197,988 research outputs found
ATAC-seq peak genomic distribution.
No full textA. Bar plot showing the genomic distribution of accessible peaks identified in ATAC-seq data in Rh1>GFPKASH during aging. Promoter annotation was based on -/+ 2 kb around transcription start sites. B. DNA binding motif for Clk and Cyc derived from CIS-BP database. (PDF)</p
Current status of numerical flow prediction for separated nozzle flows
No full textThe European ‘Flow Separation Control Device’ group (FSCD) organized in collaboration with the French ‘Aérodynamiques des tuyères et Arrière-Corps’ group (ATAC) a CFD workshop with test cases on different nozzle flow topics. One of these test cases (1A) was managed by the German Aerospace Center (DLR) and Astrium ST. The objective was to compute the flow inside a strongly over-expanded truncated ideal contour nozzle with respect to the prediction of location and shape of the flow separation, the oblique shock and the Mach disc. Experimental data were provided by DLR.
An introduction to the test facility and the experimental setup is given. The numerical results are evaluated and compared to test data. A concluding synthesis illustrates the current status of nozzle flow computation
ENCODE-DCC/atac-seq-pipeline: v2.2.0
No full textUpgrade Caper to >=2.2.0 for new HPC features.
scripts/uninstall_conda_env.sh
$ scripts/install_conda_env.sh
Caper's new HPC feature
Unified command caper hpc for all HPC backend types (slurm, sge, pbs and lsf).
Read Caper's README carefully and make a backup of your Caper's conf file (~/.caper/default.conf) and run caper init YOUR_BACKEND.
caper hpc submit atac.wdl -i INPUT.json --leader-job-name GOOD_NAME_FOR_LEADER [--conda | --singularity]: submits a workflow to HPC's job engine.
caper hpc list: shows all Caper leader jobs
caper hpc abort JOB_ID: terminate a Caper leader job including child job
ATAC-seq captures chromatin accessibility in brains of wild-type monarchs and monarchs impaired for clock function.
No full textA) Correlation plot of two biological replicates showing normalized read counts in wild-type at ZT04. Correlation plots for all conditions tested are shown in S5A Fig. Correlations varied from 0.76 to 0.85. B) Visualization of ATAC-seq signal between genotypes and time points at scaffold DPSCF300015 showing no substantial gross change in chromatin accessibility in adult brain. ATAC-seq peaks from biological replicates are merged. WT, wild-type; Clk KO, Clk knockouts; Cyc-like, Bmal1 mutants lacking the C-terminal transactivation domain [6]. C) Representative ATAC-seq tracks in genomic regions of clock genes (timeless and clockwork orange) showing the lack of differential ATAC-seq peaks between time points and genotypes. D) ATAC-seq signal within consensus ATAC-seq peaks was compared between all samples using Pearson’s correlation to cluster samples. Replicates are noted as numbers following each genotype and time point. F: female; M: male. E) Venn diagrams representing lack of differences in ATAC-seq signal within consensus genome-wide ATAC-seq peaks (top) and ATAC-seq peaks associated to rhythmic genes differentially regulated in Clk knockouts (bottom) between ZT04 and ZT16 in wild-type brains and between genotypes at ZT04 (fold-change cutoff > 1.3). The complete list of cross-comparisons is provided in S9 Table. F) Log2 fold enrichment of ATAC-seq peaks within different genomic regions in the monarch genome (top) and within rhythmic genes differentially regulated in Clk knockouts (bottom) for each genotype at ZT04 and at ZT16. Except for intergenic regions, genomic features are defined within -1Kb of the transcription start site (TSS) and +1Kb of the transcription termination site (TTS). Fold enrichment is calculated as the number of peaks per genomic regions/total number of peaks relative to the length of the genomic regions/total length.</p
ATAC-seq analysis in Clk<sup>DN</sup> photoreceptors.
