is essential in the base excision repair (BER) pathway of DNA lesions caused by oxidation and alkylation. This protein hydrolyzes DNA adjacent to the 5'-end of an apurinic/apyrimidinic (AP) site to produce a nick with a 3'-hydroxyl group and a 5'-deoxyribose phosphate moiety or activates the DNA binding activity of certain transcription factors through its redox function. Studies have indicated a role for APE1/Ref-1 in the pathogenesis of cancer and in resistance to DNA-interactive drugs...
January 21, 2017: Bioorganic & Medicinal Chemistry
https://www.readbyqxmd.com/read/28129601/pluripotent-cells-display-enhanced-resistance-to-mutagenesis
#4
Daniel J Cooper, I-Chung Chen, Christine Hernandez, Yufeng Wang, Christi A Walter, John R McCarrey
Pluripotent cells have been reported to exhibit lower frequencies of point mutations and higher levels of DNA repair than differentiated cells. This predicts that pluripotent cells are less susceptible to mutagenic exposures than differentiated cells. To test this prediction, we used a lacI mutation-reporter transgene system to assess the frequency of point mutations in multiple lines of mouse pluripotent embryonic stem cells and induced pluripotent cells, as well as in multiple lines of differentiated fibroblast cells, before and after exposure to a moderate dose of the mutagen, methyl methanesulfonate...
January 6, 2017: Stem Cell Research
https://www.readbyqxmd.com/read/28129013/oxidative-dna-damage-and-reduced-expression-of-dna-repair-genes-role-in-primary-open-angle-glaucoma-poag
#5
Kuldeep Mohanty, Rima Dada, Tanuj Dada
BACKGROUND: Controversy exists regarding the role of oxidative DNA damage and DNA repair in primary open angle glaucoma (POAG). We performed a case control study to test the hypothesis that oxidative DNA damage and base excision repair (BER) genes PARP1 and OGG1 are involved in POAG pathogenesis. MATERIALS AND METHODS: The study included 116 POAG patients and 116 cataract patients as controls. The 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels were measured by ELISA...
January 27, 2017: Ophthalmic Genetics
https://www.readbyqxmd.com/read/28119421/dna-polymerase-%C3%AE-uses-its-lyase-domain-in-a-processive-search-for-dna-damage
#6
Michael J Howard, Yesenia Rodriguez, Samuel H Wilson
DNA polymerase (Pol) β maintains genome fidelity by catalyzing DNA synthesis and removal of a reactive DNA repair intermediate during base excision repair (BER). Situated within the middle of the BER pathway, Pol β must efficiently locate its substrates before damage is exacerbated. The mechanisms of damage search and location by Pol β are largely unknown, but are critical for understanding the fundamental features of the BER pathway. We developed a processive search assay to determine if Pol β has evolved a mechanism for efficient DNA damage location...
January 23, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28110804/differential-role-of-base-excision-repair-proteins-in-mediating-cisplatin-cytotoxicity
#7
Akshada Sawant, Ashley M Floyd, Mohan Dangeti, Wen Lei, Robert W Sobol, Steve M Patrick
Interstrand crosslinks (ICLs) are covalent lesions formed by cisplatin. The mechanism for the processing and removal of ICLs by DNA repair proteins involves nucleotide excision repair (NER), homologous recombination (HR) and fanconi anemia (FA) pathways. In this report, we monitored the processing of a flanking uracil adjacent to a cisplatin ICL by the proteins involved in the base excision repair (BER) pathway. Using a combination of extracts, purified proteins, inhibitors, functional assays and cell culture studies, we determined the specific BER proteins required for processing a DNA substrate with a uracil adjacent to a cisplatin ICL...
March 2017: DNA Repair
https://www.readbyqxmd.com/read/28098985/hmgb1-stimulates-activity-of-polymerase-%C3%AE-on-nucleosome-substrates
#8
Angela Balliano, Fanfan Hao, Catherine Njeri, Lata Balakrishnan, Jeffrey J Hayes
The process of base excision repair (BER) recognizes and repairs small lesions or inappropriate bases on DNA through either a short-patch or long-patch pathway. The enzymes involved in BER have been well-characterized on DNA substrates, and, somewhat surprisingly, many of these enzymes, including several DNA glycosylases, AP endonuclease (APE), FEN1 endonuclease, and DNA ligases, have been shown to have activity on DNA substrates within nucleosomes. DNA polymerase β (Pol β), however, exhibits drastically reduced or no activity on nucleosomal DNA...
