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https://www.readbyqxmd.com/read/29750271/ape1-deficiency-promotes-cellular-senescence-and-premature-aging-features
#1
Mengxia Li, Xiao Yang, Xianfeng Lu, Nan Dai, Shiheng Zhang, Yi Cheng, Lei Zhang, Yuxin Yang, Yie Liu, Zhenzhou Yang, Dong Wang, David M Wilson
Base excision repair (BER) handles many forms of endogenous DNA damage, and apurinic/apyrimidinic endonuclease 1 (APE1) is central to this process. Deletion of both alleles of APE1 (a.k.a. Apex1) in mice leads to embryonic lethality, and deficiency in cells can promote cell death. Unlike most other BER proteins, APE1 expression is inversely correlated with cellular senescence in primary human fibroblasts. Depletion of APE1 via shRNA induced senescence in normal human BJ fibroblasts, a phenotype that was not seen in counterpart cells expressing telomerase...
May 10, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29747595/the-search-for-a-melanoma-tailored-chemotherapy-in-the-new-era-of-personalized-therapy-a-phase-ii-study-of-chemo-modulating-temozolomide-followed-by-fotemustine-and-a-cooperative-study-of-goim-gruppo-oncologico-italia-meridionale
#2
Michele Guida, Stefania Tommasi, Sabino Strippoli, Maria Iole Natalicchio, Simona De Summa, Rosamaria Pinto, Antonio Cramarossa, Anna Albano, Salvatore Pisconti, Michele Aieta, Ruggiero Ridolfi, Amalia Azzariti, Gabriella Guida, Vito Lorusso, Giusepe Colucci
BACKGROUND: It is frequently asked whether chemotherapy can still play a role in metastatic melanoma considering the effectiveness of the available drugs today, including antiCTLA4/antiPD1 immunotherapy and antiBRAF/antiMEK inhibitors. However, only approximately half of patients respond to these drugs, and the majority progress after 6-11 months. Therefore, a need for other therapeutic options is still very much apparent. We report the first large trial of a sequential full dose of fotemustine (FM) preceded by a low dose of temozolomide (TMZ) as a chemo-modulator in order to inactivate the DNA repair action of O(6)-methylguanine DNA-methyltransferase (MGMT)...
May 10, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29747151/role-of-pon1-sod2-ogg1-xrcc1-and-xrcc4-polymorphisms-on-modulation-of-dna-damage-in-workers-occupationally-exposed-to-pesticides
#3
Vivian F Silva Kahl, Fernanda Rabaioli da Silva, Jodel da Silva Alves, Gabrieli Flesch da Silva, Juliana Picinini, Varinderpal Singh Dhillon, Michael Fenech, Melissa Rosa de Souza, Johnny F Dias, Claudia Telles de Souza, Mirian Salvador, Cátia Dos Santos Branco, Flávia Valadão Thiesen, Daniel Simon, Juliana da Silva
Tobacco farming has been proving to induce poor health outcomes in agricultural workers, genomic instability being the triggering one. This study evaluated influence of PON1 (paraoxonase 1), SOD2 (superoxide dismutase), OGG1 (8-oxoguanine glycosylase), XRCC1 (X-ray repair cross-complementing protein 1), and XRCC4 (X-ray repair cross-complementing protein 4) genes polymorphisms on DNA damage in 121 subjects occupationally exposed to pesticides mixtures and nicotine at tobacco fields and 121 non-exposed individuals...
May 7, 2018: Ecotoxicology and Environmental Safety
https://www.readbyqxmd.com/read/29741625/dna-repair-in-the-archaea-an-emerging-picture
#4
Malcolm F White, Thorsten Allers
There has long been a fascination in the DNA Repair pathways of archaea, for two main reasons. Firstly, many archaea inhabit extreme environments where the rate of physical damage to DNA is accelerated. These archaea might reasonably be expected to have particularly robust or novel DNA repair pathways to cope with this. Secondly, the archaea have long been understood to be a lineage distinct from the bacteria, and to share a close relationship with the eukarya, particularly in their information processing systems...
