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548 results for “DNA repair”
Slimfield: Escherichia coli DNA repair proteins (RecA-mGFP and RecB-sfGFP)
<p>Imaging modality / instrument: <em>Brightfield</em> + <em>Slimfield</em></p> <p>Image format:<em> OME TIFF (16 bit) + MicroManager metadata files</em></p> <p>Microscope settings:</p> <p><em>488 nm triggered excitation; split detection, cropped to GFP or RFP/GFP (left/right) channels; 3 ms/frame laser exposure; Photometrics Prime95b CMOS</em></p> <p>Samples and acquisitions:</p> <p>Fluorescent fusions in live E.coli cells. MMC = mitomycin C</p> <table> <tbody> <tr> <td> <p>No. fields of view</p> </td> <td> <p>MMC-</p> </td> <td> <p>MMC+ (0.5 ug/ml 3h)</p> </td> </tr> <tr> <td> <p>RecA-mGFP</p> </td> <td> <p>7</p> </td> <td> <p>15</p> </td> </tr> <tr> <td> <p>RecB-sfGFP</p> </td> <td> <p>17</p> </td> <td> <p>21</p> </td> </tr> <tr> <td> <p>MG1655 control</p> </td> <td> <p>10</p> </td> <td> <p>10</p> </td> </tr> </tbody> </table> <p>Approx. size before/after compression: 21 GB / 7 GB</p>
Supplementary Data for the manuscript 'The Rad9-Rad1-Hus1 DNA repair clamp is found in Microsporidia'
<p>This dataset contains the supplementary data files for the manuscript titled 'The Rad9-Rad1-Hus1 DNA repair clamp is found in Microsporidia'.</p>
Phase I trial of CX-5461, a first-in-class G-quadruplex stabilizer in patients with advanced solid tumors enriched for DNA-repair deficiencies (CCTG IND.231) - Variant Calls
<p>Variant Calls from Phase I trial of CX-5461, a first-in-class G-quadruplex stabilizer in patients with advanced solid tumors enriched for DNA-repair deficiencies (CCTG IND.231)</p> <p>See publication for methodology.</p>
Data from: Seasonal brain regeneration and chromosome instability are linked to selection on DNA repair in Sorex araneus
Open the record for dataset details and reuse information.
Human DNA Cross-Link Repair 1A (DCLRE1A. SNM1A); A Target Enabling Package
<p>Cancer cells experience genomic instability, probably through a combination of excessive replicative activity and the loss of function of checkpoint and DNA repair pathways that may have contributed to the oncogenic transformation. Chemotherapy by DNA-damaging agents such as cisplatin and nitrogen mustards create DNA interstrand crosslinks (ICL), which can lead to double-strand breaks and cell death when the cells replicate their DNA. Genotoxic drugs are counteracted by the cell’s DNA damage response. Hence, it is expected that inhibiting DNA repair proteins would sensitise cells to chemotherapy.<br> Here we address an enzyme that participates in the repair of ICLs, DCLRE1A. The TEP includes expression clones and methods for producing the catalytic domain and high-throughput activity assays. Furthermore, we provide a crystallization system that generates thousands of reproducible crystals that allow soaking of small-molecule ligands. We provide crystal structures of several small molecule fragments and inhibitors, opening the way to development of more potent and selective inhibitors.</p>
Next-generation Sequencing Data Associated with "Genome Editing Outcomes Reveal Mycobacterial NucS Participates in a Short-Patch Repair of DNA Mismatches"
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Uncoupling of programmed DNA cleavage and repair jeopardizes the assembly of the Paramecium somatic genome
<p>In the ciliate <i>Paramecium</i>, the precise excision of numerous Internal Eliminated Sequences (IESs) from the somatic genome is essential at each sexual cycle. DNA double strands breaks (DSBs) are introduced by the PiggyMac endonuclease, and repaired in a highly concerted manner by the Non-Homologous End Joining pathway (NHEJ), as illustrated by the complete inhibition of DNA cleavage when Ku70/80 proteins are missing. We show here that expression of a DNA binding-deficient Ku70 mutant (Ku70-6E) permits DNA cleavage but not DSB repair, leading to accumulation of unrepaired DSBs. When wildtype and mutant Ku are co-expressed, the DSBs induced by Ku70-6E can be repaired by wildtype Ku, which uncouples DNA repair from the cleavage step. High-throughput sequencing of the developing MAC genome in these conditions reveals the presence of extremities healed by <i>de novo</i> telomere addition and numerous translocations between IES-flanking sequences. We conclude that coupling the two steps of IES excision ensures that both extremities are maintained together throughout the process, and propose that Ku assists PiggyMac during assembly of the synaptic pre-cleavage complex.</p>
