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916 results for “DNA damage”
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor therapy reduces the level of DNA damage in patients with heterozygous familial hypercholesterolemia
<p><span><span>Heterozygous Familial Hypercholesterolaemia (HeFH) is a common autosomal dominant genetic disease (1:300) characterized by elevated LDL-C leading to premature atherosclerosis. Treatment with a PCSK9 inhibitor (iPCSK9) is recommended in high cardiovascular risk FH patients if the treatment goal is not achieved on maximal tolerated statin plus ezetimibe. </span></span><span>The aim of this study was to </span><span><span>examine the changes in DNA damage in HeFH patients associated with iPCSK9 use. </span></span><span>Fifty-seven patients were included: a normolipidemic group (control; n=20) and patients with HeFH (study group; n=36). DNA damage was determined by alkaline comet assay. PCSK9 protein level was assessed by ELISA. </span><span>The levels of Lp(a) in human serum were quantitatively turbidimetrically assay.</span><span> </span><span>PCSK9i treatment was associated with lower DNA damage, Lp(a), PCSK9 and lipid profile than before treatment. However, 20 of 36 patients still had Lp(a) values above 125 nmol/L, and reduced Lp(a) did not correlate with reduced DNA damage. Reduced PCSK9 moderately (r=0.48) correlates with reduced DNA damage</span><span><span>. PCSK9i therapy reduces the level of DNA damage in HeFH patients, regardless of the type of inhibitor. The reduction in DNA damage is not related to the changes in lipid profile or Lp(a) induced by PCSK9i, but it is dependent on PCSK9 level.</span></span></p>
Vertebrate DNA damage tolerance requires the C-terminus but not BRCT or transferase domains of REV1: Additional Files
<p>Additional information for Ross et al. (2005) Vertebrate DNA damage tolerance requires the C-terminus but not BRCT or transferase domains of REV1 published in Nucleic Acids Research Volume 33, Issue 4 doi:10.1093/nar/gki279, requested by an anonymous poster on PubPeer.</p> <p>A description of the individual files can be found in the README.txt file</p>
An Integrated Structural Model of the DNA Damage Responsive H3K4me3 Binding WDR76:SPIN1 Complex with the Nucleosome
<p>Serial Capture Affinity Purification (SCAP) is a powerful method to isolate a specific protein complex. When combined with cross linking mass spectrometry (XL-MS) and computational approaches one can build an integrated structural model of the isolated complex. Here, we applied SCAP to dissect a subpopulation of WDR76 in complex with SPIN1, a histone marker reader that specifically recognizes trimethylated histone H3 lysine4 (H3K4me3). In contrast to a previous SCAP analysis of the SPIN1:SPINDOC complex, histones and the H3K4me3 mark were copurified with the WDR76:SPIN1 complex. Next, interaction network analysis of copurifying proteins and microscopy analysis revealed a potential role of the WDR76:SPIN1 complex in the DNA damage response. Since we detected an extensive number of cross-linked sites were found between WDR76, SPIN1, and histones, we first built an integrated structural model of the complex which revealed that SPIN1 recognized the H3K4me3 epigenetic mark while interacting with WDR76. Finally, we then used the powerful Integrative Modeling Platform to build a structural model of WDR76 and SPIN1 bound to the nucleosome.</p>
METADATA for results of irradiation-induced complex DNA damage measurements using plasmid pBR322 along a typical Proton Treatment Plan at the MedAustron proton and carbon beam therapy facility (energy 137–198 MeV and Linear Energy Transfer (LET) range 1–9 keV/μm), by means of Agarose Gel Electrophoresis and DNA fragmentation using Atomic Force Microscopy (AFM)
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A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage - Fig. 4e
<p>The single-molecule FRET dataset underlying Fig. 4e of "A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage", DOI: 10.1039/C8SC00681D</p>
A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage - Fig. 4f
<p>The single-molecule FRET dataset underlying Fig. 4f of "A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage", DOI: 10.1039/C8SC00681D</p>
A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage - Fig. 4d
<p>The single-molecule FRET dataset underlying Fig. 4d of "A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage", DOI: 10.1039/C8SC00681D</p>
Figure 1 in DNA damage, oxidative stress, decreased viability and motility in common carp (Cyprinuscarpio L.) spermatozoa induced by tryptophan, phenylalanine and cysteine amino acids during short-term storage
Figure 1. Effect of tryptophan (T), phenylalanine (P), cysteine (C) at concentrations of 1, 5, 25, and 50 mM on DNA fragmentation of common carp (Cyprinuscarpio L.) spermatozoa at 6 (a), 24 (b), and 48 (c) h.