May 5, 2018: FEMS Microbiology Reviews
https://www.readbyqxmd.com/read/29737460/association-between-ogg1-s326c-cc-genotype-and-elevated-relapse-risk-in-acute-myeloid-leukemia
#5
Nanami Gotoh, Takayuki Saitoh, Noriyuki Takahashi, Tetsuhiro Kasamatsu, Yusuke Minato, Alkebsi Lobna, Tsukasa Oda, Takumi Hoshino, Toru Sakura, Hiroaki Shimizu, Makiko Takizawa, Hiroshi Handa, Akihiko Yokohama, Norifumi Tsukamoto, Hirokazu Murakami
Recent studies have shown that tumors of relapsed acute myeloid leukemia (AML) present additional genetic mutations compared to the primary tumors. The base excision repair (BER) pathway corrects oxidatively damaged mutagenic bases and plays an important role in maintaining genetic stability. The purpose of the present study was to investigate the relationship between BER functional polymorphisms and AML relapse. We focused on five major polymorphisms: OGG1 S326C, MUTYH Q324H, APE1 D148E, XRCC1 R194W, and XRCC1 R399Q...
May 8, 2018: International Journal of Hematology
https://www.readbyqxmd.com/read/29724592/potential-genetic-modifiers-of-disease-risk-and-age-at-onset-in-patients-with-frontotemporal-lobar-degeneration-and-grn-mutations-a-genome-wide-association-study
#6
Cyril Pottier, Xiaolai Zhou, Ralph B Perkerson, Matt Baker, Gregory D Jenkins, Daniel J Serie, Roberta Ghidoni, Luisa Benussi, Giuliano Binetti, Adolfo López de Munain, Miren Zulaica, Fermin Moreno, Isabelle Le Ber, Florence Pasquier, Didier Hannequin, Raquel Sánchez-Valle, Anna Antonell, Albert Lladó, Tammee M Parsons, NiCole A Finch, Elizabeth C Finger, Carol F Lippa, Edward D Huey, Manuela Neumann, Peter Heutink, Matthis Synofzik, Carlo Wilke, Robert A Rissman, Jaroslaw Slawek, Emilia Sitek, Peter Johannsen, Jørgen E Nielsen, Yingxue Ren, Marka van Blitterswijk, Mariely DeJesus-Hernandez, Elizabeth Christopher, Melissa E Murray, Kevin F Bieniek, Bret M Evers, Camilla Ferrari, Sara Rollinson, Anna Richardson, Elio Scarpini, Giorgio G Fumagalli, Alessandro Padovani, John Hardy, Parastoo Momeni, Raffaele Ferrari, Francesca Frangipane, Raffaele Maletta, Maria Anfossi, Maura Gallo, Leonard Petrucelli, EunRan Suh, Oscar L Lopez, Tsz H Wong, Jeroen G J van Rooij, Harro Seelaar, Simon Mead, Richard J Caselli, Eric M Reiman, Marwan Noel Sabbagh, Mads Kjolby, Anders Nykjaer, Anna M Karydas, Adam L Boxer, Lea T Grinberg, Jordan Grafman, Salvatore Spina, Adrian Oblak, M-Marsel Mesulam, Sandra Weintraub, Changiz Geula, John R Hodges, Olivier Piguet, William S Brooks, David J Irwin, John Q Trojanowski, Edward B Lee, Keith A Josephs, Joseph E Parisi, Nilüfer Ertekin-Taner, David S Knopman, Benedetta Nacmias, Irene Piaceri, Silvia Bagnoli, Sandro Sorbi, Marla Gearing, Jonathan Glass, Thomas G Beach, Sandra E Black, Mario Masellis, Ekaterina Rogaeva, Jean-Paul Vonsattel, Lawrence S Honig, Julia Kofler, Amalia C Bruni, Julie Snowden, David Mann, Stuart Pickering-Brown, Janine Diehl-Schmid, Juliane Winkelmann, Daniela Galimberti, Caroline Graff, Linn Öijerstedt, Claire Troakes, Safa Al-Sarraj, Carlos Cruchaga, Nigel J Cairns, Jonathan D Rohrer, Glenda M Halliday, John B Kwok, John C van Swieten, Charles L White, Bernardino Ghetti, Jill R Murell, Ian R A Mackenzie, Ging-Yuek R Hsiung, Barbara Borroni, Giacomina Rossi, Fabrizio Tagliavini, Zbigniew K Wszolek, Ronald C Petersen, Eileen H Bigio, Murray Grossman, Vivianna M Van Deerlin, William W Seeley, Bruce L Miller, Neill R Graff-Radford, Bradley F Boeve, Dennis W Dickson, Joanna M Biernacka, Rosa Rademakers
BACKGROUND: Loss-of-function mutations in GRN cause frontotemporal lobar degeneration (FTLD). Patients with GRN mutations present with a uniform subtype of TAR DNA-binding protein 43 (TDP-43) pathology at autopsy (FTLD-TDP type A); however, age at onset and clinical presentation are variable, even within families. We aimed to identify potential genetic modifiers of disease onset and disease risk in GRN mutation carriers. METHODS: The study was done in three stages: a discovery stage, a replication stage, and a meta-analysis of the discovery and replication data...
