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916 results for “DNA damage”
Nutritional Intervention and DNA Damage of Patients With HBOC
ClinicalTrials.gov study NCT05306002. IPD Sharing: NO. Countries: 1. Publications: 5.
Niraparib Before Surgery in Treating Patients With High Risk Localized Prostate Cancer and DNA Damage Response Defects
ClinicalTrials.gov study NCT04030559. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Trial of Niraparib in BAP1 and Other DNA Damage Response (DDR) Deficient Neoplasms (UF-STO-ETI-001)
ClinicalTrials.gov study NCT03207347. IPD Sharing: NO. Countries: 1. Publications: 1.
Data from: Attractive male sticklebacks carry more oxidative DNA damage in the soma and germline
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Data from: PITAR, a DNA damage-inducible Cancer/Testis long noncoding RNA, inactivates p53 by binding and stabilizing TRIM28 mRNA
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Data from: DNA damage signaling in Drosophila macrophages modulates systemic cytokine levels in response to oxidative stress
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Data from: Differences in RAD51 transcriptional response and cell cycle dynamics reveal varying sensitivity to DNA damage among Arabidopsis thaliana root cell types
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Data from: Evidence of centromeric histone 3 chaperone involved in DNA damage repair pathway in budding yeast
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Data from: Tissue-specific mutagenesis from endogenous guanine damage is suppressed by PolK and DNA repair
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Data from: Prolonged cell cycle arrest in response to DNA damage in yeast requires the maintenance of DNA damage signaling and the spindle assembly checkpoint
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Data from: Gal-1 promotes lung cancer cell survival by enhancing PARP1/H1.2 interaction to promote DNA repair upon DNA damage response
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Differential cytotoxicity induced by the titanium(IV)salan complex Tc52in G2-phase independent of DNA damage
<p>Chemotherapy is one of the major treatment modalities for cancer. Metal-based compounds such as derivatives of cisplatin are in the front line of therapy against a subset of cancers, but their use is restricted by severe side-effects and the induction of resistance in treated tumors. Subsequent research focused on development of cytotoxic metal-complexes without cross-resistance to cisplatin and reduced side-effects. This led to the discovery of first-generation titanium(IV)salan complexes, which reached clinical trials but lacked efficacy. New-generation titanium (IV)salan-complexes show promising anti-tumor activity in mice, but their molecular mechanism of cytotoxicity is completely unknown.</p> <p>4 different human cell lines were analyzed in their responses to a toxic (Tc52) and a structurally highly related but non-toxic (Tc53) titanium(IV)salan complex. Viability assays were used to reveal a suitable treatment range, flow-cytometry analysis was performed to monitor the impact of dosage and treatment time on cell-cycle distribution and cell death. Potential DNA strand break induction and crosslinking was investigated by immunostaining of damage markers as well as automated fluorometric analysis of DNA unwinding. Changes in nuclear morphology were analyzed by DAPI staining. Acidic beta-galactosidase activity together with morphological changes was monitored to detect cellular senescence. Western blotting was used to analyze induction of pro-apoptotic markers such as activated caspase7 and cleavage of PARP1, and general stress kinase p38.</p> <p>Here we show that the titanium(IV)salan Tc52 is effective in inducing cell death in the lower micromolar range. Surprisingly, Tc52 does not target DNA contrary to expectations deduced from the reported activity of other titanium complexes. Instead, Tc52 application interferes with progression from G2-phase into mitosis and induces apoptotic cell death in tested tumor cells. Contrarily, human fibroblasts undergo senescence in a time and dose-dependent manner. As deduced from fluorescence studies, the potential cellular target seems to be the cytoskeleton.</p> <p>In summary, we could demonstrate in four different human cell lines that tumor cells were specifically killed without induction of major cytotoxicity in non-tumorigenic cells. Absence of DNA damaging activity and the cell-cycle block in G2 instead of mitosis makes Tc52 an attractive compound for further investigations in cancer treatment.</p>