No full textA. Bar plot showing the genomic distribution of accessible peaks identified in ATAC-seq data from the indicated genotypes and ages. Promoter annotation was based on -/+ 2 kb around transcription start sites. B. Volcano plots representing the differentially accessible peaks in Rh1>ClkDN relative to Rh1>Ctrl. Differentially accessible peaks are defined as having a False Discovery Rate (FDR) 1.5. (PDF)</p
Chromatin accessibility profiling by ATAC-seq
No full textThe assay for transposase-accessible chromatin using sequencing (ATAC-seq) provides a simple and scalable way to detect the unique chromatin landscape associated with a cell type and how it may be altered by perturbation or disease. ATAC-seq requires a relatively small number of input cells and does not require a priori knowledge of the epigenetic marks or transcription factors governing the dynamics of the system. Here, we describe an updated and optimized protocol for ATAC-seq, called Omni-ATAC, that is applicable across a broad range of cell and tissue types. The ATAC-seq workflow has five main steps: sample preparation, transposition, library preparation, sequencing, and data analysis. This protocol details the steps to generate and sequence ATAC-seq libraries, with recommendations for sample preparation and downstream bioinformatic analysis. ATAC-seq libraries for ~12 samples can be generated in 10 hours by someone familiar with basic molecular biology and downstream sequencing analysis can be implemented using benchmarked pipelines by someone with basic bioinformatics skills and access to a high-performance computing environment
SCXRD dataset for "Synthesis of 2-amino-5-methylpyridinium tetrachloridocadmate(II) (C6H9N2)2[CdCl4]: Structure, DFT-calculated descriptors and molecular docking study"
No full textDataset del artículo Jomaa, Ikram; Bardak, Fehmi; ISSAOUI, N.; Cabeza, Aurelio; Choquesillo-Lazarte, Duane CSIC ORCID; Atac, A.; Marouani, Houda; Al-Dossary, Omar M. Synthesis of 2-amino-5-methylpyridinium tetrachloridocadmate(II) (C6H9N2)2[CdCl4]: Structure, DFT-calculated descriptors and molecular docking study. Journal of King Saud University - Science 36 (2024)King Saud UniversityPeer reviewe
An improved ATAC-seq protocol reduces background and enables interrogation of frozen tissues
No full textWe present Omni-ATAC, an improved ATAC-seq protocol for chromatin accessibility profiling that works across multiple applications with substantial improvement of signal-to-background ratio and information content. The Omni-ATAC protocol generates chromatin accessibility profiles from archival frozen tissue samples and 50-mu m sections, revealing the activities of disease-associated DNA elements in distinct human brain structures. The Omni-ATAC protocol enables the interrogation of personal regulomes in tissue context and translational studies
Identification of transcription factor binding sites using ATAC-seq
No full textAbstract Transposase-Accessible Chromatin followed by sequencing (ATAC-seq) is a simple protocol for detection of open chromatin. Computational footprinting, the search for regions with depletion of cleavage events due to transcription factor binding, is poorly understood for ATAC-seq. We propose the first footprinting method considering ATAC-seq protocol artifacts. HINT-ATAC uses a position dependency model to learn the cleavage preferences of the transposase. We observe strand-specific cleavage patterns around transcription factor binding sites, which are determined by local nucleosome architecture. By incorporating all these biases, HINT-ATAC is able to significantly outperform competing methods in the prediction of transcription factor binding sites with footprints
Preventative therapies for healthy women at high risk of breast cancer
No full textIvana Sestak Centre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Queen Mary University of London, Charterhouse Square, London, UKAbstract: Tamoxifen has been shown to reduce the risk of developing estrogen receptor (ER)-positive breast cancer by at least 50%, in both pre- and postmenopausal women. The current challenge is to find new agents with fewer side effects and to find agents that are specifically suitable for premenopausal women with ER-negative breast cancer. Other selective estrogen receptor modulators (SERMs), such as raloxifene, arzoxifene, and lasofoxifene, have been shown to reduce the incidence of breast cancer by 50%–80%. SERMs are interesting agents for the prevention of breast cancer, but longer follow-up is needed for some of them for a complete risk–benefit profile of these drugs. Aromatase inhibitors have emerged as new drugs in the prevention setting for postmenopausal women. In the Mammary Prevention 3 (MAP3) trial, a 65% reduction in invasive breast cancer with exemestane was observed, and the Breast Cancer Intervention Study-II trial, which compared anastrozole with placebo, reported a 60% reduction in those cancers. Although SERMs and aromatase inhibitors have been proven to be excellent agents in the preventive setting specifically for postmenopausal women and ER-positive breast cancer, newer agents have to be found specifically for ER-negative breast cancers, which mostly occur in premenopausal women. Keywords: breast cancer, preventive therapy, selective estrogen receptor modulators, aromatase inhibitors, high-risk wome
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