Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: MPRA in K562 cells for JIA risk haplotypes

PROVIDER: PRJNA818294 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18399500.fastq.gz	Fastqsanger.gz
	SRR18398001.fastq.gz	Fastqsanger.gz
	SRR18399501.fastq.gz	Fastqsanger.gz
	SRR18398002.fastq.gz	Fastqsanger.gz
	SRR18399502.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Homo sapiens strain:K562

Project description:MPRA libraries in K562 cells

| PRJNA389101 | ENA

Systematic dissection of regulatory motifs in 2,000 predicted human enhancers using a massively parallel reporter assay

Project description:We employ a massively parallel reporter assay (MPRA) to measure the ex vivo activities of hundreds of K562 and HepG2 enhancers with known transcription factor motif instances. For seven selected motifs that correspond to known or predicted activators and repressors in the two cell types, we make directed modifications of the bases corresponding to these motifs and observe the changes in enhancer activity. Reporter mRNA-seq from HepG2 and K562 cells transfected with a ~55,000-plex MPRA plasmid pool containing 5,418 mutated human enhancer sequences, each linked to 10 distinct 10-nt tags. The reporter mRNA tags facilitate quantitation of their abundances. The same tags were also sequenced from the transfected MPRA plasmid pool to facilitate normalization to plasmid copy numbers.

2013-03-15 | E-GEOD-33367 | biostudies-arrayexpress

Massively Parallel Reporter Assay Confirms Regulatory Potential of hQTLs and Reveals Important Variants in Lupus and Other Autoimmune Diseases

Project description:We designed a massively parallel reporter assay (MPRA) in an Epstein-Barr virus transformed B cell line to directly characterize the potential for histone post-translational modifications, i.e., histone quantitative trait loci (hQTLs), expression QTLs (eQTLs), and variants on SLE and autoimmune (AI) disease risk haplotypes to modulate regulatory activity in an allele dependent manner. Our study demonstrates that hQTLs, as a group, are more likely to modulate regulatory activity in an MPRA compared to other variant classes tested, including a set of eQTLs previously shown to interact with hQTLs and tested AI risk variants. In addition, we nominate 17 variants (including 11 previously unreported) as putative causal variants for SLE and another 14 for various other AI diseases, prioritizing these variants for future functional studies primary and immortalized B cells. Thus, we uncover important insights into the mechanistic relationships between genotype, epigenetics, and gene expression in SLE and AI disease phenotypes.

2024-03-10 | GSE254502 | GEO

Transcription profiling of peripheral blood from patients with primary progressive multiple sclerosis to compare risk and protective PRF1 haplotypes

Project description:A genetic study of the PRF1 gene has shown association of several polymorphisms with multiple sclerosis (MS). Haplotype analysis identified risk haplotypes strongly associated with male patients having the primary-progressive form of MS (PPMS). Gene expression microarrays were performed in 10 male PPMS patients carrying the risk (n=6) and protective haplotypes (n=4) in order to identify pathways associated with the risk haplotypes. Pathway analysis revealed overrepresentation of the cell killing gene ontology category among down-regulated genes in patients carrying risk haplotypes compared with patients carrying protective haplotypes. Number of samples analyzed: 10 Protective haplotype samples: UOM982, EMA1473, MMC-998, CDP1842 Risk haplotype samples: UUS1554, RAU1550, RPS1011, AGS1013, PFB1530, MGA1014

2010-07-28 | E-GEOD-23205 | biostudies-arrayexpress

Microarray expression analysis of PRF1 (perforin 1) haplotypes in patients with primary progressive multiple sclerosis

2010-07-28 | GSE23205 | GEO

CD4+ T cells From Children With Active Juvenile Idiopathic Arthritis Show Altered Chromatin Features Associated With Transcriptional Abnormalities (ATAC-seq)

Project description:We used a multi-omics approach in an attempt to identify mechanisms driving the transcriptional abnormalities in peripheral blood CD4+ T cells of children with active JIA. We demonstrate that active JIA is associated with distinct alterations in CD4+ T cell chromatin, as assessed by ATAC-seq studies. However, 3D chromatin architecture, assessed by HiChIP and simultaneous mapping of CTCF anchors of chromatin loops, reveals that normal 3D chromatin architecture is largely preserved in JIA CD4+ T cells. However, overlapping CTCF binding, ATACseq, and RNAseq data with known JIA genetic risk loci demonstrated the presence of genetic influences on the observed transcriptional abnormalities and identified candidate target genes. These studies demonstrate the utility of multi-omics approaches for unraveling some of the most vexing questions regarding the pathobiology of autoimmune diseases.

2021-01-05 | GSE164214 | GEO

CD4+ T cells From Children With Active Juvenile Idiopathic Arthritis Show Altered Chromatin Features Associated With Transcriptional Abnormalities (ChIP-seq)

2021-01-05 | GSE164212 | GEO

CD4+ T cells From Children With Active Juvenile Idiopathic Arthritis Show Altered Chromatin Features Associated With Transcriptional Abnormalities (RNA-seq)

2021-01-05 | GSE164213 | GEO

Epigenetic profiling of Juvenile Idiopathic Arthritits (JIA) patients

Project description:With H3K27ac chromatin immunoprecipitation we identified a disease-specific, inflammation-associated, (super-)enhancer signature in JIA patient synovial fluid-derived CD4+ memory/effector T cells. This signature consists of unique pathogenesis-associated epigenetic changes which extend beyond general T cell activation-induced alterations, indicating that disease-specific (super-)enhancers contribute to JIA pathogenesis. In addition, our analysis shows that there is a profound enrichment of JIA-related SNPs in (super-)enhancers in JIA patients compared to controls, illustrating the importance of these non-coding regions for disease pathogenesis. H3K27ac ChIP-sequencing of CD4+ memory/effector T cells derived from peripheral blood (PB) from healthy controls (HC) and PB or synovial fluid (SF) from JIA patients.

2015-09-15 | E-GEOD-71596 | biostudies-arrayexpress

Genome-scale high-resolution mapping of activating and repressive nucleotides in regulatory regions

Project description:We employ a massively parallel reporter assay (MPRA) to measure the ex vivo activities in K562 and HepG2 cells of more than 15,000 human candidate regulatory regions. The regulatory regions were tiled with overlapping constructs enabling high resolution computational inference of activating and repressive nucleotides.

2016-08-12 | GSE71279 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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