Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inactivation of ARID1A-SWI/SNF Complex Alters Chromatin Compactness at Enhancer Regions and Affects Transcription of Key Tumor Signaling Circuitry [ChIP-Seq]

ABSTRACT: For ATAC-seq data processing, we used the ENCODE ATAC-seq pipeline (https://www.encodeproject.org/atac-seq/). In detail, for each sample, ATAC-seq reads were first checked for adaptor contamination. Then, adaptor trimmed reads were aligned to hg19 using Bowtie2 under paired-end mode with parameter “-X2000”, which permits 2000 bp for the maximum allowable insert size between two paired ends of each read. Using the ENCODE ATAC-seq pipeline, duplicated reads were properly filtered out. ATAC-seq enriched peaks were called using MACS2 (Zhang et al., 2008) based on remaining unique reads with parameters “-f BAMPE -q 0.05 --nomodel”. In total, we collected 45,569 peaks for the ARID1AWT sample and 27,480 peaks for the ARID1AKO sample.

ORGANISM(S): Homo sapiens

PROVIDER: GSE106660 | GEO | 2020/06/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Subtelomeric CTCF and Cohesin binding site organization using improved subtelomere assemblies and a novel annotation pipeline

Project description:We investigated the reported binding of telomere associated factor TERF1 and TERF2 to internal telomere sites using ChIP-Seq for these two factors in a lymphoblastoid cell line. We mapped over 40 million reads for each sample to a custom reference genome that incorporates our subtelomere assembly, and generated signal tracks using only uniquely mapping reads, and also using a multimapping pipeline we developed. We find that peaks are misshapen and made up of reads that cannot be distinguished from true telomere sequence. Removing telomere identified reads removes all internal signal.

2014-02-18 | GSE55053 | GEO

Subtelomeric CTCF and Cohesin binding site organization using improved subtelomere assemblies and a novel annotation pipeline

2014-02-18 | E-GEOD-55053 | biostudies-arrayexpress

Determine differences in chromatin accessibility in primary human AML samples by ATAC-seq.

Project description:ATAC-Seq was performed for 35 AML primary specimens from primary AML cells, followed by a detailed ATAC-Seq pipeline for data processing. We provide both raw files as well as various processed files such as individual and consensus peaks.

2022-02-06 | GSE150868 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of C57BL/6J mice.

Project description:Purpose: Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq) is a method for mapping chromatin accessibility genome-wide. The goals of this study are to investigate chromatin accessibility of C57BL/6J mice through ATAC-seq. Results: ATAC-seq reads were aligned to the UCSC mm10 reference genome with BWA-MEM. ATAC-seq peaks were called through MACS2 . Peaks were annotated and known transcription factor binding motifs were further analyzed in the ATAC-seq peaks by HOMER.

2020-07-08 | GSE153993 | GEO

The SWI/SNF subunit Dpf2 licenses Nrf2-dependent gene expression to enforce multilineage control of inflammation [ATAC-seq]

Project description:Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For ATACseq, Lin- cKit+ cells were processed following the OMIM-ATAC-seq protocol (Corces MR et al., Nature Methods 2017). Libraries were sequenced on a NextSeq (75bp, paired end reads) to obtain more than 40 million reads/sample. Results: For ATACseq, we obtained more than 40 million reads per sample. ATAC-Seq chromatin accessible regions were determined using ENCODE pipeline standards (https://github.com/ENCODE-DCC/atac-seq-pipeline; git commit 2b693ab). Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells.

2023-06-06 | GSE192776 | GEO

Integration of kinase and calcium signaling at the level of chromatin underlines inducible gene activation in T cells

Project description:Aim: to perform a genome-wide investigation of chromatin landscape and gene expression patterns downstream of calcium and kinase signaling in Jurkat T cells. Methods: PMA and ionomycin were used to activate the calcium and kinase signalling networks involved in T cell activation. Global gene expression was measured using RNA-seq, whilst ATAC-seq was used to probe chromatin landscape following 3 hours of stimulation with PMA, ionomycin or both. All experiments were performed in triplicate. For RNA-seq all sequencing was performed using paired-end sequencing on an Illumina HiSeq2500 instrument. For ATAC-seq sequencing was performed using a HiSeq 1500. Results: we mapped approximately 60 million reads per sample for ATAC-seq, and 22 million reads per library for RNA-seq. Overall we identified 57,825 transcripts and 19,763 ATAC-seq peaks. We identifiead 1648 genes whose expression was increased by 2-fold or more by at least one treatment in comparison to untreated cells. Similarly, we identified 3972 ATAC peaks that were induced by at least 2-fold by treatment in comparison to untreated cells. Conclusions: we found that chromatin landscape was associated with gene expression downstream of calcium and kinase signaling in Jurkat cells. Further to this we found that activation of the full complement of TCR-responsive genes is dependent upon both PMA and ionomycin, and amounts to more than just the sum of both.