Cell-cycle dependent DNA repair and replication unifies patterns of chromosome instability
<p>This repository contains the data used to generate the figures in paper: Cell-cycle dependent DNA repair and replication unifies patterns of chromosome instability.</p>
Microscopy data from: Identification of genetic interactions with priB links the PriA/PriB DNA replication restart pathway to double-strand DNA break repair in Escherichia coli
<p>Collisions between DNA replication complexes (replisomes) and impediments such as damaged DNA or proteins tightly bound to the chromosome lead to premature dissociation of replisomes at least once per cell cycle in <em>Escherichia coli</em>. Left unrepaired, these events produce incompletely replicated chromosomes that cannot be properly partitioned into daughter cells. DNA replication restart, the process that reloads replisomes at prematurely terminated sites, is therefore essential in <em>E. coli</em> and other bacteria. Three replication restart pathways have been identified in <em>E. coli</em>: PriA/PriB, PriA/PriC, and PriC/Rep. A limited number of genetic interactions between replication restart and other genome maintenance pathways have been defined, but a systematic study placing replication restart reactions in a broader cellular context has not been performed. We have utilized transposon insertion sequencing to identify new genetic interactions between DNA replication restart pathways and other cellular systems. Known genetic interactors with the <em>priB</em> replication restart gene (uniquely involved in the PriA/PriB pathway) were confirmed and several novel <em>priB </em>interactions were discovered. Far fewer connections were found with the PriA/PriC or PriC/Rep pathways, suggesting a primacy role for the PriA/PriB pathway in <em>E. coli</em>. Targeted genetic and imaging-based experiments with <em>priB</em> and its genetic partners revealed significant double-strand DNA break (DSB) accumulation in strains with mutations in <em>dam</em>, <em>rep</em>, <em>rdgC</em>, <em>lexA</em>, or <em>polA</em>. Modulating the activity of the RecA recombinase partially suppressed the detrimental effects of <em>rdgC</em> or <em>lexA</em> mutations in Δ<em>priB</em> cells. Taken together, our results highlight roles for several genes in DSB homeostasis and define a genetic network that facilitates DNA repair/processing upstream of PriA/PriB-mediated DNA replication restart in <em>E. coli</em>.</p>
RBBP4 regulates the expression of Mre11-Rad50-NBS1(MRN)complex and promotes DNA double-strand breaks repair to mediate glioblastoma Chemoradiotherapy resistance
<p>Article <a>related</a> SUPPLEMENTARY data.</p> <p> </p>
The effect of presence and absence of DNA repair genes on the rate and pattern of mutation in bacteria
<p>This repository contains the code, data, and outputs used in the manuscript "The effect of presence and absence of DNA repair genes on the rate and pattern of mutation in bacteria".</p> <ul> <li><strong>Script.py:</strong> This is a Python script for estimating the number of polymorphisms and mutation rates of bacterial clusters of orthologous genes found in ATGC_data.zip. It produces individual strain outputs to<em> Polymorphism_Results/</em> and<em> Rate_Results/ </em>directories.</li> <li><strong>ATGC_data.zip: </strong>This is a data set of bacterial clusters of orthologous genes downloaded from the ATGC database by Kristensen et al. (2017). The fasta files are utilised by <em>Script.py</em> and should be extracted to the same working directory, under <em>ATGC_data/.</em></li> <li><strong>mutation_rate_data.csv: </strong>This file contains the outputs of <em>Script.py </em>merged into a single file, alongside additional information regarding the presence and absence of particular repair genes, and the calculation of overall mutation rate and Watterson's corrected mutation rate.</li> <li><strong>Phylogenetic_Comparisons.xlsx:</strong> This file contains the averages of overall mutation rate, transition/transversion ratio, and GC-AT bias, for 50 phylogenetic comparisons under presence and absence of repair enzymes. </li> </ul>
Dynamic interplay of cNHEJ and MMEJ pathways of DNA double-strand break repair during embryonic development in zebrafish.
