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ataxia telangiectasia mutated

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https://www.readbyqxmd.com/read/29024033/impact-of-x-irradiation-on-microglia
#1
Franziska Menzel, Nicole Kaiser, Susann Haehnel, Felicitas Rapp, Ina Patties, Nina Schöneberg, Zhana Haimon, Kerstin Immig, Ingo Bechmann
Irradiation is widely used to treat brain tumors, and also to create bone marrow (BM) chimeras. BM chimeras are widely used to dissect functions and origin of microglia and blood-derived mononuclear cells under homeostatic or pathological conditions. This is facilitated by the fact that microglia survive irradiation and are thus regarded radio-resistant. In this study, we tested whether microglia are indeed radio-resistant and looked for potential mechanisms that might explain this phenomenon. We analyzed the radio-resistance of microglia independently of their physiological brain environment compared to other mononuclear cells from spleen and brain after X-irradiation with 7 Gy or 30 Gy...
October 10, 2017: Glia
https://www.readbyqxmd.com/read/29018054/the-induction-of-myeloma-cell-death-and-dna-damage-by-tetrac-a-thyroid-hormone-derivative
#2
Keren Cohen, Uri Abadi, Aleck Hercbergs, Paul J Davis, Martin Ellis, Osnat Ashur-Fabian
Multiple myeloma (MM) is a plasma cell malignancy in which involvement of the thyroid hormone-integrin αvβ3 pathway was shown and pharmacologic inhibition of this pathway is a rational approach to disease management. A thyroid hormone derivative, tetraiodothyroacetic acid (tetrac), which inhibits L-thyroxine (T4) and 3,5,3'-triiodo-L-thyronine (T3) binding to αvβ3 integrin, was studied in five MM cell lines and primary bone marrow (BM) MM cells. Tetrac inhibited MM cell proliferation (absolute cell number/viability) and induced caspase-dependent apoptosis (annexin-V/PI and cell cycle)...
October 10, 2017: Endocrine-related Cancer
https://www.readbyqxmd.com/read/28992350/radon-inhalation-induces-manganese-superoxide-dismutase-in-mouse-brain-via-nuclear-factor-%C3%AE%C2%BAb-activation
#3
Takahiro Kataoka, Reo Etani, Norie Kanzaki, Yusuke Kobashi, Yuto Yunoki, Tsuyoshi Ishida, Akihiro Sakoda, Yuu Ishimori, Kiyonori Yamaoka
Although radon inhalation increases superoxide dismutase (SOD) activities in mouse organs, the mechanisms and pathways have not yet been fully clarified. The aim of this study was to determine the details of SOD activation in mouse brain tissue following the inhalation of radon at concentrations of 500 or 2000 Bq/m3 for 24 h. After inhalation, brains were removed quickly for analysis. Radon inhalation increased the manganese (Mn)-SOD level and mitochondrial SOD activity. However, the differences were not significant...
September 4, 2017: Journal of Radiation Research
https://www.readbyqxmd.com/read/28981872/telomere-length-atm-mutation-status-and-cancer-risk-in-ataxia-telangiectasia-families
#4
Anne-Laure Renault, Noura Mebirouk, Eve Cavaciuti, Dorothée Le Gal, Julie Lecarpentier, Catherine Dubois d'Enghien, Anthony Laugé, Marie-Gabrielle Dondon, Martine Labbé, Gaetan Lesca, Dominique Leroux, Laurence Gladieff, Claude Adenis, Laurence Faivre, Brigitte Gilbert-Dussardier, Alain Lortholary, Jean-Pierre Fricker, Karin Dahan, Jacques-Olivier Bay, Michel Longy, Bruno Buecher, Nicolas Janin, Hélène Zattara, Pascaline Berthet, Audrey Combès, Isabelle Coupier, Janet Hall, Dominique Stoppa-Lyonnet, Nadine Andrieu, Fabienne Lesueur
Recent studies have linked constitutive telomere length (TL) to aging-related diseases including cancer at different sites. ATM participates in the signaling of telomere erosion, and inherited mutations in ATM have been associated with increased risk of cancer, particularly breast cancer. The goal of this study was to investigate whether carriage of an ATM mutation and TL interplay to modify cancer risk in ataxia-telangiectasia (A-T) families.The study population consisted of 284 heterozygous ATM mutation carriers (HetAT) and 174 non-carriers (non-HetAT) from 103 A-T families...