April 30, 2018: Lancet Neurology
https://www.readbyqxmd.com/read/29721771/oxidative-stress-stimulates-invasive-potential-in-rat-c6-and-human-u-87-mg-glioblastoma-cells-via-activation-and-cross-talk-between-pkm2-enpp2-and-ape1-enzymes
#7
Ravi P Cholia, Monisha Dhiman, Raj Kumar, Anil K Mantha
Maintaining genomic integrity is essential for cell survival and viability. Reactive oxygen species (ROS) overproduction results in oxidative stress leading to the genomic instability via generation of small base lesions in DNA and these unrepaired DNA damages lead to various cellular consequences including cancer. Recent data support the concept "oxidative stress is an indispensable participant in fostering proliferation, survival, and migration" in various cancer cell types including glioblastoma cells...
May 2, 2018: Metabolic Brain Disease
https://www.readbyqxmd.com/read/29717169/ung-1-and-apn-1-are-the-major-enzymes-to-efficiently-repair-5-hydroxymethyluracil-dna-lesions-in-c-elegans
#8
Arturo Papaluca, J Richard Wagner, H Uri Saragovi, Dindial Ramotar
In Caenorhabditis elegans, two DNA glycosylases, UNG-1 and NTH-1, and two AP endonucleases, APN-1 and EXO-3, have been characterized from the base-excision repair (BER) pathway that repairs oxidatively modified DNA bases. UNG-1 removes uracil, while NTH-1 can remove 5-hydroxymethyluracil (5-hmU), an oxidation product of thymine, as well as other lesions. Both APN-1 and EXO-3 can incise AP sites and remove 3'-blocking lesions at DNA single strand breaks, and only APN-1 possesses 3'- to 5'-exonulease and nucleotide incision repair activities...
May 1, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29717115/non-canonical-activation-of-dapk2-by-ampk-constitutes-a-new-pathway-linking-metabolic-stress-to-autophagy
#9
Ruth Shiloh, Yuval Gilad, Yaara Ber, Miriam Eisenstein, Dina Aweida, Shani Bialik, Shenhav Cohen, Adi Kimchi
Autophagy is an intracellular degradation process essential for adaptation to metabolic stress. DAPK2 is a calmodulin-regulated protein kinase, which has been implicated in autophagy regulation, though the mechanism is unclear. Here, we show that the central metabolic sensor, AMPK, phosphorylates DAPK2 at a critical site in the protein structure, between the catalytic and the calmodulin-binding domains. This phosphorylation activates DAPK2 by functionally mimicking calmodulin binding and mitigating an inhibitory autophosphorylation, providing a novel, alternative mechanism for DAPK2 activation during metabolic stress...
May 1, 2018: Nature Communications
https://www.readbyqxmd.com/read/29698889/acetylation-of-oxidized-base-repair-initiating-neil1-dna-glycosylase-required-for-chromatin-bound-repair-complex-formation-in-the-human-genome-increases-cellular-resistance-to-oxidative-stress
#10
Shiladitya Sengupta, Chunying Yang, Muralidhar L Hegde, Pavana M Hegde, Joy Mitra, Arvind Pandey, Arijit Dutta, Abdul Tayyeb Datarwala, Kishor K Bhakat, Sankar Mitra
Posttranslational modifications of DNA repair proteins have been linked to their function. However, it is not clear if posttranslational acetylation affects subcellular localization of these enzymes. Here, we show that the human DNA glycosylase NEIL1, which is involved in repair of both endo- and exogenously generated oxidized bases via the base excision repair (BER) pathway, is acetylated by histone acetyltransferase p300. Acetylation occurs predominantly at Lys residues 296, 297 and 298 located in NEIL1's disordered C-terminal domain...
