Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dissecting the Mechanisms of Transcriptional Synergy in Response to Proinflammatory Cytokines in Endothelial Cells

ABSTRACT: Dissecting the Mechanisms of Transcriptional Synergy in Response to Proinflammatory Cytokines in Endothelial Cells

PROVIDER: PRJNA971164 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24492108_1.fastq.gz	Fastqsanger.gz
	SRR24492108_2.fastq.gz	Fastqsanger.gz
	SRR24492109_1.fastq.gz	Fastqsanger.gz
	SRR24492109_2.fastq.gz	Fastqsanger.gz
	SRR24492110_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 160

Similar Datasets

Dissecting the Mechanisms of Transcriptional Synergy in Response to Proinflammatory Cytokines in Endothelial Cells

Project description:Combinatorial cytokine signaling is implicated in the pathogenesis of diseases of the cardiovascular system ranging from acute combinatorial cytokine signaling observed in complications from SARS-COVID19 infection to chronic combinatorial cytokine signaling observed in atherosclerosis. There remains a large gap of our understanding how combinatorial cytokine signaling interface to drive proinflammatory programs. We hypothesize that stimulation of HAECs with IFNg and TNFa promotes synergistic gene transcription through the coordinated interplay between p65, STAT1, p300/CBP, and BRD4. Our work demonstrates through the generation of novel statistical framework that IFNg and TNFa dual stimulation for one hour results in the synergistic induction of a small subset of proinflammatory genes. Prolonged dual cytokine stimulation results in synergistic levels of protein expression and cell death. Treatment with A-485 and/or JQ1 reduces levels of synergistic gene and protein expression along with improvements in cell viability. Defining synergistic responses and identifying their unique transcriptional dependencies opens the door to understanding how disparate cytokine signaling drives proinflammatory responses and how these responses can be targeted.

2024-05-02 | GSE232168 | GEO

RPSA and proinflammatory cytokines after HSV-1 infection

Project description:RPSA and proinflammatory cytokines after HSV-1 infection

| PRJNA842678 | ENA

IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

Project description:IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

| PRJNA416508 | ENA

Deficiency of RPSA reduces binding of P65 to proinflammatory cytokines promoter regions in HSV-1 infection

Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the enrichment of P65 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.

2023-11-12 | GSE204891 | GEO

Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

Project description:Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

| PRJNA656998 | ENA

Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines [18hrs]

Project description:Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines [18hrs]

| PRJNA758807 | ENA

Circulating proinflammatory cytokines alter transcriptional activity within fibrotic tissue of Dupuytren’s disease patients

Project description:In this project, we have utilized blood and tissue samples from patients with Dupuytren’s disease (DD), a common fibroproliferative disorder of the hand, to identify increased circulating proinflammatory cytokines and assess alterations in the tissue using RNAseq and FTIR analysis. Our results indicate that specific cytokines in circulation play a direct role in local disease progression and may be useful for prospective identification of patients at risk for disease progression or recurrence as well as the development of novel therapeutic strategies. Furthermore, these results help to mechanistically link the well understood association of DD with chronic low-grade inflammatory states.

2021-06-01 | GSE169477 | GEO

Circulating proinflammatory cytokines alter transcriptional activity within fibrotic tissue of Dupuytren’s disease patients

Project description:Circulating proinflammatory cytokines alter transcriptional activity within fibrotic tissue of Dupuytren’s disease patients

| PRJNA716676 | ENA

Proinflammatory cytokines promote TET2-mediated DNA demethylation during CD8 T cell effector differentiation

Project description:Proinflammatory cytokines promote TET2-mediated DNA demethylation during CD8 T cell effector differentiation

| PRJNA758558 | ENA

Single-cell RNA-sequencing of mouse islets exposed to proinflammatory cytokines

Project description:Exposure to proinflammatory cytokines is believed to contribute to pancreatic β-cells during diabetes development. While some cytokine-mediated changes in islet gene expression are known, the heterogeneity of the response is not well-understood. Following 6 hour treatment with interleukin-1 beta (IL-1β) and interferon-gamma (IFN-γ) alone or together, mouse islets were subjected to single-cell RNA-sequencing (scRNA-seq). Inducible nitric oxide synthase (iNOS) mRNA (Nos2), antiviral genes, and immune-associated genes were induced in a subset of β-cells in response to both cytokines, while IL-1β alone activated only antiviral genes. Subsets of α- and δ-cells expressed Nos2 and exhibited similar gene expression changes as β-cells, including induction of antiviral genes and repression of identity genes. Finally, cytokine-responsiveness was inversely correlated with expression of genes encoding heat shock proteins. Our findings show that all endocrine cell types respond to cytokines, IL-1β induces the expression of protective genes in β-cells, and cellular stress gene expression is associated with an inhibition in cytokine signaling.

2021-04-15 | GSE156175 | 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