July 21, 2017: Carcinogenesis
https://www.readbyqxmd.com/read/28979810/enhancing-chemotherapy-sensitivity-by-targeting-pcg-via-the-atm-p53-pathway
#5
Shu-Bin Gao, Kang-Li Li, Huan Qiu, Ling-Yu Zhu, Chang-Bao Pan, Yue Zhao, Shu-Hua Wei, Shu Shi, Guang-Hui Jin, Li-Xiang Xue
Histone modification and chromatin remodeling are important events in response to DNA damage, and Polycomb group (PcG) proteins, catalyzing H3K27 methylation, are involved. However, the biological function and mechanism of PcG in DNA damage are not fully understood. Additionally, downstream effectors in hepatocellular carcinoma (HCC) remain unclear. The present study investigated the biological and mechanistic roles of PcG in the DNA damage response induced by chemotherapeutic drugs in HCC. It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion...
2017: American Journal of Cancer Research
https://www.readbyqxmd.com/read/28977657/h2ax-facilitates-classical-non-homologous-end-joining-at-the-expense-of-limited-nucleotide-loss-at-repair-junctions
#6
Yi-Li Feng, Ji-Feng Xiang, Si-Cheng Liu, Tao Guo, Guo-Fang Yan, Ye Feng, Na Kong, Hao-Dan Li, Yang Huang, Hui Lin, Xiu-Jun Cai, An-Yong Xie
Phosphorylated histone H2AX, termed 'γH2AX', mediates the chromatin response to DNA double strand breaks (DSBs) in mammalian cells. H2AX deficiency increases the numbers of unrepaired DSBs and translocations, which are partly associated with defects in non-homologous end joining (NHEJ) and contributing to genomic instability in cancer. However, the role of γH2AX in NHEJ of general DSBs has yet to be clearly defined. Here, we showed that despite little effect on overall NHEJ efficiency, H2AX deficiency causes a surprising bias towards accurate NHEJ and shorter deletions in NHEJ products...
August 10, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28973861/ctcf-prevents-genomic-instability-by-promoting-homologous-recombination-directed-dna-double-strand-break-repair
#7
Fengchao Lang, Xin Li, Wenhai Zheng, Zhuoran Li, Danfeng Lu, Guijun Chen, Daohua Gong, Liping Yang, Jinlin Fu, Peng Shi, Jumin Zhou
CTCF is an essential epigenetic regulator mediating chromatin insulation, long-range regulatory interactions, and the organization of large topological domains in the nucleus. Phenotypes of CTCF haploinsufficient mutations in humans, knockout in mice, and depletion in cells are often consistent with impaired genome stability, but a role of CTCF in genome maintenance has not been fully investigated. Here, we report that CTCF maintains genome stability, is recruited to sites of DNA damage, and promotes homologous recombination repair of DNA double-strand breaks (DSBs)...
September 25, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28972393/aryl-hydrocarbon-receptor-suppresses-the-prostate-cancer-lncap-cell-growth-and-invasion-by-promoting-dna-damage-response-under-oxidative-stress
#8
Jing-Song Yu, Peng-Fei Leng, Yi-Fu Li, Yong-Quan Wang, Yan Wang, Rui-Hua An, Ji-Ping Qi
Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that interacts with multiple signaling pathways during prostate development. In the present study, LNCaP cells were knocked down of AhR by siRNA, or treated with the AhR agonist 3-methylcholanthrene (3MC). The effects of AhR on LNCaP cells and the associated mechanisms were studied both under normal condition and under hydrogen peroxide (H2O2)-induced oxidative stress. MTT, transwell chamber assays and flow cytometry were employed to investigate cell proliferation, invasion, and apoptosis, respectively, whereas the DNA damage response (DDR) signaling (phosphorylation of ataxia-telangiectasia mutated [ATM], check-point kinase 2 [Chk2], histone H2AX, p53, and cleaved poly-ADP-ribose polymerase [PARP]) was detected by western blotting...
October 3, 2017: DNA and Cell Biology
https://www.readbyqxmd.com/read/28968864/atm-activated-autotaxin-atx-propagates-inflammation-and-dna-damage-in-lung-epithelial-cells-a-new-mode-of-action-for-silica-induced-dna-damage
#9
Huiyuan Zheng, Johan Högberg, Ulla Stenius
Silica exposure is a common risk factor for lung cancer. It has been claimed that key elements in cancer development are activation of inflammatory cells that indirectly induce DNA damage and proliferative stimuli in respiratory epithelial cells. We studied DNA damage induced by silica particles in respiratory epithelial cells and focused the role of the signaling enzyme autotaxin (ATX). A549 and 16HBE lung epithelial cells were exposed silica particles. Reactive oxidative species (ROS), NLRP3 inflammasome activation, ATX, ataxia telangiectasia mutated (ATM), and DNA damage (γH2AX, pCHK1, pCHK2, comet assay) were endpoints...