April 17, 2018: DNA Repair
https://www.readbyqxmd.com/read/29668892/sumoylation-of-xrcc1-activated-by-poly-adp-ribosyl-ation-regulates-dna-repair
#11
Ling-Yueh Hu, Che-Chang Chang, Yen-Sung Huang, Wen-Cheng Chou, Ying-Mei Lin, Chun-Chen Ho, Wei-Ting Chen, Hsiu-Ming Shih, Chia-Ni Hsiung, Pei-Ei Wu, Chen-Yang Shen
XRCC1 is an essential scaffold protein for base excision repair (BER) and helps to maintain genomic stability. XRCC1 has been indicated as a substrate for small ubiquitin-like modifier modification (SUMOylation); however, how XRCC1 SUMOylation is regulated in cells and how SUMOylated XRCC1 regulates BER activity are not well understood. Here we show that SUMOylation of XRCC1 is regulated in cells under methyl-methanesulfonate (MMS) treatment and facilitates BER. Poly(ADP-ribose) polymerase 1 (PARP1) is activated by MMS immediately and synthesizes poly(ADP-ribose) (PAR), which in turn promotes recruitment of SUMO E3 TOPORS to XRCC1 and facilitates XRCC1 SUMOylation...
April 16, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29662639/polymorphisms-in-ber-genes-and-risk-of-breast-cancer-evidences-from-69-studies-with-33760-cases-and-33252-controls
#12
Lele Qiao, Xiaoshan Feng, Gongping Wang, Bo Zhou, Yantong Yang, Mengxiang Li
Recently, numerous studies have reported an association between single nucleotide polymorphisms in base-excision repair genes and the risk of developing breast cancer, however there is no consensus. The aim of this meta-analysis was to review and quantitatively assess the relationship between single nucleotide polymorphisms in base-excision repair genes and breast cancer risk. The results suggested that a mutation of T to G in rs1760944 may lead to a higher risk of developing breast cancer in the Mongoloid population, and G to A of rs25487 significantly reduced the risk of breast cancer in Mongoloid and Caucasoid populations...
March 23, 2018: Oncotarget
https://www.readbyqxmd.com/read/29660759/parp-inhibitors-in-breast-cancer-bringing-synthetic-lethality-to-the-bedside
#13
REVIEW
Anita A Turk, Kari B Wisinski
Individuals with breast and ovarian cancer susceptibility gene 1 (BRCA1) or BRCA2 germline mutations have a significantly increased lifetime risk for breast and ovarian cancers. BRCA-mutant cancer cells have abnormal homologous recombination (HR) repair of DNA. In these tumors, the base excision repair (BER) pathway is important for cell survival. The poly(adenosine diphosphate-ribose) polymerase (PARP) enzymes play a key role in BER, and PARP inhibitors are effective in causing cell death in BRCA-mutant cells while sparing normal cells-a concept called synthetic lethality...
April 16, 2018: Cancer
https://www.readbyqxmd.com/read/29643057/defective-base-excision-repair-of-oxidative-dna-damage-in-vascular-smooth-muscle-cells-promotes-atherosclerosis
#14
Aarti Shah, Kelly Gray, Nichola Figg, Alison Finigan, Lakshi Starks, Martin Bennett
Background -Atherosclerotic plaques demonstrate extensive accumulation of oxidative DNA damage, predominantly as 8-oxoguanine (8oxoG) lesions. 8oxoG is repaired by base excision repair (BER) enzymes; however, the mechanisms regulating 8oxoG accumulation in vascular smooth muscle cells (VSMCs) and its effects on their function and in atherosclerosis are unknown. Methods -We studied levels of 8oxoG and its regulatory enzymes in human atherosclerosis, the mechanisms regulating 8oxoG repair and the BER enzyme 8oxoG DNA glycosylase I (OGG1) in VSMCs in vitro, and the effects of reducing 8oxoG in VSMCs in atherosclerosis in ApoE-/- mice...
