Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Liangxi Wang

PROVIDER: E-MTAB-12212 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Multi-species RELA ChIP-seq of mammalian aortic endothelial cells before and after TNFα stimulation

Project description:TNFα has an evolutionary conserved role in mediating inflammation via activation of the transcription factor NF-κB. The functions of individual NF-κB binding sites are not well understood. To identify conserved and functionally important NF-κB binding sites in mammals, we performed ChIP-seq to map the genome-wide binding of RELA and select histone modifications in primary vascular endothelial cells (ECs) isolated from the aortas of human (HAEC), mouse (MAEC) and cow (BAEC), before and after TNFα. The conserved RELA binding sites show strong epigenetic changes in response to TNFα and enrich near genes controlling vascular development and pro-inflammatory responses. Our method identifies novel modes of RELA-chromatin interactions that are conserved in mammals and shared between multiple cell-types. Particularly, genomic regions bound by RELA prior to stimulation are important responders during TNFα stimulation. We use CRISPR/Cas9 genome editing to validate the roles of the conserved RELA pre-bound sites near pro-inflammatory genes such as CCL2 and PLK2. Our evolutionary approach describes new aspects of mammalian NF-κB biology including its role within super-enhancers and relevance in inflammatory disorders.

2020-10-03 | E-MTAB-7889 | biostudies-arrayexpress

H3K4me3 HiChIP of immortalized human 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. The process of transcriptional activation is dependent on the context of chromatin interactions/loops. However, the chromatin conformation in response to the cytokine challenge TNFα in human aortic endothelial cells has not been described. Our approach characterized chromatin interactions from active enhancers to promoters as well as active promoters to promoters on a genome-wide scale and highlighted important enhancer candidates for target genes.

2023-03-01 | E-MTAB-12213 | biostudies-arrayexpress

ATAC-seq of primary mammalian aortic endothelial cells before and after TNFα stimulation

Project description:To identify conserved TNFα-induced changes in chromatin-accessibility in mammals, we performed ATAC-seq in primary vascular endothelial cells (ECs) isolated from the aortas of human (HAEC), mouse (MAEC) and cow (BAEC), before and after TNFα. We overlay our data with multi-species NF-κB binding data and identify multiple modes of NF-κB-chromatin interactions that are conserved during mammalian TNFα response. Our cross-species approach identifies conserved changes in chromatin-accessibility at NF-κB binding sites that are disease-relevant and essential during mammalian acute inflammation.

2020-06-01 | E-MTAB-7878 | biostudies-arrayexpress

The NF-kB genomic landscape in lymphoblastoid B-cells

Project description:The nuclear factor kB (NF-kB) subunits RelA, RelB, c-Rel, p50 and p52 are each critical for B-cell development and function. To systematically characterize their responses to canonical and non-canonical NF-kB pathways activity, we performed ChIP-seq analysis in lymphoblastoid B-cells. We found a surprisingly complex NF-kB binding landscape, which did not readily reflect the two NF-kB pathway paradigm. Instead, ten subunit binding patterns were observed at promoters and eleven at enhancers. Surprisingly, nearly one-third of NF-kB binding sites lacked kB motifs. De novo motif finding uncovered distinct modes of NF-kB recruitment at these sites. The oncogenic forkhead box protein FOXM1 and NF-kB co-occupied many kB sites despite the absence of a FOXM1 DNA motif. FoxM1 knockdown decreased expression of key NF-kB targets and caused apoptosis. Our study highlights opportunities for selective therapeutic NF-kB blockade. ChIP-seq was used to define the genomic landscape of NF-kB DNA binding in lymphoblastoid cells.

2014-08-29 | E-GEOD-55105 | biostudies-arrayexpress

TNFalpha signaling primes chromatin for NF-kappaB binding and induces rapid and widespread nucleosome repositioning

Project description:Background The rearrangement of nucleosomes along the DNA fiber profoundly affects gene expression, but little is known about how signaling reshapes the chromatin landscape, in 3D space and over time, to allow the establishment of new transcriptional programs. Results Using micrococcal nuclease treatment and high-throughput sequencing, we map genome-wide changes in nucleosome positioning in primary human endothelial cells stimulated with tumour necrosis factor alpha (TNFalpha) - a proinflammatory cytokine that signals through nuclear factor kappaB (NF-kappaB). Within 10 minutes, nucleosomes reposition at regions both proximal and distal to NF-kappaB binding sites, before the transcription factor quantitatively binds thereon. Similarly, in long TNFalpha-responsive genes, repositioning precedes transcription by pioneering elongating polymerases and appears to nucleate from intragenic enhancer clusters resembling super-enhancers. By 30 minutes, widespread repositioning occurs throughout Mbp-long chromosomal segments, with consequential effects on 3D structure, detected using chromosome conformation capture. Conclusions Whilst nucleosome repositioning is viewed as a local phenomenon, our results point to effects occurring over multiple scales. Here, we present data in support of a TNFalpha-induced priming mechanism, mostly independent of NF-kappaB binding and/or elongating RNA polymerases, leading to a plastic network of interactions that affects DNA accessibility over large domains. MNase-Seq of HUVEC cells after stimulation with TNFÎ± for 0, 10 or 30 min. Biological replicates for 0 and 30 min.

2014-11-05 | E-GEOD-53343 | biostudies-arrayexpress

4C-seq of CCL2 promoter contacts in primary human aortic endothelial cells and TeloHAEC cell line before and after TNFα stimulation

Project description:We characterized DNA contacts of CCL2 promoter to show its interactions with RELA binding sites within a super-enhancer in primary human aortic endothelial cells and TeloHAEC cell line under basal and TNFα stimulated conditions

2020-06-01 | E-MTAB-8272 | biostudies-arrayexpress

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers [Chem-Seq]

Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. Chem-Seq for the biotinylated small molecule JQ1 in untreated or TNFalpha treated human endothelial cells

2014-09-29 | E-GEOD-60051 | biostudies-arrayexpress

NF-kB coordinates rapid, BRD4-dependent remodeling of proinflammatory super-enhancers [ChIP-Seq]

Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. ChIP-Seq for various transcription factors, RNA Polymerase II, and histone modifications in human endothelial cells

2014-09-29 | E-GEOD-53998 | 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

A novel YDDX linear motif mediates docking of the IKK kinase to substrates: structural and functional insights

Project description:The inhibitor of kB kinase (IKK) is the master regulator of the nuclear factor kB (NF-kB) pathway, involved in inflammatory, immune and apoptotic responses. In the ‘canonical’ NF-kB pathway, IKK phosphorylates inhibitor of kB (IkB) proteins and this triggers ubiquitin-mediated degradation of IkB, leading to release and nuclear translocation of NF-B transcription factors. The data presented show that the IKK and IKK subunits recognize a YDDX docking site located within the disordered C-terminal region of IkBa. Our results also suggest that IKK contributes to the docking interaction with higher affinity as compared to IKK.

2024-05-09 | PXD037534 | JPOST Repository

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