<p><span>Fastq sequences from zebrafish embryos corresponding to 9 amplicons sequenced by </span><span>Illumina MiSeq. DNA sample were obtained from non-treated wildtype controls (ctrl) or from wildtype (WT), polq mutants, lig3 mutant or lig4 mutant injected with Cas9 protein and a pool of 5 or 4 different sgRNA (numbered from 1#1 to 5#2). Each target site corresponds to one amplicon. </span></p>
Confocal microscopy of gH2AX and 53BP1 DNA repair foci of cells exposed to gamma-irradiation, pt. 2/3
<p><strong>Summary</strong></p> <p>Dataset of confocal microscopy data of cells exposed to gamma-irradiation and immunostained with gH2AX and 53BP1.</p> <ul> <li><strong>Part 1/3: </strong>Head and neck primocultures immunostained with gH2AX/53BP1, Testing dataset. DOI <a href="https://doi.org/10.5281/zenodo.2564980">10.5281/zenodo.2564980</a></li> <li><strong>Part 2/3 (this dataset)</strong>: U-87 and NHDF Cells exposed to 1-4 Gy confocal microscopy data of head and neck tumor primocultures immunostained with gH2AX/53BP1. Testing dataset. DOI <a href="https://doi.org/10.5281/zenodo.2572450">10.5281/zenodo.2572450</a>. 174 TIFFs</li> <li><strong>Part 3/3</strong>: training dataset for nuclei and gH2AX foci with ground truth annotation masks, head and neck primocultures (head and neck non-tumor and spinocellular tumor cells). DOI <a href="https://doi.org/10.5281/zenodo.2576241">10.5281/zenodo.2576241</a>. 150 TIFFs for nuclei learning incl 150 png nuclei masks + 99 TIFFs for DNA repair foci training</li> <li><strong>Code</strong>: the code is available at <a href="https://github.com/tomasvicar/LearnFoci">https://github.com/tomasvicar/LearnFoci</a></li> </ul> <p><strong>Materials and methods</strong></p> <p><em>Dataset</em></p> <p>Following cells were used: (1) patient primocultures of patients with spinocellular head and neck tumors (histologically verified tumor and tumor-adjacent tissues), isolation protocol descibed in <em>Svobodova et al, 2017</em>, (2) primary glioblastoma cell line U-87 (ATCC HTB-14, LGC Standards, United Kingdom), (3) primary normal human dermal fibroblasts (NHDF, PromoCell, Hedelberg, Germany) isolated from the dermis of juvenile foreskin or adult skin.<br> The study was conducted in accord with the Helsinki Declaration of 1964 and all subsequent revisions thereof. It was approved by the ethical committee of St. Anne’s Faculty Hospital, Brno. Primoculture cells were cultivated in Pen/Strep antibiotic solution (PAA Laboratories GmbH, Austria) in RPMI-1640 medium with 10% FBS (Biochrom, USA) at 37 °C and 50% CO2 in humidified atmosphere up to 50% confluence. U-87 were grown in Eagle's MEM with 10% FBS.</p> <p><em>Gamma irradiation</em></p> <p>The cells were irradiated at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic in a following schemes: (a) patient-derived primoculture was irradiated with a single dose of 2 Gy (D = 1 Gy/min) of gamma-rays (60Co, Chisostat, Chirana, CR) , (b) U-87 and NHDF cells were irradiated with doses 1, 2, and 4 Gy (D = 1 Gy/min). Cells were irradiated in RPMI 1640 medium (37 °C, normal atmosphere). Confocal microscopy of gammaH2AX and 53BP1 foci immunodetection was consequently performed.</p> <p><em>Fluorescent staining </em></p> <p>DNA double strand breaks (DSBs) were quantified in different periods of time post-irradiation (30 min, 8h and 24h post irradiation) by means of $\gamma$H2AX and 53BP1 foci immunodetection combined with confocal microscopy. For details see \cite{falk2007chromatin}.