April 11, 2018: Circulation
https://www.readbyqxmd.com/read/29625008/study-of-the-lyase-activity-of-human-dna-polymerase-%C3%AE-using-analogues-of-the-intermediate-schiff-base-complex
#15
Sasha M Daskalova, Xiaoguang Bai, Sidney M Hecht
DNA polymerase β (Pol β) participates in mammalian base excision repair (BER). The enzyme has a two-domain architecture, reflecting its dual functionality. The polymerase activity, which replaces damaged nucleosides removed during an initial excision process, is within the C-terminal 31 kDa domain, while the N-terminal 8 kDa domain participates in a lyase function, working to remove a 5'-deoxyribose phosphate (5'-dRP) moiety from the damaged DNA substrate. The currently accepted mechanism of the lyase reaction involves a transient covalent enzyme‒DNA intermediate in the form of a Schiff base connecting Lys72 of the enzyme with the 5'-dRP moiety...
April 6, 2018: Biochemistry
https://www.readbyqxmd.com/read/29575156/the-overexpression-of-tcap1-endonuclease-confers-resistance-to-infective-trypanosoma-cruzi-trypomastigotes-against-oxidative-dna-damage
#16
Lucía Valenzuela, Soía Sepúlveda, Iván Ponce, Norbel Galanti, Gonzalo Cabrera
Trypanosoma cruzi, the causative agent of Chagas' disease survives to DNA damage generated by ROS/RNS inside to their different hosts. In recent eukaryotes, oxidative DNA damage is repaired mainly by the Base Excision Repair (BER) pathway, being essential the apurinic/apyrimidinic endonuclease activity. Using a pTREX-gfp vector, the nucleotide sequence that encodes T. cruzi AP endonuclease TcAP1 (orthologue of human APE1) and a putative TcAP1 dominant negative (TcAP1DN), were transfectedand expressed in T. cruzi epimastigotes...
March 25, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29547780/monitoring-base-excision-repair-in-chlamydomonas-reinhardtii-cell-extracts
#17
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
https://www.readbyqxmd.com/read/29536659/transcriptional-coupling-mfd-and-dna-damage-scanning-disa-coordinate-excision-repair-events-for-efficient-bacillus-subtilis-spore-outgrowth
#18
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
https://www.readbyqxmd.com/read/29524558/egfr-tki-induced-hsp70-degradation-and-ber-suppression-facilitate-the-occurrence-of-the-egfr-t790-m-resistant-mutation-in-lung-cancer-cells
#19
Xiang Cao, Yi Zhou, Hongfang Sun, Miao Xu, Xiaowen Bi, Zhihui Zhao, Binghui Shen, Fengyi Wan, Zhuan Hong, Lei Lan, Lan Luo, Zhigang Guo, Zhimin Yin
Non-small cell lung cancer (NSCLC) patients harboring EGFR-activating mutations initially respond to EGFR tyrosine kinase inhibitors (EGFR-TKIs) and have shown favorable outcomes. However, acquired drug resistance to EGFR-TKIs develops in almost all patients mainly due to the EGFR T790 M mutation. Here, we show that treatment with low-dose EGFR-TKI results in the emergence of the EGFR T790 M mutation and in the reduction of HSP70 protein levels in HCC827 cells. Erlotinib treatment inhibits HSP70 phosphorylation at tyrosine 41 and increases HSP70 ubiquitination, resulting in HSP70 degradation...
June 28, 2018: Cancer Letters
https://www.readbyqxmd.com/read/29522991/the-c-terminal-tail-of-the-neil1-dna-glycosylase-interacts-with-the-human-mitochondrial-single-stranded-dna-binding-protein
#20
Nidhi Sharma, Srinivas Chakravarthy, Matthew J Longley, William C Copeland, Aishwarya Prakash
The 16.5 kb mitochondrial genome is subjected to damage from reactive oxygen species (ROS) generated in the cell during normal cellular metabolism and external sources such as ionizing radiation and ultraviolet light. ROS cause harmful damage to DNA bases that could result in mutagenesis and various diseases, if not properly repaired. The base excision repair (BER) pathway is the primary pathway involved in maintaining the integrity of mtDNA. Several enzymes that partake in BER within the nucleus have also been identified in the mitochondria...
May 2018: DNA Repair
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