January 18, 2017: Biochemistry
https://www.readbyqxmd.com/read/28087410/repair-of-8-oxog-a-mismatches-by-the-mutyh-glycosylase-mechanism-metals-and-medicine
#9
REVIEW
Douglas M Banda, Nicole N Nuñez, Michael A Burnside, Katie M Bradshaw, Sheila S David
Reactive oxygen and nitrogen species (RONS) may infringe on the passing of pristine genetic information by inducing DNA inter- and intra-strand crosslinks, protein-DNA crosslinks, and chemical alterations to the sugar or base moieties of DNA. 8-Oxo-7,8-dihydroguanine (8-oxoG) is one of the most prevalent DNA lesions formed by RONS and is repaired through the base excision repair (BER) pathway involving the DNA repair glycosylases OGG1 and MUTYH in eukaryotes. MUTYH removes adenine (A) from 8-oxoG:A mispairs, thus mitigating the potential of G:C to T:A transversion mutations from occurring in the genome...
January 10, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28067485/honokiol-inhibits-dna-polymerases-%C3%AE-and-%C3%AE-and-increases-bleomycin-sensitivity-of-human-cancer-cells
#10
A S Prakasha Gowda, Zucai Suo, Thomas E Spratt
A major concept to sensitize cancer cells to DNA damaging agents is by inhibiting proteins in the DNA repair pathways. X-family DNA polymerases play critical roles in both base excision repair (BER) and nonhomologous end joining (NHEJ). In this study, we examined the effectiveness of honokiol to inhibit human DNA polymerase β (pol β), which is involved in BER, and DNA polymerase λ (pol λ), which is involved in NHEJ. Kinetic analysis with purified polymerases showed that honokiol inhibited DNA polymerase activity...
February 20, 2017: Chemical Research in Toxicology
https://www.readbyqxmd.com/read/28067232/oxidized-nucleotide-insertion-by-pol-%C3%AE-confounds-ligation-during-base-excision-repair
#11
Melike Çağlayan, Julie K Horton, Da-Peng Dai, Donna F Stefanick, Samuel H Wilson
Oxidative stress in cells can lead to accumulation of reactive oxygen species and oxidation of DNA precursors. Oxidized purine nucleotides can be inserted into DNA during replication and repair. The main pathway for correcting oxidized bases in DNA is base excision repair (BER), and in vertebrates DNA polymerase β (pol β) provides gap filling and tailoring functions. Here we report that the DNA ligation step of BER is compromised after pol β insertion of oxidized purine nucleotides into the BER intermediate in vitro...
January 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28049757/smug2-dna-glycosylase-from-pedobacter-heparinus-as-a-new-subfamily-in-udg-superfamily
#12
Panjiao Pang, Ye Yang, Jing Li, Zhong Wang, Weiguo Cao, Wei Xie
Base deamination is a common type of DNA damage that occurs in all organisms. DNA repair mechanisms are essential to maintain genome integrity, in which the base excision repair (BER) pathway plays a major role in the removal of base damage. In the BER pathway, the uracil DNA glycosylase superfamily is responsible for excising the deaminated bases from DNA and generates apurinic/apyrimidinic (AP) sites. Using bioinformatics tools, we identified a family 3 SMUG1-like DNA glycoyslase from Pedobacter heparinus (named as Phe SMUG2), which display catalytic activities towards DNA containing uracil or hypoxanthine/xanthine...
January 3, 2017: Biochemical Journal
https://www.readbyqxmd.com/read/28040648/enhanced-degradation-of-azo-dye-by-a-stacked-microbial-fuel-cell-biofilm-electrode-reactor-coupled-system
#13
Xian Cao, Hui Wang, Xiao-Qi Li, Zhou Fang, Xian-Ning Li
In this study, a microbial fuel cell (MFC)-biofilm electrode reactor (BER) coupled system was established for degradation of the azo dye Reactive Brilliant Red X-3B. In this system, electrical energy generated by the MFC degrades the azo dye in the BER without the need for an external power supply, and the effluent from the BER was used as the inflow for the MFC, with further degradation. The results indicated that the X-3B removal efficiency was 29.87% higher using this coupled system than in a control group...
March 2017: Bioresource Technology
https://www.readbyqxmd.com/read/28039326/proximity-to-agct-sequences-dictates-mmr-independent-versus-mmr-dependent-mechanisms-for-aid-induced-mutation-via-ung2
#14
Eddy Sanchai Thientosapol, George Sharbeen, K K Edwin Lau, Daniel Bosnjak, Timothy Durack, Igor Stevanovski, Wolfgang Weninger, Christopher J Jolly
AID deaminates C to U in either strand of Ig genes, exclusively producing C:G/G:C to T:A/A:T transition mutations if U is left unrepaired. Error-prone processing by UNG2 or mismatch repair diversifies mutation, predominantly at C:G or A:T base pairs, respectively. Here, we show that transversions at C:G base pairs occur by two distinct processing pathways that are dictated by sequence context. Within and near AGCT mutation hotspots, transversion mutation at C:G was driven by UNG2 without requirement for mismatch repair...
