Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

45 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Leveraging cell type-specific regulatory regions to detect SNPs associated with tissue factor pathway inhibitor plasma levels

ABSTRACT: Using human aortic enhancers to prioritize genomic regions for GWAS analysis

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Jessica Dennis

PROVIDER: E-MTAB-4935 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Systematic interaction profiling of human bromodomain-containing proteins reveals complex modes of binder recruitment for BET proteins

Project description:ChIP-seq of GFP tagged wild type and mutant human BRD3 in U-2 O3 cells

2018-04-01 | E-MTAB-5670 | biostudies-arrayexpress

ChIP-seq of ERG-bound regulatory elements in human and bovine vascular endothelial cells

Project description:In this study we set out to discover conserved orthologous ERG-bound gene regulatory elements in primary vascular endothelial cells isolated from human and cow

2017-06-15 | E-MTAB-5148 | biostudies-arrayexpress

ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.

2014-03-02 | E-GEOD-54191 | biostudies-arrayexpress

Genome-wide mapping of H3K4me3 and H3K27ac in chicken immature erythrocyte cells

Project description:Transcriptional regulation is impacted by multiple layers of genome organization. Here, we report that highly expressed genes were associated with H3K4me3 and H3K27ac.Our data provide a genome-wide profile of chromatin signatures in relation to expression levels in chicken immature erythrocytes. Examination of two different histone modifications in immature erythrocyte cells

2016-07-03 | E-GEOD-75845 | biostudies-arrayexpress

The chicken erythrocyte epigenome

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-03 | E-GEOD-75955 | biostudies-arrayexpress

Genomic localization of Topoisomerase II beta

Project description:ChIP-seq of Top2b, CTCF, Rad21, H3K4me2, H3K36me3 in mouse liver. ChIP-exo of CTCF, Rad21 and Top2b

2016-08-05 | E-MTAB-3587 | biostudies-arrayexpress

Histone ChIP-seq of primary mouse aortic endothelial cells treated with TNFα against untreated controls

Project description:TNFα is a potent cytokine to mediate inflammatory response by activation of the master transcription factor NF-kB. Endothelial cells are important participants in inflammatory responses in animals. NF-kB is a major mediator to activate endothelial cells by inducing multiple pro-inflammatory genes in response to TNFα. NF-kB mediated gene transcription is known to accompany rapid changes in epigenetic states. However, the epigenetic landscape in response to the cytokine challenge TNFα in mouse endothelial cells has not been described. Our approach characterized the epigenetic profiles on a genome-wide scale and mapped putative active enhancers in primary mouse aortic endothelial cells.

2023-03-01 | E-MTAB-12212 | biostudies-arrayexpress

Single Cell Sequencing Identifies Key Epigenetic Regulators in Nuclear Transfer Mediated Reprogramming [RRBS]

Project description:Differentiated cell can be reprogrammed into totipotent embryo through somatic cell nuclear transfer (SCNT). However, this process is highly inefficient and most cloned embryos arrest at certain developmental stages. Through single cell sequencing combined with embryo biopsy, here we generate a global map of DNA methylome and RNA transcriptome for SCNT embryos with distinct developmental fates. We subsequently demonstrate that the unfaithful reactivation of two histone demethylases, Kdm4b and Kdm5b, accounts for the arrest of cloned embryos at 2-cell and 4-cell stage, respectively. Ectopic expression of Kdm4b and Kdm5b in SCNT can remove H3K9me3 barrier, restore the transcription profile and facilitate the blastocyst developmental efficiency over 95%. Moreover, these cloned embryos can further support full-term development and the derivation of SCNT-embryonic stem cells with greater efficiency. Our study reveals that histone methylation reset is crucial for the development of SCNT embryos, which provides a clue to further improve therapeutic cloning. For SCNT embryos 4-8 replicates were performed for each stage . As the control, 3 replicates were performed for each stage of wild type samples

2016-05-17 | E-GEOD-70607 | biostudies-arrayexpress

High-resolution enzymatic mapping of genomic 5-hydroxymethylcytosine in mouse embryonic stem cells

Project description:We describe the use of a novel DNA modification-dependent restriction endonuclease AbaSI coupled with sequencing (Aba-seq) to map high-resolution hydroxymethylome of mouse E14 embryonic stem cells. The specificity of AbaSI enables sensitive detection of 5hmC at low occupancy regions. Bioinformatic analysis suggests 5hmCs in genic regions closely follows the 5mC distribution. 5hmC is generally depleted in CpG islands and only enriched in a small set of repetitive elements. A regularly spaced and oscillating 5hmC pattern was observed at the binding sites of CTCF. 5hmC is enriched at the poised enhancers with the mono-methylated histone H3 lysine 4 (H3K4me1) marks, but not at the active enhancers with the acetylated histone H3 lysine 27 (H3K27Ac) marks. Non-CG hydroxymethylation appears to be prevalent in the mitochondrial genome. We propose that some amounts of transiently stable 5hmCs may indicate a poised epigenetic state or de-methylation intermediate, while others may suggest a locally accessible chromosomal environment to the TET enzymatic apparatus. Mapping of genomic 5-hydroxymethylcytosine in mouse embryonic stem cell by enzymatic digistion of AbaSI coupled with high-throughput sequencing, in replicates.

2013-01-01 | E-GEOD-42898 | biostudies-arrayexpress

Tet1 is a tumor suppressor of hematopoietic malignancy

Project description:Epigenetic pathways that regulate DNA methylation and chromatin modifications are frequently found to be dysregulated in human cancers. The TET methylcytosine dioxygenase 1 (TET1) enzyme is an important regulator of hydroxymethylcytosine (5hmC) in embryonic stem cells, neural progenitors,adult cells and reprogrammed cells. Decreased expression of TET proteins and loss of 5hmC has been reported in many tumors, suggesting a critical role for the maintenance of this epigenetic modification in normal cellular function. However, loss of TET1 function in the etiology of cancer has not been directly investigated. Here, we show that deletion of the Tet1 gene promotes the development of B cell lymphoma. Tet1 is required for maintaining normal levels of 5hmC, preventing aberrant DNA hypermethylation and for the regulation of transcriptional programs involved in B-cell lineage specification, chromosome maintenance, and DNA repair. Progenitor B cells in the absence of Tet1 accumulate DNA damage and whole-exome sequencing of Tet1-deficient tumors revealed a high correlation of mutations with those most frequently found in Non-Hodgkin B cell lymphoma (B-NHL) patients. In addition, we show that the TET1 gene is deleted, hypermethylated and transcriptionally silenced in B-NHL patients. These findings provide the first in vivo evidence of TET1 function as a tumor suppressor of hematopoietic malignancy. We did hydroxymethylation tests for two wild type mice and two Tet1 knockout mice.

2015-04-12 | E-GEOD-65895 | biostudies-arrayexpress

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