</p> <p><em>Confocal microscopy</em></p> <p>The microscopy of samples was performed at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic. Leica DM RXA microscope (equipped with DMSTC motorized stage, Piezzo z-movement, MicroMax CCD camera, CSU-10 confocal unit and 488, 562, and 714 nm laser diodes with AOTF) was used for acquiring detailed cell images (100× oil immersion Plan Fluotar lens, NA 1.3). Total 50 Z slices was captured with Z step size 0.3 μm.</p> <p><strong>File description</strong></p> <p>all files are compressed hyperstack tiffs (50 Z slices and 3 fluorescent channels, XYCZ order), 100x magnification</p> <ul> <li>Confocal_NHDF_cells_IR_1-4Gy.zip: Human fibroblast NHDF cell line, exposed to gamma irradiation doses 1, 2, and 4 Gy, 64 TIFFs</li> <li>Confocal_U-87_cells_IR_1-4Gy.zip: Human glioblastoma U-87 cell line, exposed to gamma irradiation doses 1, 2, and 4 Gy, 108 TIFFs</li> </ul>
Confocal microscopy of gH2AX and 53BP1 DNA repair foci of cells exposed to gamma-irradiation, pt. 1/3
<p><strong>Summary</strong></p> <p>Dataset of confocal microscopy data of cells exposed to gamma-irradiation and immunostained with gH2AX and 53BP1.</p> <ul> <li><strong>Part 1/3 (this dataset): </strong>Head and neck primocultures immunostained with gH2AX/53BP1, Testing dataset. DOI <a href="https://doi.org/10.5281/zenodo.2564980">10.5281/zenodo.2564980</a></li> <li><strong>Part 2/3</strong>: U-87 and NHDF Cells exposed to 1-4 Gy confocal microscopy data of head and neck tumor primocultures immunostained with gH2AX/53BP1. Testing dataset. DOI <a href="https://doi.org/10.5281/zenodo.2572450">10.5281/zenodo.2572450</a>. 174 TIFFs</li> <li><strong>Part 3/3</strong>: training dataset for nuclei and gH2AX foci with ground truth annotation masks, head and neck primocultures (head and neck non-tumor and spinocellular tumor cells). DOI <a href="https://doi.org/10.5281/zenodo.2576241">10.5281/zenodo.2576241</a>. 150 TIFFs for nuclei learning incl 150 png nuclei masks + 99 TIFFs for DNA repair foci training</li> <li><strong>Code</strong>: the code is available at <a href="https://github.com/tomasvicar/LearnFoci">https://github.com/tomasvicar/LearnFoci</a></li> </ul> <p><strong>Materials and methods</strong></p> <p><em>Dataset</em></p> <p>Following cells were used: (1) patient primocultures of patients with spinocellular head and neck tumors (histologically verified tumor and tumor-adjacent tissues), isolation protocol descibed in <em>Svobodova et al, 2017</em>, (2) primary glioblastoma cell line U-87 (ATCC HTB-14, LGC Standards, United Kingdom), (3) primary normal human dermal fibroblasts (NHDF, PromoCell, Hedelberg, Germany) isolated from the dermis of juvenile foreskin or adult skin.<br> The study was conducted in accord with the Helsinki Declaration of 1964 and all subsequent revisions thereof. It was approved by the ethical committee of St. Anne’s Faculty Hospital, Brno. Primoculture cells were cultivated in Pen/Strep antibiotic solution (PAA Laboratories GmbH, Austria) in RPMI-1640 medium with 10% FBS (Biochrom, USA) at 37 °C and 50% CO2 in humidified atmosphere up to 50% confluence. U-87 were grown in Eagle's MEM with 10% FBS.