Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CUT&Tag analysis uncovered Pou4f1-bound DNA elements in E16.5 retinas

ABSTRACT: To understand how Pou4f1 functions in RGC lineage specification and subtype formation, we performed “Cleavage Under Targets & Tagmentation” (CUT&Tag) analysis using a rabbit anti-Pou4f1 antibody and embryonic 16.5 (E16.5) retinal cells to generate barcoded PCR libraries that are enriched for Pou4f1-mediated binding. In parallel, rabbit IgG was used as a negative control for peak calling analysis, and rabbit anti-H3K9ac antibody was used to mark active enhancers and promoters.

ORGANISM(S): Mus musculus

PROVIDER: GSE221209 | GEO | 2023/04/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CUT&Tag analysis uncovered Pou4f1-bound DNA elements in E16.5 retinas

Project description:CUT&Tag analysis uncovered Pou4f1-bound DNA elements in E16.5 retinas

| PRJNA913195 | ENA

POU4F1 is associated with t(8;21) AML and contributes directly to its unique transcriptional signature

Project description:POU4F1 is associated with t(8;21) acute myeloid leukemia (AML) and contributes directly to its unique transcriptional signature To identify targets of POU4F1, we performed gene expression profiling, comparing Pou4f1+/+ or Pou4f1-/- fetal liver cells to cells overexpressing POU4F1 and identified 140 differentially expressed genes.

2010-04-09 | E-GEOD-19997 | biostudies-arrayexpress

Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer

Project description:Basal-like breast cancer (BLBC) is the most aggressive molecular subtype of breast cancer with worse prognosis and fewer treatment options. The underlying mechanisms upon BLBC transcriptional dysregulation and its upstream transcription factors (TFs) remain unclear. Here, among the hyperactive candidate TFs of BLBC identified by bioinformatic analysis, POU4F1 is uniquely upregulated in BLBC and is associated with poor prognosis. POU4F1 is necessary for the tumor growth and malignant phenotypes of BLBC through regulating G1/S transition by direct binding at the promoter of CDK2 and CCND1. More importantly, POU4F1 maintains BLBC identity by repressing ERα expression through CDK2-mediated EZH2 phosphorylation and subsequent H3K27me3 modification in ESR1 promoter. Knocking out POU4F1 in BLBC cells reactivates functional ERa expression, rendering BLBC sensitive to tamoxifen treatment. In-depth epigenetic analysis reveals that the subtype-specific re-configuration and activation of the bivalent chromatin in the POU4F1 promoter contributes to its unique expression in BLBC, which is maintained by DNA demethylase TET1. Together, these results reveal a subtype-specific epigenetically activated TF with critical role in promoting and maintaining BLBC, suggesting that POU4F1 is a potential therapeutic target for BLBC.

2024-03-14 | GSE261462 | GEO

ISL1 and POU4F1 Directly Interact to Regulate the Differentiation and Survival of Inner Ear Sensory Neurons

Project description:Isl1 and Pou4f1 regulate a unique set of CVG gene cooperatively or individually. GO term analysis shows these genes are crucial for CVGs development. To estimate Isl1 and Pou4f1 directly or indirectly regulate these downstream genes and how they act to affect these genes, we performed the CUT&Tag of ISL1 and POU4F1 with the histone modifications, H3K4me3, H3K27ac and H3K27me3 in CVGs. The identity of the peaks were characterized and big chromatin profiles were obtained.

2024-05-31 | GSE233840 | GEO

POU4F1 is associated with t(8;21) AML and contributes directly to its unique transcriptional signature

Project description:POU4F1 is associated with t(8;21) acute myeloid leukemia (AML) and contributes directly to its unique transcriptional signature

2010-04-09 | GSE19997 | GEO

ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

Project description:To investigate the downstream genes of Isl1 and Pou4f1 in CVGs, we examined the gene expression level of each single knockout and double knockout compared with control.

2024-05-31 | GSE233755 | GEO

ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

Project description:The inner ear sensory neurons play a pivotal role in auditory processing and balance control. Though significant progresses have been made, the underlying mechanisms controlling the differentiation and survival of the inner ear sensory neurons remain largely unknown. During development, ISL1 and POU4F transcription factors are co-expressed and are required for terminal differentiation, pathfinding, axon outgrowth and the survival of neurons in the central and peripheral nervous systems. However, little is understood about their functional relationship and regulatory mechanism in neural development. Here, we have knocked out Isl1 or Pou4f1 or both in mice of both sexes. In the absence of Isl1, the differentiation of cochleovestibular ganglion (CVG) neurons is disturbed and with that Isl1-deficient CVG neurons display defects in migration and axon pathfinding. Compound deletion of Isl1 and Pou4f1 causes a delay in CVG differentiation and results in a more severe CVG defect with a loss of nearly all of spiral ganglion neurons (SGNs). Moreover, ISL1 and POU4F1 interact directly in developing CVG neurons and act cooperatively as well as independently in regulating the expression of unique sets of CVG-specific genes crucial for CVG development and survival by binding to the cis-regulatory elements including the promoters of Fgf10, Pou4f2, and Epha5 and enhancers of Eya1 and Ntng2 These findings demonstrate that Isl1 and Pou4f1 are indispensable for CVG development and maintenance by acting epistatically to regulate genes essential for CVG development.

2024-05-31 | GSE233706 | GEO

RNAseq changes in fibroblasts after treatment with selected protein(s) or E16.5 skin extract

Project description:Purpose: To identify the cellular processes upregulated in fibroblasts after treatment with selected protein(s) or E16.5 skin extract Methods: To explore the mechanism of extract-induced HF neogenesis, adult dermal fibroblasts were cultured in the presence of E16.5 extract or selected protein(s) for 3 days before being tested. Results: we determined how the exposure of adult fibroblasts to E16.5 extract, the selected protein mix or each of the selected proteins and compared the resultant transcriptomes with those of adult DP and embryonic dermal fibroblasts. Conclusions: Gene expression of adult fibroblasts exposed to E16.5 extract and selected proteins mix, the key DP signature genes became upregulated.

2016-08-10 | GSE85303 | GEO

RNAseq changes in human fibroblasts after treatment with E16.5 skin extract

Project description:To identify the cellular processes upregulated in fibroblasts after treatment with E16.5 skin extract

2017-02-24 | GSE95245 | GEO

ChIP-seq profiling of H3K27 tri-methylation in Ezh2-deficient and control murine lung epithelium at day E16.5

Project description:Epithelial (CD31-CD45-EpCAM+) lung cells were derived by FACS from ShhCre;Ezh2fl/fl and control ShhCre;Ezh2fl/+ mouse embryos at day E16.5 (2 biological replicates per genotype). Chromatin from each of the replicates was immunoprecipitated with H3K27me3 antibody (Millipore #07-449) and subjected to NGS library preparation using TruSeq Nano DNA Sample Preparation Kit (Illumina). Completed libraries from different samples were sequenced on HiSeq 2500 TruSeq with SBS Kit v3 - HS reagents (Illumina) as 100 bp single end reads at the Australian Genome Research Facility.

2015-05-11 | GSE57392 | 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