Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [Histons modifications ChIP-seq]

ABSTRACT: Podocytes are highly specialized cells, but their chromatin status and the precise molecular events leading to their differentiation remain poorly defined. Here we used ChIP-Seq analysis for H3K4me3, H3K4me1 and H3K27me3 to establish the histone methylation map in adult.Loss of MafB led to the deposition of extracellular matrix, progressive foot process effacement, and kidney disease. mouse podocytes. Our data demonstrate open chromatin across podocyte specific genes and reveals that genes expressed in the mesoderm lineage become actively repressed upon podocyte differentiation. To better understand the transcriptional control of podocyte differentiation, we studied the role of transcription factor MAFB.

ORGANISM(S): Mus musculus

PROVIDER: GSE233911 | GEO | 2024/09/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [WT1-MAFB_ChIP-seq]

Project description:Podocytes are highly specialized cells, but their chromatin status and the precise molecular events leading to their differentiation remain poorly defined. Here we used ChIP-Seq analysis for H3K4me3, H3K4me1 and H3K27me3 to establish the histone methylation map in adult.Loss of MafB led to the deposition of extracellular matrix, progressive foot process effacement, and kidney disease. mouse podocytes. Our data demonstrate open chromatin across podocyte specific genes and reveals that genes expressed in the mesoderm lineage become actively repressed upon podocyte differentiation. To better understand the transcriptional control of podocyte differentiation, we studied the role of transcription factor MAFB.

2024-09-30 | GSE233910 | GEO

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [MAFb KO RNA-seq]

2024-09-30 | GSE233912 | GEO

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters

Project description:MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters

| PRJNA978556 | ENA

Transcriptome profile of MafB-cKO of podocyte

Project description:The transcription factor MafB is essential for differentiation and foot process formation of podocytes. In order to identify the downstream targets of MafB, we analyzed the Mafb-deficient podocyte by RNA-seq. We found slit diaphragm-related protein (Nphs1, Magi2), Rho GTPase-activating protein (Arhgap24, Iqgap2) and podocyte-specific transcription factor (Tcf21) were significantly reduced in MafB cKO glomeruli. This indicates that one of these factors might be directly regulated by MafB to maintain its function in podocyte maintenance.

2021-08-03 | GSE96044 | GEO

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [MAFb KO RNA-seq]

Project description:MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [MAFb KO RNA-seq]

| PRJNA978562 | ENA

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [WT1-MAFB_ChIP-seq]

Project description:MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [WT1-MAFB_ChIP-seq]

| PRJNA978561 | ENA

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [Histons modifications ChIP-seq]

Project description:MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters [Histons modifications ChIP-seq]

| PRJNA978563 | ENA

MAFB permits differentiation by permitting WT1 binding to podocyte specific promoters

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

2024-09-30 | GSE233913 | GEO

Genome-wide analysis of WT1-controlled gene expression in podocytes

Project description:We identified binding sites of the Wilms' tumor suppressor protein WT1 in the mouse podocyte genome in vivo by ChIP-seq. Furthermore, we provide a podocyte transcriptome derived from primary podocytes that were isolated by FACS on mouse glomeruli. In short, we show that WT1 activates a highly specific podocyte transcriptome by binding to putative podocyte-specific enhancers and TSS of target genes. Genes bound by WT1 in podocytes include the majority of genes mutated in hereditary podocytopathies as well as components of the slit diaphragm, actin cytoskeleton, extracellular matrix, and within endocytosis pathways. Furthermore, we infer a podocyte TF network from DNA-binding motifs enriched at WT1-bound loci that includes Tead, Lmx1b, Mafb, Tcf21, and Fox-class transcription factors. Examination of transcription factor binding sites for WT1 by ChIP-seq. Transcriptome analysis of podocytes by RNA-seq.

2014-12-11 | E-GEOD-64063 | biostudies-arrayexpress

FOXC2 and WT1 regulate transcriptional reprogramming during the podocyte response to injury

Project description:In the context of human disease, the mechanisms whereby transcription factors reprogram gene expression in reparative responses to injury are not well understood. We have studied the mechanisms of transcriptional reprogramming in disease using murine kidney podocytes as a model for tissue injury. Podocytes are a crucial component of glomeruli, the filtration units of each nephron. Podocyte injury is the initial event in many processes that lead to End Stage Kidney Disease. FOXC2 is a transcription factor known to regulate gene expression in podocytes. FOXC2 and WT1 are both required for podocyte differentiation. Using murine models and human kidney organoids, we investigated FOXC2-mediated transcriptional reprogramming during the course of podocyte injury. Correlating FOXC2 and WT1 ChIP-seq analyses demonstrated that they co-bind many genes expressed in podocytes. Reprogramming the transcriptome involved highly dynamic changes in the binding of FOXC2 and WT1 to target genes during a reparative injury response.

2023-11-01 | GSE213174 | 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