Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IL-1 versus p65 overexpression [human, rat]

ABSTRACT: IL-1 versus p65 overexpression [human, rat]

PROVIDER: PRJNA510929 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8358340.fastq.gz	Fastqsanger.gz
	SRR8358341.fastq.gz	Fastqsanger.gz
	SRR8358342.fastq.gz	Fastqsanger.gz
	SRR8358333.fastq.gz	Fastqsanger.gz
	SRR8358343.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

IL-1 versus p65 overexpression [human, rat]

Project description:Comparison of cytokine signaling in rat insulinoma cells versus human islets

2022-05-26 | GSE124166 | GEO

Analysis of p65 genomic location changes with IL-17 blockade

Project description:We characterize the effect that IL-17 blockade has on p65 genomic location in epidermal aged cells

2023-03-24 | GSE213732 | GEO

Trancriptome profiling of murine overexpression of p65/RelA mutants

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

2022-07-27 | GSE98437 | GEO

Transcriptome profiling of murine overexpression of p65/RelA mutants II

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in B16 Bcr-Abl+ murine cell lines

2022-07-27 | GSE135136 | GEO

Transcriptome profiling of murine overexpression of p65/RelA mutants III

Project description:Effect of overexpression of murine p65/RelA and D361 mutant and resulting fragments in DA1-3B Bcr-Abl+ murine cell lines

2022-07-27 | GSE135137 | GEO

ADRB3 overexpression in rat

Project description:ADRB3 overexpression in rat

| PRJNA627922 | ENA

The activation of IL-1 induced enhancers depends on TAK1 kinase activity and NF-KB p65 [RNA-Seq]

Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-?B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-?B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-?B-dependent enhancers in epithelial cells. RNA-seq of KB cells either untreated or treated with IL-1 alpha

2014-12-16 | E-GEOD-64185 | biostudies-arrayexpress

p65

Project description:p65

| PRJNA811604 | ENA

The activation of IL-1 induced enhancers depends on TAK1 kinase activity and NF-KB p65 [ChIP-Seq]

Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-κB subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-κB p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-κB-dependent enhancers in epithelial cells. ChIP-seq in KB cells with 5 different antibodies under different treatment conditions

2014-12-16 | E-GEOD-64223 | biostudies-arrayexpress

The activation of IL-1-induced enhancers depends on TAK1 kinase activity and NF-kappaB p65 I

Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-M-NM-:B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-M-NM-:B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-M-NM-:B-dependent enhancers in epithelial cells. Two sets of experiments were performed as biological replicate series (rep1 and rep2) each comprising of the following 4 conditions: Human epithelial KB cells were 1) left untreated or were 2) treated with Interleukin-1-alpha (10ng/M-BM-5l) for 1 hour, 3) treated for 1.5h with the TAK1 inhibitor 5Z-7-oxozeaenol (1M-BM-5M) or were 4) treated with 5Z-7-oxozeaenol for 30 minutes followed by Interleukin-1-alpha for 1 hour.

2014-12-17 | E-GEOD-64201 | 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