Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [Cut&Tag]

ABSTRACT: The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [Cut&Tag]

PROVIDER: PRJNA1149680 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30295049_1.fastq.gz	Fastqsanger.gz
	SRR30295049_2.fastq.gz	Fastqsanger.gz
	SRR30295050_1.fastq.gz	Fastqsanger.gz
	SRR30295050_2.fastq.gz	Fastqsanger.gz
	SRR30295051_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 58

Similar Datasets

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [Cut&Tag]

Project description:Skeletal muscle fibrosis, characterized by the replacement of functional muscle tissue with fibrotic scarring, leads to muscle function loss and potentially fatal respiratory failure, particularly in muscular dystrophy. The mechanisms driving muscle fibrosis is not yet fully understood. Our study utilized single-cell RNA-seq and single-nuclei ATAC-seq to analyze the transcriptome and chromatin accessibility of regenerating and dystrophic skeletal muscle, identifying a specific subset of fibro-adipogenic precursors (FAPs) enriched in dystrophic muscles, termed fibrotic FAPs. We further demonstrated that chronic inflammation upregulates Fosl1, an early response gene, which activates the expression of Kdm6b in fibrotic FAPs. Kdm6b, a histone demethylase, specifically removes the repressive histone H3K27me3 mark. Notably, targeting Kdm6b genetically and pharmacologically inhibits fibrotic di^erentiation in human and mouse FAPs in vitro and ameliorated muscle fibrosis in mouse models in vivo. Furthermore, constitutive activation of the Fosl1-Kdm6b pathway reduced H3K27me3 modification at critical fibrotic gene loci, leading to their transcriptional activation. Taken together, our findings reveal that chronic inflammation perpetuates the Fosl1-Kdm6b axis in FAPs, causing epigenomic reprogramming and altering the H3K27me3 landscape, which is essential for preventing fibrotic di^erentiation of FAPs and skeletal muscle fibrosis.

2025-02-28 | GSE275142 | GEO

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [HiCAR]

2025-02-28 | GSE275143 | GEO

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [scRNA-seq]

2025-02-28 | GSE275141 | GEO

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [bulk RNA-seq]

2025-02-28 | GSE275140 | GEO

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [HiCAR]

Project description:The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [HiCAR]

| PRJNA1149681 | ENA

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [scRNA-seq]

Project description:The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [scRNA-seq]

| PRJNA1149682 | ENA

The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [bulk RNA-seq]

Project description:The Fosl1-Kdm6b Axis Controls Skeletal Muscle Fibrosis by Regulating Histone H3K27me3 [bulk RNA-seq]

| PRJNA1149675 | ENA

KDM6B promotes activation of the oncogenic CDK4/6-pRB-E2F pathway by maintaining enhancer activity in MYCN-amplified neuroblastoma [CUT&TAG]

Project description:The H3K27me2/me3 histone demethylase KDM6B is over-expressed in neuroblastoma and is essential to neuroblastoma cell survival. While the KDM6B inhibitor, GSK-J4, has shown activity in in vitro and in vivo preclinical models, the mechanism of action remains poorly defined. We demonstrate that genetic and pharmacologic inhibition of KDM6B downregulates the pRB-E2F transcriptome and MYCN expression. Chemical genetic analyses show that high expression of the E2F transcriptome is positively correlated with sensitivity of cancer cells to GSK-J4. Mechanistically, inhibition of KDM6B activity 1) reduces the chromatin accessibility of E2F target genes and MYCN, 2) selectively leads to an increase of H3K27me3 but a decrease of the enhancer mark H3K4me1 at the CTCF and BORIS binding sites, which may, consequently, disrupt the long-range chromatin interaction of MYCN and E2F target genes, and 3) phenocopies the transcriptome induced by the specific CDK4/6 inhibitor palbociclib. Overexpression of CDK4/6 or Rb1 knockout confers neuroblastoma cell resistance to both palbociclib and GSK-J4. A gene signature targeted by KDM6B inhibition is associated with poor survival of patients with neuroblastoma regardless of the MYCN status. These data indicate that KDM6B activity promotes an oncogenic CDK4/6-pRB-E2F pathway in neuroblastoma cells via H3K27me3-dependent enhancer-promoter interactions, providing a rationale to target KDM6B for high-risk neuroblastoma.

2021-10-29 | GSE182884 | GEO

H3K27me3 localization in UTX deficient Plasma cells by CUT&Tag

Project description:To understand the role of the H3K27me3 demethylases, UTX and JMJD3, in B cell differentiation. CUT&Tag for H3K27me3 was performed on CreCtrl and dKO (UTX and JMJD3-deficient) PC at day three post in vivo stimulation with LPS.

2022-02-01 | GSE185098 | GEO

ChIP-seq analysis of MED1 and FOSL1 in SCC1 cells after depletion of FOSL1

Project description:To explore genome-wide alteration MED1 and FOSL1 after depletion of FOSL1, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of MED1 and FOSL1 following FOSL1 knockdown. Depletion of FOSL1 led to dramatically loss of the recruitment of MED1 and FOSL1 at a cohort of key oncogenes associate with tumorigenesis and metastasis.

2021-04-14 | GSE151132 | 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