Expression quantitative trait loci influence DNA damage-induced apoptosis in cancer
<p><strong>Exposure expression quantitative trait loci (e2QTL)</strong></p> <p>The analysis of e2QTL allows for the identification of context-specific eQTL effects (Kim-Hellmuth et al. (2017), PMID: 28814792). To evaluate how inter-individual genetic variability influences the regulation of DNA damage-induced apoptosis, we performed e2QTL analysis of CD8+ T cells from 461 healthy European participants stimulated with high doses of 5 different carcinogens. These include Methyl-methanesulfonate (MMS), tert-butyl-hydroperoxide (TBOOH), benzo(a)pyrene-7,8-diol-9,10-epoxide (BPDE), 4-hydroxycyclophosphamide (HC) and UVC radiation.</p> <p><code>eQTL_DNA_damage_induced_apoptosis.csv:</code> eQTL data. FastQTL was used to analyze cis-eQTL within a 1 MB window of a gene’s transcription start site. Filtering and normalization of expression data was performed as described by the Genotype Tissue Expression (GTEx) project (The GTEx Consortium (2015), PMID: 25954001) including 60 PEER factors, top 3 genotype PCs and sex as covariates. Genotypes were filtered by PHWE > 10-6 and MAF > 5 %. Adjusted p-values were generated using 1,000 to 10,000 permutations. Variant IDs (CHR:POS:REF:ALT) are based on GRCh38.</p> <p><code>e2QTL_DNA_damage_induced_apoptosis.csv:</code> e2QTL data. The most significant variant for each analyzed gene was determined based on eQTL data to calculate e2QTL in a z-test that were corrected for multiple testing using Bonferroni correction as described by Kim-Hellmuth et al. (2017). Variant IDs (CHR:POS:REF:ALT) are based on GRCh38.</p> <p> </p>
Data for "Influences of Glyphosate Contaminations and Concentrate Feed on Performance, Blood Parameters, Blood Cell Functionality and DNA Damage Properties in Fattening Bulls"
<p>The deposited data consist of three data tables and three tables containing legends for the data:</p> <p><a href="https://zenodo.org/api/files/afb9373a-d44c-4441-ba97-052c0b6ec1b6/oneTimepoint.txt">oneTimepoint.txt</a> contains data from statistical tests within one timepoint; <a href="https://zenodo.org/api/files/afb9373a-d44c-4441-ba97-052c0b6ec1b6/oneTimepoint_legend.txt">oneTimepoint_legend.txt</a> contains the corresponding legend.</p> <p><a href="https://zenodo.org/api/files/afb9373a-d44c-4441-ba97-052c0b6ec1b6/threeTimepoints.txt">threeTimepoints.txt</a> contains data from statistical tests inclduing three distinct timepoints; <a href="https://zenodo.org/api/files/afb9373a-d44c-4441-ba97-052c0b6ec1b6/threeTimepoints_legend.txt">threeTimepoints_legend.txt</a> contains the corresponding legend.</p> <p><a href="https://zenodo.org/api/files/afb9373a-d44c-4441-ba97-052c0b6ec1b6/Performance.txt">Performance.txt</a> contains data from statistical tests inclduing two time periods in fattening; <a href="https://zenodo.org/api/files/afb9373a-d44c-4441-ba97-052c0b6ec1b6/Performance_legend.txt">Performance_legend.txt</a> contains the corresponding legend.</p>
Hybrid lizards with introgressed mtDNA show increased resistance to DNA damage from Reactive Oxygen Species
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Data from: Attractive male sticklebacks carry more oxidative DNA damage in the soma and germline
<p>Trade-offs between the expression of sexual signals and the maintenance of somatic and germline tissues are expected when these depend upon the same resources. Despite the importance of sperm DNA integrity, its trade-off with sexual signalling has rarely been explored. We experimentally tested the trade-off between carotenoid-based sexual colouration and oxidative DNA damage in skeletal muscle, testis and sperm by manipulating reproductive schedule (early <i>vs.</i> late onset of breeding) in male three-spined sticklebacks. Oxidative DNA damage was measured as the amount of 8-hydroxy-2-deoxy-Guanosine in genomic DNA. Irrespective of the experimentally manipulated reproductive schedule, individuals investing more in red colouration showed higher levels of oxidative DNA damage in muscle, testis and sperm during the peak breeding season. Our results show that the expression of red colouration traded off against the level of oxidative DNA damage possibly due to the competing functions of carotenoids as colorants and antioxidants. Thus, female sticklebacks may risk fertility and viability of offspring by choosing redder, more deteriorated partners with decreased sperm DNA integrity. The evolution of sexual signal may be constrained by oxidative DNA damage in the soma and germline. </p>
