Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNA-Seq]

ABSTRACT: Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNA-Seq]

PROVIDER: PRJNA851251 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19760833_1.fastq.gz	Fastqsanger.gz
	SRR19760833_2.fastq.gz	Fastqsanger.gz
	SRR19760834_1.fastq.gz	Fastqsanger.gz
	SRR19760834_2.fastq.gz	Fastqsanger.gz
	SRR19760835_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [ChIP-seq]

Project description:We previously demonstrated that the NF-κB inhibitor IκBα binds the chromatin together with PRC2 to regulate a subset of developmental- and stem cell-related genes. This alternative function has been elusive in both physiological and disease conditions because of the predominant role of IκBα as a negative regulator of NF-κB. We here uniquely characterize specific residues of IκBα that allow the generation of separation-of-function (SOF) mutants that are defective for either NF-κBrelated (SOF DeltaNF-κB) or chromatin-related (SOF DeltaH2A,H4) activities. Expression of IκBα SOF DeltaNF-κB, but not SOF DeltaH2A/H4, is sufficient to negatively regulate a specific stemness program in intestinal cells, thus rescuing the differentiation blockage imposed by IκBα deficiency. . By ChIP assay we demonstrated IκBα binding to several stem cell genes that are transcriptionally repressed following IκBα SOF DeltaNF-κB induction. Our data indicate that SOF mutants represent an exclusive tool for studying IκBα functions in physiology and disease.

2025-05-18 | GSE271349 | GEO

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNA-Seq]

2025-05-18 | GSE206515 | GEO

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNAseq Knock-ins IKBa]

2025-05-18 | GSE292288 | GEO

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness

Project description:Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness

| PRJNA1000982 | ENA

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [ChIP-seq]

Project description:Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [ChIP-seq]

| PRJNA1130975 | ENA

Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNAseq Knock-ins IKBa]

Project description:Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNAseq Knock-ins IKBa]

| PRJNA1237823 | ENA

Chromatin activity of IκBα mediates the exit from naïve pluripotency (Methylation array)

Project description:Inflammatory signals are key in development and cell differentiation but their orchestration with pluripotency and stemness signals is poorly understood. Our previous work identified a chromatin function of IκBα, the NF-κB inhibitor, that is crucial for differentiation in different types of somatic stem cells. Here we demonstrate that deficiency of IκBα imposes a profound chromatin rewiring defect that impacts on DNA methylation, histone post-translational modifications and transcriptional regulation, stabilizing mouse embryonic stem cells (ESCs) in a ground state of pluripotency while preventing them from pluripotency exit and differentiation. By engineering separation-of-function mutants of IκBα with specific binding to either NF-κB or histones, we demonstrate that regulation of pluripotency state by IκBα is independent of NF-kB but requires the chromatin-related IκBα function.

2025-03-25 | GSE239562 | GEO

Chromatin activity of IκBα mediates the exit from naïve pluripotency (RNA-Seq)

2025-03-25 | GSE239563 | GEO

Chromatin activity of IκBα mediates the exit from naïve pluripotency (ChIP-seq Histone marks)

2025-03-25 | GSE239564 | GEO

Expression data from RH30 vector and RH30 IκBα SR cells

Project description:Classical NF-κB activity can be inhibited by overexpression of the IκBα super repressor (SR). To determine the role of NF-κB in rhabdomyosarcoma cells, we overexpressed the IκBα SR in RH30 rhabdomyosarcoma cells. IκBα SR was overexpressed in RH30 cells. RH30 vector cells were used as control group.

2018-03-30 | GSE112119 | 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