September 15, 2017: Carcinogenesis
https://www.readbyqxmd.com/read/28962138/radioresistance-of-chordoma-cells-is-associated-with-the-atm-atr-pathway-in-which-rad51-serves-as-an-important-downstream-effector
#10
Chao Zhang, Bing Wang, Lei Li, Yawei Li, Pengzhi Li, Guohua Lv
Surgery followed by radiotherapy is the standard treatment for chordomas, which are a rare but low-grade type of bone cancer arising from remnants of the embryonic notochord. However, disease recurrence following radiotherapy is common, most likely due to endogenous DNA repair mechanisms that promote cell survival upon radiation strikes. The ataxia telangiectasia mutated/ataxia telangiectasia mutated and Rad3 related (ATM/ATR)-mediated pathway has a critical role in DNA repair mechanisms; however, it has rarely been investigated in chordomas...
September 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28959360/role-of-wild-type-p53-induced-phosphatase-1-in-cancer
#11
Zhi-Peng Wang, Ye Tian, Jun Lin
Wild-type p53-induced phosphatase (Wip1) is a member of the protein phosphatase type 2C family and is an established oncogene due to its dephosphorylation of several tumor suppressors and negative control of the DNA damage response system. It has been reported to dephosphorylate p53, ataxia telangiectasia mutated, checkpoint kinase 1 and p38 mitogen activated protein kinases, forming negative feedback loops to inhibit apoptosis and cell cycle arrest. Wip1 serves a major role in tumorigenesis, progression, invasion, distant metastasis and apoptosis in various types of human cancer...
October 2017: Oncology Letters
https://www.readbyqxmd.com/read/28952912/measurement-of-dna-dependent-protein-kinase-phosphorylation-using-flow-cytometry-provides-a-reliable-estimate-of-dna-repair-capacity
#12
Andris Abramenkovs, Bo Stenerlöw
Uncontrolled generation of DNA double-strand breaks (DSBs) in cells is regarded as a highly toxic event that threatens cell survival. Radiation-induced DNA DSBs are commonly measured by pulsed-field gel electrophoresis, microscopic evaluation of accumulating DNA damage response proteins (e.g., 53BP1 or γ-H2AX) or flow cytometric analysis of γ-H2AX. The advantage of flow cytometric analysis is that DSB formation and repair can be studied in relationship to cell cycle phase or expression of other proteins. However, γ-H2AX is not able to monitor repair kinetics within the first 60 min postirradiation, a period when most DSBs undergo repair...
September 27, 2017: Radiation Research
https://www.readbyqxmd.com/read/28929041/severe-late-toxicity-after-adjuvant-breast-radiotherapy-in-a-patient-with-a-germline-ataxia-telangiectasia-mutated-gene-future-treatment-decisions
#13
Maryam Dosani, Kasmintan A Schrader, Alan Nichol, Sophie Sun, Tamara Shenkier, Zoe Lohn, Gudrun Aubertin, Scott Tyldesley
Ataxia telangiectasia mutated (ATM) gene mutations may confer increased sensitivity to ionizing radiation and increased risk of late toxicity for cancer patients. We present the case of a 55-year-old female treated with adjuvant breast and regional nodal radiation following lumpectomy and axillary lymph node dissection for stage II invasive ductal carcinoma of the breast. She developed severe telangiectasia, fibrosis, induration, chest wall pain (with evidence of rib fractures on imaging), and painful limitation in her range of motion at the shoulder...
July 11, 2017: Curēus
https://www.readbyqxmd.com/read/28928376/oligo-fucoidan-prevents-il-6-and-ccl2-production-and-cooperates-with-p53-to-suppress-atm-signaling-and-tumor-progression
#14
Li-Mei Chen, Po-Yen Liu, Yen-An Chen, Hong-Yu Tseng, Pei-Chun Shen, Pai-An Hwang, Hsin-Ling Hsu
Low-molecular-weight Fucoidan (Oligo-Fucoidan) is a sulfated polysaccharide that has a variety of biological effects and has also been shown to have beneficial health effects. However, the molecular mechanisms underlying the therapeutic effects of Oligo-Fucoidan in patients with cancer remain unclear. Using human colorectal cancer HCT116 cells with (p53(+/+)) or without (p53(-/-)) normal p53 expression, we found that Oligo-Fucoidan treatment reduces the occurrence of spontaneous DNA lesions. Etoposide induces double strand DNA breaks...