December 29, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/28011149/chromatin-associated-mechanisms-in-base-excision-repair-nucleosome-remodeling-and-dna-transcription-two-key-players
#15
REVIEW
Hervé Menoni, Paolo Di Mascio, Jean Cadet, Stefan Dimitrov, Dimitar Angelov
Genomic DNA is prone to a large number of insults by a myriad of endogenous and exogenous agents. The base excision repair (BER) is the major mechanism used by cells for the removal of various DNA lesions spontaneously or environmentally induced and the maintenance of genome integrity. The presence of persistent DNA damage is not compatible with life, since abrogation of BER leads to early embryonic lethality in mice. There are several lines of evidences showing existence of a link between deficient BER, cancer proneness and ageing, thus illustrating the importance of this DNA repair pathway in human health...
December 20, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27994037/destabilization-of-the-pcna-trimer-mediated-by-its-interaction-with-the-neil1-dna-glycosylase
#16
Aishwarya Prakash, Kedar Moharana, Susan S Wallace, Sylvie Doublié
The base excision repair (BER) pathway repairs oxidized lesions in the DNA that result from reactive oxygen species generated in cells. If left unrepaired, these damaged DNA bases can disrupt cellular processes such as replication. NEIL1 is one of the 11 human DNA glycosylases that catalyze the first step of the BER pathway, i.e. recognition and excision of DNA lesions. NEIL1 interacts with essential replication proteins such as the ring-shaped homotrimeric proliferating cellular nuclear antigen (PCNA). We isolated a complex formed between NEIL1 and PCNA (±DNA) using size exclusion chromatography (SEC)...
December 19, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/27994014/human-ap-endonuclease-ape1-is-acetylated-at-dna-damage-sites-in-chromatin-and-acetylation-modulates-its-dna-repair-activity
#17
Shrabasti Roychoudhury, Somsubhra Nath, Heyu Song, Muralidhar L Hegde, Larry J Bellot, Anil K Mantha, Shiladitya Sengupta, Sutapa Ray, Amarnath Natarajan, Kishor K Bhakat
Apurinic/apyrimidinic (AP) sites, the most frequently formed DNA lesions in the genome, inhibit transcription and block replication. The primary enzyme to repair AP sites in mammalian cells is the AP endonuclease (APE1), which functions through the Base Excision Repair (BER) pathway. Although the mechanism by which APE1 repairs AP sites in vitro has been extensively investigated, it is largely unknown how APE1 repairs AP sites in cells. Here, we show that APE1 is acetylated (AcAPE1) after binding to the AP sites in chromatin and that AcAPE1 is exclusively present on chromatin throughout the cell cycle...
December 19, 2016: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/27974818/cadmium-ii-inhibition-of-human-uracil-dna-glycosylase-by-catalytic-water-supplantation
#18
Trevor Gokey, Bo Hang, Anton B Guliaev
Toxic metals are known to inhibit DNA repair but the underlying mechanisms of inhibition are still not fully understood. DNA repair enzymes such as human uracil-DNA glycosylase (hUNG) perform the initial step in the base excision repair (BER) pathway. In this work, we showed that cadmium [Cd(II)], a known human carcinogen, inhibited all activity of hUNG at 100 μM. Computational analyses based on 2 μs equilibrium, 1.6 μs steered molecular dynamics (SMD), and QM/MM MD determined that Cd(II) ions entered the enzyme active site and formed close contacts with both D145 and H148, effectively replacing the catalytic water normally found in this position...
December 15, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27932076/single-nucleotide-polymorphisms-in-dna-glycosylases-from-function-to-disease
#19
Mariarosaria D'Errico, Eleonora Parlanti, Barbara Pascucci, Paola Fortini, Sara Baccarini, Valeria Simonelli, Eugenia Dogliotti
Oxidative stress is associated with a growing number of diseases that span from cancer to neurodegeneration. Most oxidatively induced DNA base lesions are repaired by the base excision repair (BER) pathway which involves the action of various DNA glycosylases. There are numerous genome wide studies attempting to associate single-nucleotide polymorphisms (SNPs) with predispositions to various types of disease; often, these common variants do not have significant alterations in their biochemical function and do not exhibit a convincing phenotype...
December 6, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27909884/differential-role-of-wnt-signaling-and-base-excision-repair-pathways-in-gastric-adenocarcinoma-aggressiveness
#20
Alireza Korourian, Raheleh Roudi, Ahmad Shariftabrizi, Elham Kalantari, Kambiz Sotoodeh, Zahra Madjd
Aberrant activation of Wnt and base excision repair (BER) signaling pathways are implicated in tumor progression and chemotherapy resistance in gastric adenocarcinoma. This study was conducted to clarify the role of E2F6 and RhoA, components of the Wnt signaling pathway, and SMUG1, a component of the BER pathway in gastric adenocarcinoma. Expression levels and clinicopathological significance of three biomarkers, namely E2F6, RhoA, and SMUG1, as potential signaling molecules involved in tumorigenesis and aggressive behavior, were examined using tissue microarray...
December 1, 2016: Clinical and Experimental Medicine
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