</p> <p><em>Gamma irradiation</em></p> <p>The cells were irradiated at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic in a following schemes: (a) patient-derived primoculture was irradiated with a single dose of 2 Gy (D = 1 Gy/min) of gamma-rays (60Co, Chisostat, Chirana, CR) , (b) U-87 and NHDF cells were irradiated with doses 1, 2, and 4 Gy (D = 1 Gy/min). Cells were irradiated in RPMI 1640 medium (37 °C, normal atmosphere). Confocal microscopy of gammaH2AX and 53BP1 foci immunodetection was consequently performed.</p> <p><em>Fluorescent staining </em></p> <p>DNA double strand breaks (DSBs) were quantified in different periods of time post-irradiation (30 min, 8h and 24h post irradiation) by means of $\gamma$H2AX and 53BP1 foci immunodetection combined with confocal microscopy. For details see \cite{falk2007chromatin}.</p> <p><em>Confocal microscopy</em></p> <p>The microscopy of samples was performed at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic. Leica DM RXA microscope (equipped with DMSTC motorized stage, Piezzo z-movement, MicroMax CCD camera, CSU-10 confocal unit and 488, 562, and 714 nm laser diodes with AOTF) was used for acquiring detailed cell images (100× oil immersion Plan Fluotar lens, NA 1.3). Total 50 Z slices was captured with Z step size 0.3 μm.</p> <p><strong>File description</strong></p> <p>all files are compressed hyperstack tiffs (50 Z slices and 3 fluorescent channels, XYCZ order), 100x magnification</p> <ul> <li>Confocal_HN_tumor_primocultures.zip: dataset of patient-derived primocultures (gamma-irradiated with 2 Gy and controls), for description see file below, 100 FOVs,</li> <li>Confocal_HN_tumor_primocultures_description.xlsx: description of confocal dataset files and patient tumor characteristics</li> <li>Confocal_HN_tumor_primocultures_train_nuclei.zip: annotated training subset 1 of dataset of patient-derived primocultures (gamma-irradiated with 2 Gy and controls) used for nuclei segmentation training, 150 FOVs, includes TIFF and manually annotated binary mask for nuclei (data_###.tif and respective mask_###.png)</li> <li>Confocal_HN_tumor_primocultures_train_nuclei_description.xlsx: description of above-mentioned files (tissue type, TNM stage, grade, time post irradiation)</li> </ul>
The role of TAp63g and p53 point mutations in regulating DNA repair, mutational susceptibility and invasion of bladder cancer cell
<p>Raw data set for the manuscript submitted to e-Life (10-06-2021-RA-eLife-71184 ) for peer-review. </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.
BrUOG 337: Olaparib Prior to Radical Prostatectomy For Advanced Prostate Cancer Defects in DNA Repair Genes
ClinicalTrials.gov study NCT03432897. IPD Sharing: NO. Countries: 1. 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.
Combination Chemotherapy With or Without Atezolizumab in Treating Patients With Stage III Colon Cancer and Deficient DNA Mismatch Repair
ClinicalTrials.gov study NCT02912559. IPD Sharing: Not stated. Countries: 3. Publications: 1.
A Study of Talazoparib in Men With DNA Repair Defects and Metastatic Castration-Resistant Prostate Cancer
ClinicalTrials.gov study NCT03148795. IPD Sharing: YES. Countries: 14. Publications: 2.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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)
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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.