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916 results for “DNA damage”
Data from: A significant component of ageing (DNA damage) is reflected in fading breeding colors: an experimental test using innate antioxidant mimetics in painted dragon lizards
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Data from: Increased sensitivity of DNA damage response-deficient cells to stimulated microgravity-induced DNA lesions
Microgravity is a major stress factor that astronauts have to face in space. In the past, the effects of microgravity on genomic DNA damage were studied, and it seems that the effect on genomic DNA depends on cell types and the length of exposure time to microgravity or simulated microgravity (SMG). In this study we used mouse embryonic stem (MES) and mouse embryonic fibroblast (MEF) cells to assess the effects of SMG on DNA lesions. To acquire the insight into potential mechanisms by which cells resist and/or adapt to SMG, we also included Rad9-deleted MES and Mdc1-deleted MEF cells in addition to wild type cells in this study. We observed significant SMG-induced DNA double strand breaks (DSBs) in Rad9-/- MES and Mdc1-/- MEF cells but not in their corresponding wild type cells. A similar pattern of DNA single strand break or modifications was also observed in Rad9-/- MES. As the exposure to SMG was prolonged, Rad9-/- MES cells adapted to the SMG disturbance by reducing the induced DNA lesions. The induced DNA lesions in Rad9-/- MES were due to SMG-induced reactive oxygen species (ROS). Interestingly, Mdc1-/- MEF cells were only partially adapted to the SMG disturbance. That is, the induced DNA lesions were reduced over time, but did not return to the control level while ROS returned to a control level. In addition, ROS was only partially responsible for the induced DNA lesions in Mdc1-/- MEF cells. Taken together, these data suggest that SMG is a weak genomic DNA stress and can aggravate genomic instability in cells with DNA damage response (DDR) defects.
Data from: Ribosomal RNA gene repeats associate with the nuclear pore complex for maintenance after DNA damage
The ribosomal RNA genes (rDNA) comprise a highly repetitive gene cluster. The copy number of genes at this locus can readily change and is therefore one of the most unstable regions of the genome. DNA damage in rDNA occurs after binding of the replication fork blocking protein Fob1 in S phase, which triggers unequal sister chromatid recombination. However, the precise mechanisms by which such DNA double-strand breaks (DSBs) are repaired is not well understood. Here, we demonstrate that the conserved protein kinase Tel1 maintains rDNA stability after replication fork arrest. We show that rDNA associates with nuclear pores, which is dependent on DNA damage checkpoint kinases Mec1/Tel1 and replisome component Tof1. These findings suggest that rDNA-nuclear pore association is due to a replication fork block and subsequent DSB. Indeed, quantitative microscopy revealed that rDNA is relocated to the nuclear periphery upon induction of a DSB. Finally, rDNA stability was reduced in strains where this association with the nuclear envelope was prevented, which suggests its importance for avoiding improper recombination repair that could induce repeat instability.
TSG101 Associates with PARP1 and is Essential for PARylation and DNA Damage-induced NF-κB Activation
<p>This dataset contains the raw luciferase assay data generated in the genome-wide siRNA screen.</p>
Figure 2 in Investigation of the effect of silymarin on oxidative DNA damage and inflammatory markers in ischemia/reperfusion injury following experimental testicular torsion/detorsion in rats
Figure 2. Testicular tissue, control group, negative Tnf-α expression (A). T 3 h / D 3 h group: very severe Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (B). T 3 h / D 24 h group: severe Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (C). T 3 h / D 3 h + silymarin group: medium level Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (D). T 3 h / D 24 h + silymarin group: mild Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (E). IHC-P, bar: 50 µm.
Figure 1 in Investigation of the effect of silymarin on oxidative DNA damage and inflammatory markers in ischemia/reperfusion injury following experimental testicular torsion/detorsion in rats
Figure 1. Testicular tissue, control group, normal histological view (A). T 3 h / D 3 h group: necrosis in spermatocytes (arrowheads); severe congestion in intertubular intervals (thick arrows); hemorrhage, thinning in the tubulus wall (B). T 3 h / D 24 h: necrosis in spermatocytes (arrowheads); severe edema in the intertubular space (stars); thinning of the tubulus wall (C). T 3 h / D 3 h + silymarin group: moderate edema in the intertubular intervals (star); congestion (thick arrow) (D). T 3 h / D 24 h + silymarin group: mild edema at intertubular intervals (star) (E); H and E, bar: 50 µm.
Figure 3 in Investigation of the effect of silymarin on oxidative DNA damage and inflammatory markers in ischemia/reperfusion injury following experimental testicular torsion/detorsion in rats
Figure 3. Testicular tissue, control group, negative 8-OHdG expression (A). T 3 h / D 3 h group: severe cytoplasmic 8-OHdG expression in spermatocytes (arrowheads) (B). T 3 h / D 24 h group: severe cytoplasmic 8-OHdG expression in spermatocytes (arrowheads) (C). T 3 h / D 3 h + silymarin group: moderate cytoplasmic 8-OHdG expression in spermatocytes (arrowheads) (D). T 3 h / D 24 h + silymarin group: mild cytoplasmic 8-OHdG expression in spermatocytes (E), IHC-P, bar: 50 µm.