2017-09-18 | GSE90718 | GEO

ATAC sequencing of control siRNA and Zmiz1 siRNA treated Human dermal lymphatic endothelial cell (HDLECs)

Project description:Purpose: Zinc Finger MIZ-Type Containing 1 (Zmiz1) is a member of the PIAS family of protein and function as a transcriptional coactivator of Notch, Androgen Receptor (AR), p53, Estrogen Receptor (ER), and Smad3/4 . Despite Zmiz1 critical role in angiogenesis, its role in lymphatic vasculature is unknown. Here, we use HDLECs cell line to profileepigenetic changes upon Zmiz1 knockdown using siRNA. Methods: ATAC sequencing library was prepared as per manufacturer instruction (Active Motif, 53150). Briefly, intact nuclei were isolated from control and Zmiz1 siRNA transfected HDLECs. Samples were treated with a hyperactive Tn5 transposase which tag the target DNA with sequencing adapters and fragment the DNA simultaneously. Library was then quantified using Qubit dsDNA High Sensitivity Assay Kit (Thermo Fisher Scientific, Q32851) and verified using the Bioanalyzer DNA High Sensitivity Assay Kit (Agilent, 5067-4626). Validated samples were sequenced using the NextSeq1000/2000 P2 Reagents (100 Cycles) v3 (Illumina, 20046811) on a Nextseq1000/2000. Resulting sequencing data were analyzed using basepairtech ATAC-Seq pipeline (www.basepairtech.com). Briefly, sequenced reads were aligned to the human (hg19) reference genome using Bowtie2. ATAC-Seq peaks and differentially accessible regions were quantified using MACS2 and DESeq2. Results: ATAC seq peaks analysis using MACS2 identified 576 peaks of which are mostly located in intergenic regions followed by introns. We found significantly reduced open chromatin near Prox1 loci upol loss of Zmiz1. Conclusions: We identify Zmiz1 regulates chromatin accessibility near Prox1 genomic loci in lymphatic endothelial cells

2023-11-29 | GSE225130 | GEO

To detect CENP-A enrichment on Chromosome 1,5 &7 in C. albicans centromere deleted clones

Project description:ChIP Seq revealed presence of unique CEN-proximal neocentromere peaks in CEN deleted clones. Using 10 million reads generated from ChIP-seq for each sample, chromosome wide maps for CENP-A enrichment were generated .

2012-12-21 | GSE42907 | GEO

Genome-wide maps of H3K27me3 in endpoint Ezh2+/+ or Ezh2-/- Tet ON PyVmT mouse mammary gland tumours

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in endpoint tumours from Ezh2+/+ or Ezh2-/- Tet ON PyVmT mammary gland tumours. In order to understand the H3K27me3 targets in the context of mouse mamamry gland tumorigenesis, data were generated by deep sequencing a pool of 5 tumours per genoype, in duplicate using Illumina HiSeq2500. Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm10). Raw reads were trimmed for length (n>=32), quality (phred score >= 30) and adaptor sequence using fastx v0.0.13.1.Trimmed reads were (pools of 5 different tumors per genotype) then aligned to the mouse reference genome mm10 using BWA v0.5.9 Broad peaks were called using MACS v1.4.1 software (mfold=10,30; bandwith=300; pvalue cutoff=1E-5) using sequenced libraries of input DNA as control. Peak list intersections were done using BEDTools v2.12.0. Binding peaks were considered overlapping if at least 1 base of the peaks overlapped. Our study demonstrated the first mapping of H3K27me3 in the endpint tumours of tetracycline ducible PyVmT mouse mamary tumours.

2018-03-01 | GSE108899 | GEO

RNAtag-seq and term-seq samples of E. coli K12 MG1655 cells grown to exponential phase in rich and minimal media.

Project description:In this study we developed TRS, a computational approach to determine the 3’ termini of transcripts from total RNA data generated by the RNAtag-seq protocol. To show the applicability of our approach, we applied our algorithm to sequencing data generated by the RNAtag-seq and the term-seq protocols. In term-seq, a 3’ adaptor is ligated to the RNA 3' termini prior to the RNA fragmentation, and thus, the sequences adjacent to the adapter sequence in the library reads represent original 3' termini that were present in the RNA sample. The RNAtag-seq protocol involves ligation of a 3’ adaptor after the RNA fragmentation and thus, the sequences adjacent to the adapter sequence in the library reads represent genuine 3’ termini that were present in the RNA sample and artificial 3’ termini generated by the RNA fragmentation. We show that our computational approach can reliably identify genuine 3’ termini from RNAtag-seq data by comparing the set of identified 3’ termini based on the RNAtag-seq and the term-seq protocols.

2023-07-15 | E-MTAB-12429 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data