Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide map of NFIB/MLL1 complex binding and H3K4me3 deposition during osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

ABSTRACT: To explore direct targets of NFIB/MLL1 complex and to examine the role of NFIB/MLL1 complex in genome-wide deposition of histone H3-K4 tri-methylation (H3K4me3), we conducted chromatin immunoprecipitation (ChIP) followed by deep sequencing (ChIP-seq) analysis of six different samples at two time points.

ORGANISM(S): Mus musculus

PROVIDER: GSE227536 | GEO | 2023/09/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

Project description:To examine the impact of the NFIB/MLL1 complex on the transcriptome of C3H10T1/2 mesenchymal stem cells (MSCs) and to identify NFIB/MLL1-dependent genes during osteogenic differentiation, we performed RNA-sequencing (RNA-seq) analysis of six different samples at two time points.

2023-09-05 | GSE227537 | GEO

Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:To investigate the cooperative function KDM4D/NFIB/MLL1 complex in the regulation of adipogenic differentiation, we established 10T1/2 cell lines in which each target gene has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2020-02-26 | GSE131369 | GEO

Chromatin immunoprecipitation of human MLL1 to understand its role in cell type specification

Project description:An experiment was performed to understand its role in cell type specification, we have determined the human genomic binding sites of MLL1. MLL1 localizes with Pol II to the 5' end of actively transcribed genes, where histone H3 lysine 4 (H3-K4) trimethylation occurs. The ability of MLL1 to serve as a start site-specific global transcriptional regulator and to participate in larger chromatin domains at the Hox genes reveals the dual roles MLL1 plays in maintenance of cellular identity.

2005-06-03 | E-WMIT-4 | biostudies-arrayexpress

Histone demethylase KDM4D cooperates with NFIB and MLL1 complex to regulate adipogenic differentiation of C3H10T1/2 mesenchymal stem cells.

Project description:The coordinated and sequential actions of lineage-specific transcription factors and epigenetic regulators are essential for the initiation and maintenance of cellular differentiation. We here report KDM4D histone demethylase as a key regulator of adipogenesis in C3H10T1/2 mesenchymal stem cells. The depletion of KDM4D results in impaired differentiation, which can be rescued by exogenous KDM4D, PPAR?, and C/EBP?, but not by C/EBP?. In addition, KDM4D interacts physically and functionally with both NFIB and MLL1 complex to regulate C/EBP? and PPAR? expression upon adipogenic hormonal induction. Although KDM4D is dispensable for the binding of both NFIB and MLL1 complex to the target promoters, the demethylation of tri-methylated H3K9 by KDM4D is required for NFIB and MLL1 complex to deposit tri-methylated H3K4 and activate PPAR? and C/EBP? expression. Taken together, our data provide a molecular framework for lineage-specific transcription factor and histone modifiers to cooperate in adipogenic differentiation, in which KDM4D removes repressive histone marks at genes with a bivalent chromatin domain and allows NFIB and MLL1 complex to promote the expression of key adipogenic regulators.

| S-EPMC7033117 | biostudies-literature

Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

| PRJNA543354 | ENA

NFIB/MLL1 complex is required for the stemness and the Dlx5-dependent osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-05 | GSE227538 | GEO

Expression analysis on Mll1+/+ and Mll1-/- MEFs

Project description:Global analysis of H3K4 methylation defines MLL family member targets and points to a role for MLL1-mediated H3K4 methylation in the regulation of transcriptional initiation by RNA polymerase II A common landmark of activated genes is the presence of trimethylation on lysine 4 of histone H3 (H3K4) at promoter regions. The Set1/COMPASS was the founding member and the only H3K4 methylases in S. cerevisiae, however, in mammals at least six H3K4 methylases Set1A/B and MLL1-4 are found in COMPASS-like complexes capable of methylating H3K4. To gain further insight into the different roles and functional targets for the H3K4 methylases, we have undertaken a genome-wide analysis of H3K4 methylation pattern in wild-type Mll1+/+ and Mll1-/- mouse fibroblasts (MEFs). We found that Mll1 is required for the H3K4 trimethylation of less than 5% of promoters carrying this modification. Many of these genes, which include developmental regulators such as Hox genes show decreased levels of RNA polymerase II recruitment and expression concomitant with the loss of H3K4 methylation. Although Mll1 is only required for the methylation of a subset of Hox genes, Menin, a component of the Mll1 and Mll2 complexes, is required for the overwhelming majority of H3K4 methylation at Hox loci. However, the loss of MLL3/4 and/or the Set1 complexes have little to no effect on the Hox loci H3K4 methylation or expression levels in these MEFs. Together these data provide insight into redundancy and specialization of COMPASS-like complexes in mammals and provide evidence on a possible role for Mll1-mediated H3K4 methylation in the regulation of transcriptional initiation. Expression arrays were done with Mll1+/+ and Mll1-/- mouse embryonic fibroblasts. Four replicates were done (dyes were swapped). DNA was hybridized to Agilent Mouse Whole Genome Expression Arrays (4x44k).

2009-10-20 | E-GEOD-18261 | biostudies-arrayexpress

Identifying NFIB target genes in mammalian cells

Project description:NFIB is a transcription factor that can both positively and negatively regulate gene transcription. We have identified NFIB as an arginine methylation substrate of CARM1. To elucidate how CARM1 could regulate NFIB target genes by methylating NFIB, we performed this ChIP-seq to firstly identify NFIB direct binding gengs.

2022-12-15 | GSE219265 | GEO

NFIB Is a Pioneer Factor for DNA Replication by Acting as a Genome Organizer [H3K4me3 CUT&Tag]

Project description:Genome-wide profiling of histone H3K4me3 of G1 or S phase U2OS cells without or with NFIB depletion.

2023-08-22 | GSE223438 | GEO

The NFIB/CARM1 Partnership is a Therapeutic Target for Small Cell Lung Cancer

Project description:This project identified NFI family members as CARM1 substrates. NFIB was previously reported to play a critical role in the development of small cell lung cancer. We provided evidence that the arginine methylation of NFIB is required for its oncogenic function in small cell lung cancer.

2023-02-07 | PXD038237 | Pride

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