September 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28916473/down-regulation-of-nox2-activity-in-phagocytes-mediated-by-atm-kinase-dependent-phosphorylation
#15
Sylvain Beaumel, Antoine Picciocchi, Franck Debeurme, Corinne Vivès, Anne-Marie Hesse, Myriam Ferro, Didier Grunwald, Heather Stieglitz, Pahk Thepchatri, Susan M E Smith, Franck Fieschi, Marie José Stasia
NADPH oxidases (NOX) have many biological roles, but their regulation to control production of potentially toxic ROS molecules remains unclear. A previously identified insertion sequence of 21 residues (called NIS) influences NOX activity, and its predicted flexibility makes it a good candidate for providing a dynamic switch controlling the NOX active site. We constructed NOX2 chimeras in which NIS had been deleted or exchanged with those from other NOXs (NIS1, 3 and 4). All contained functional heme and were expressed normally at the plasma membrane of differentiated PLB-985 cells...
September 13, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28898322/-new-mutation-in-atm-gen-in-patient-whith-ataxia-telangiectasia-clinical-case
#16
Felipe Ruiz-Botero, Juliet T Rodríguez-Guerrero
INTRODUCTION: The ataxia telangiectasia syndrome (AT) is a genetic disease with an autosomal recessive inheritance pattern, with multisystem involvement and a broad clinical spectrum. It is caused by the mutation of the ATM gene, causing reduction or absence of the ATM proteinkinase, altering processes in the cell cycle, DNA repair and apoptosis. The objective of this article is to report the case of a patient with ataxia telangiectasia syndrome, caused by a mutation not previously reported in the literature...
2017: Revista Chilena de Pediatría
https://www.readbyqxmd.com/read/28895705/-complete-heart-block-and-asystole-in-a-child-with-ataxia-telangiectasia
#17
Daniel Palanca Arias, Ariadna Ayerza Casas, Mercedes Domínguez Cajal, Marta López Ramón, Lorenzo Jiménez Montañés
Ataxia-telangiectasia is a disorder characterized by cerebellar ataxia, telangiectasia, immunodeficiency, and increased predisposition to cancer susceptibility. Mutations in the ataxia telangiectasia mutated gene seem to play an important role in normal cell function and in cardiovascular remodeling. We report a case of a 14-year-old boy with ataxia-telangiectasia and high-grade B-non-Hodgkin lymphoma who remained in continuous complete remission after chemotherapy and who was admitted into our Emergency Room presenting with episodes of presyncope...
October 1, 2017: Archivos Argentinos de Pediatría
https://www.readbyqxmd.com/read/28894253/atm-deficiency-increases-genomic-instability-and-metastatic-potential-in-a-mouse-model-of-pancreatic-cancer
#18
Yiannis Drosos, David Escobar, Ming-Yi Chiang, Kathryn Roys, Virginia Valentine, Marc B Valentine, Jerold E Rehg, Vaibhav Sahai, Lesa A Begley, Jianming Ye, Leena Paul, Peter J McKinnon, Beatriz Sosa-Pineda
Germline mutations in ATM (encoding the DNA-damage signaling kinase, ataxia-telangiectasia-mutated) increase Familial Pancreatic Cancer (FPC) susceptibility, and ATM somatic mutations have been identified in resected human pancreatic tumors. Here we investigated how Atm contributes to pancreatic cancer by deleting this gene in a murine model of the disease expressing oncogenic Kras (Kras(G12D)). We show that partial or total ATM deficiency cooperates with Kras(G12D) to promote highly metastatic pancreatic cancer...
September 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28894083/ataxia-telangiectasia-mutated-atm-protein-signaling-participates-in-development-of-pulmonary-arterial-hypertension-in-rats
#19
Fan Hu, Caijun Liu, Hanmin Liu, Liang Xie, Li Yu
BACKGROUND Previous studies revealed physiological and pathogenetic similarity between vascular smooth muscles cells with severe pulmonary arterial hypertension and tumors. The DNA damage response was found in both pulmonary arterial hypertension (PAH) cells and tumors. The ataxia-telangiectasia mutated proteins (ATM) pathway is considered an important factor in the DNA damage response of tumor formation, but its function in the development of PAH remains unknown. MATERIAL AND METHODS The Sprague-Dawley rat PAH model was established...
September 12, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28893936/take-your-pikk-tumour-viruses-and-dna-damage-response-pathways
#20
REVIEW
Neha J Pancholi, Alexander M Price, Matthew D Weitzman
Viruses regulate cellular processes to facilitate viral replication. Manipulation of nuclear proteins and pathways by nuclear replicating viruses often causes cellular genome instability that contributes to transformation. The cellular DNA damage response (DDR) safeguards the host to maintain genome integrity, but DNA tumour viruses can manipulate the DDR to promote viral propagation. In this review, we describe the interactions of DNA tumour viruses with the phosphatidylinositol 3-kinase-like protein kinase (PIKK) pathways, which are central regulatory arms of the DDR...
October 19, 2017: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
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