In-depth comparative toxicogenomics of glyphosate and Roundup herbicides: Histopathology, transcriptome and epigenome signatures, and DNA damage
<p><span><span><span><span><span><span><span><span><span><span><span>Whether or not glyphosate activates cellular mechanisms involved in carcinogenesis remains controversial. We tested whether glyphosate and three glyphosate-based commercial herbicide formulations activate mechanisms known to be key characteristics of carcinogens. The mammalian stem cell-based genotoxicity ToxTracker assay showed that the representative EU formulation Roundup MON 52276 and the UK formulation Roundup MON 76473, but not glyphosate and the US Roundup formulation MON 76207, activated oxidative stress and unfolded protein responses. High-throughput molecular profiling of liver function was performed in female Sprague-Dawley rats exposed to glyphosate or MON 52276 (both at 0.5, 50, 175 mg/kg bw/day glyphosate equivalent concentration) for 90 days. Histopathology and serum biochemistry analysis showed that MON 52276 but not glyphosate treatment increased hepatic steatosis and necrosis. MON 52276 and glyphosate altered the expression of genes in liver reflecting TP53 activation by DNA damage and the regulation of circadian rhythms. The most affected genes in liver also had their expression similarly altered in kidneys. Small RNA profiling in liver showed miR-22 and miR-17 had their levels decreased by MON 52276, while mir-30 levels were decreased, whilst miR-10 levels were increased by glyphosate. DNA methylation profiling of liver revealed 5,727 and 4,496 differentially methylated CpG sites between the control and glyphosate and MON 52276 exposed groups of animals respectively. Direct DNA damage measurement by apurinic/apyrimidinic lesion formation in liver was increased with glyphosate exposure. Altogether, our results show that Roundup herbicide formulations are causing more biological changes than glyphosate alone, activating mechanisms involved in cellular carcinogenesis.</span></span></span></span></span></span></span></span></span></span></span></p>
The 'dark matter' of protein variants carries a distinct DNA signature and predicts damaging variant effects
<p>Data generated for the manuscript "The 'dark matter' of protein variants carries a distinct DNA signature and predicts damaging variant effects".</p> <p> </p> <p>Please consult the README file for detailed description of data files included in this dataset.</p>
DNA damage and reticular stress in cytotoxicity and oncotic cell death of MCF-7 cells treated with fluopsin C
<p>DNA damage and reticular stress in cytotoxicity and oncotic cell death of MCF-7 cells treated with fluopsin C</p>
Data set releted to article "Pressure overload activates DNA-damage response in cardiac stromal cells"
<p>Repository data from a study on effects of pressure overload on DNA-damage activation in cardiac stromal cells</p>
Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas
<p>Supplementary data for Kazansky, Kentsis et al., "Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas."</p> <p>All files are labeled with their corresponding figure numbers.</p>
Histopathological, Oxidative Stress, and DNA Damage Assessment in the Vas Deferens Tissue of the Freshwater Leech Erpobdella johanssoni (Johansson, 1927) Following BTEX Exposure
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MADDD-seq, a novel massively parallel sequencing tool for simultaneous detection of DNA damage and mutations
<p>The file "data.tar" contains the output of the MADDD-seq pipepline. There is one sub-folder per sample. For each sample, the most important files are:</p> <ul> <li>max_variants_2.adduct.gtf : A GTF file with the location (and details) about each adduct called by the pipepline</li> <li>max_variants_2.DSC.vcf.gz : A VCF (Variant Call File) with information about mutations called.</li> <li>coverage.rds : pre-computed coverage information in binary format to be loaded in R.</li> </ul> <p>To analyze this data, use the following R files: adducts.R, mutations.R and jason-function-2022-04.R</p> <p> </p> <p>The file "kallisto-h5.tar" contains the output of running Kallisto on the regular RNAseq data (for expression level analysis). To analyze this data, use the following R files: Yeast-MNNG-MGT.Rmd and myDESeq2.R</p> <p> </p> <p>The source code of the R files will need to be modified to point at the location of files on the computer being used. These modifications are pointed by comments in the code and are located towards the start of each file.</p>
Eosinophilia and Leucocytic DNA damage
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.