Melanism protects alpine zooplankton from DNA damage caused by ultraviolet radiation
<p>Melanism is widely observed among animals, and is adaptive in various contexts for its thermoregulatory, camouflaging, mate-attraction, or photoprotective properties. Many organisms exposed to ultraviolet radiation show increased fitness resulting from melanin pigmentation; this has been assumed to result in part from reduced UV-induced damage to DNA. However, to effectively test the hypothesis that melanin pigmentation reduces UV-induced DNA damage requires quantification of UV-specific DNA damage lesions following UV exposure under controlled conditions using individuals that vary in pigmentation intensity. We accomplished this using alpine genotypes of the freshwater microcrustacean <i>Daphnia melanica </i>for which we quantified cyclobutane pyrimide dimers in DNA, a damage structure that can only be generated by UV exposure. For genotypes with carapace melanin pigmentation, we found that individuals with greater melanin content sustained lower levels of UV-induced DNA damage. Individuals with more melanin were also more likely to survive exposure to ecologically relevant levels of UV-B radiation. Parallel experiments with conspecific genotypes that lack carapace melanin pigmentation provide additional support for our conclusion that melanism protects individuals from UV-induced DNA damage. Finally, within-genotype comparisons with asexually-produced clonal siblings demonstrate that melanin content influences DNA damage even among genetically identical individuals raised in the same environment.</p>
Data from: The telomeric DNA damage response occurs in the absence of chromatin decompaction
Telomeres are specialized nucleoprotein structures that protect chromosome ends from DNA damage response (DDR) and DNA rearrangements. The telomeric shelterin protein TRF2 suppresses the DDR, and this function has been attributed to its abilities to trigger t-loop formation or prevent massive decompaction and loss of density of telomeric chromatin. Here, we applied stochastic optical reconstruction microscopy (STORM) to measure the sizes and shapes of functional human telomeres of different lengths and dysfunctional telomeres that elicit a DDR. Telomeres have an ovoid appearance with considerable plasticity in shape. Examination of many telomeres demonstrated that depletion of TRF2, TRF1, or both affected the sizes of only a small subset of telomeres. Costaining of telomeres with DDR markers further revealed that the majority of DDR signaling telomeres retained a normal size. Thus, DDR signaling at telomeres does not require decompaction. We propose that telomeres are monitored by the DDR machinery in the absence of telomere expansion and that the DDR is triggered by changes at the molecular level in structure and protein composition.
Figure 4 in Comparative analysis of the karyotype sensitivities of Apodemus flavicollis and laboratory mice to DNA-damaging agents
Figure 4. Pericentric inversions in bone marrow cell of A. flavicollis after Mitomycin C treatment.
Figure 2 in Comparative analysis of the karyotype sensitivities of Apodemus flavicollis and laboratory mice to DNA-damaging agents
Figure 2. Breaks and fragments in bone marrow cell of A. flavicollis after Mitomycin C treatment.
Segmentations of carcinogenic DNA damages in WSI
<p>The dataset includes patches from WSI images of the carcinogenic DNA damages caused by ultraviolet (UV) radiation on excised abdominal human skin, excised porcine skin and in vitro skin models with different melanin indices. Two predominant types of DNA damage are featured in this dataset: Cyclobutane pyrimidine dimers (CPD) and pyrimidine (6-4) pyrimidone photoproducts (6-4PP). The dataset spans 804 patches.</p> <p>A regression score, concerning the relative amount of damaged nuclei was annotated for all samples, segmentation maps were annotated for a subset of 202 samples. All files were anonymized and processed in accordance with the institutional guidelines and cannot be traced back to an individual person.</p>
The mitochondrial protease OMA1 acts as a metabolic safeguard upon nuclear DNA damage
<p>The provided Dataset contains the liquid-chromatography mass spectrometry (LC-MS) raw files (3 zipped files containing the Thermo .raw files) and one zipped file containing three tables extracted containing the peak information (Compound ID, expected RT (min), Filename, Injection Volume (uL), peak height, peak area, actual RT (min), RT Delta, formula, adduct, m/z (Expected), m/z (Apex), m/z (Delta in ppm) and S/N (signa-to-noise)) of the steady state and the 13C6 glucose-traced metabolite measurements for the above mentioned (see title) publication in Cell Reports.</p> <p>The data was measured using either anion-chromatography coupled to high resolution mass spectrometry (for anionic compounds, including intermediates from the TCA cycle, glycolysis, pentose phosphate pathway and nucleotides) or ultra high performance liquid chromatography coupled to high resolution mass spectrometry (amine-containing compounds, including amino acids and polyamines). The methods used for extracting and analyzing the samples are described in detail in the above mentioned publication. The data deposited here is shown in figure 7a and b and figure S7a, b and c.</p> <p> </p> <p> </p>
A Study Investigating DNA-damage Response Agents in Molecularly Altered Advanced Cancer
ClinicalTrials.gov study NCT04564027. IPD Sharing: YES. Countries: 3. Publications: 0.
Randomised Controlled Trial of an Antioxidant and Sunscreen Combination Cream for Reducing DNA Damage in Human Skin
ClinicalTrials.gov study NCT07301515. IPD Sharing: YES. Countries: 1. Publications: 0.
Trial of Olaparib in Patients With Metastatic Urothelial Cancer Harboring DNA Damage Response Gene Alterations
ClinicalTrials.gov study NCT03448718. IPD Sharing: NO. Countries: 1. Publications: 0.
Correlate BRCA1 Protein Expression With Response to DNA Damaging Chemotherapy
ClinicalTrials.gov study NCT01990352. IPD Sharing: Not stated. Countries: 1. Publications: 0.
RP-3500 and Olaparib in DNA Damage Repair Pathway Deficient Relapsed/Refractory Chronic Lymphocytic Leukemia
ClinicalTrials.gov study NCT05405309. IPD Sharing: NO. Countries: 1. Publications: 0.
Pembrolizumab in Metastatic Castration Resistant Prostate Cancer (mCRPC) With or Without DNA Damage Repair Defects
ClinicalTrials.gov study NCT03248570. IPD Sharing: NO. Countries: 1. Publications: 0.
Prevention of Oral DNA Damage by Black Raspberries
ClinicalTrials.gov study NCT04372914. IPD Sharing: NO. Countries: 1. Publications: 0.
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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.