Distinct mobility patterns of BRCA2 molecules at DNA damage sites - source data
<p>This repository contains source data from the publication "Distinct mobility patterns of BRCA2 molecules at DNA damage sites"</p><p>- Source data of FRAP experiments. Text files contain time and intensity data of the individual FRAP curves including the normalized intensities as plotted in the figure.</p><p>- Source data for BRCA2 protein quantification </p><p>- dSTORM localization data</p><p>- Single-molecule tracks of BRCA2-Halo Mitomycin and untreated tracks. Original movies can be found here: http://doi.orig/10.5281/zenodo.10144073</p><p>For questions please contact Maarten Paul (m.w.paul [at] erasmusmc.nl</p>
Distinct mobility patterns of BRCA2 molecules at DNA damage sites v2
<p>This repository contains source data and processed data accompanied with the paper:</p><p>"Distinct mobility patterns of BRCA2 molecules at DNA damage sites"</p><p>The repository contains the following files:</p><p>single molecule tracking data of BRCA2-HaloTag (JF549) in mouse ES cells either untreated or Mitomycin C (MMC) treated cells. For details on the experimental conditions please check the methods section of the accompanying paper.</p><p>At http://doi.org/10.5281/zenodo.8143173 the corresponding tracking data can be found, among other source data of this study.</p><p>For questions please contact Maarten Paul (m.w.paul [at] erasmusmc.nl</p>
Replication stalling activates SSB for recruitment of DNA damage tolerance factors
<p>This repository contains four zipped folders with data and code related to this manuscript in the form of MATLAB files. The folders contain:</p> <ol> <li>By figure: plotted data organized by figure in the manuscript (as MATLAB workspaces, .mat files).</li> <li>Variables: plotted data organized by strain number and description (as MATLAB workspaces, .mat files).</li> <li>Functions: MATLAB functions needed to 1) integrate MicrobeTracker(1) cell segmentation analysis with u-track point source detection(2) and tracking(3) analysis and 2) perform subsequent processing of u-track analysis results (as MATLAB scripts, .m files)</li> <li>Scripts: MATLAB scripts needed to perform different types of data analysis (as MATLAB scripts, .m files). These scripts are organized by integration time (short vs. long exposure) and by type of analysis (radial distribution functional analysis, diffusion coefficient analysis, etc)</li> </ol>
Data from "Evaluating the Risk of Data Loss Due to Particle Radiation Damage in a DNA Data Storage System"
<p>Raw sequencing data from irradiated DNA samples and controls.<br>Sequences for encoded files used in the irradiation studies.<br>Please see the publication's Source Data file for mapping to encoded files.</p>
CO2 Protects Cells from Iron-Fenton Oxidative DNA Damage in E. coli and Humans
<p>Whereas hydroxyl radical is commonly named as the Fenton product responsible for DNA and RNA<br>damage in cells, here we demonstrate that the cellular reaction generates carbonate radical<br>anion due to physiological levels of bicarbonate. Analysis of the metabolome, the transcriptome,<br>and the human genome shows a consistent buffering of H2O2-induced oxidative<br>stress leading to one common pathway, namely guanine oxidation. Particularly revealing are nanopore-<br>based studies of direct RNA sequencing of cytosolic and mitochondrial ribosomal RNA along with<br>glycosylase-dependent qPCR studies of oxidative DNA damage in telomeres. The focusing of oxidative<br>modification on one pathway is consistent with the highly evolved base excision repair suite of enzymes<br>and their involvement in gene regulation in response to oxidative stress.</p>
Data files for CPD-DNA damage paper
<p>This contains the data files submitted by IIIT-H faculty and students from the CCNSB group regarding the work CPD-DNA Damage.</p>
To Assess Safety and Efficacy of Agents Targeting DNA Damage Repair With Olaparib Versus Olaparib Monotherapy.
ClinicalTrials.gov study NCT03330847. IPD Sharing: YES. Countries: 15. Publications: 1.
Olaparib in Treating Patients With Relapsed or Refractory Advanced Solid Tumors, Non-Hodgkin Lymphoma, or Histiocytic Disorders With Defects in DNA Damage Repair Genes (A Pediatric MATCH Treatment Tri
ClinicalTrials.gov study NCT03233204. IPD Sharing: UNDECIDED. Countries: 2. Publications: 2.
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International Brain Laboratory public data
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OpenNeuro
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