Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ATAC-seq]

ABSTRACT: BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ATAC-seq]

PROVIDER: PRJNA882078 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21628615_1.fastq.gz	Fastqsanger.gz
	SRR21628615_2.fastq.gz	Fastqsanger.gz
	SRR21628616_1.fastq.gz	Fastqsanger.gz
	SRR21628616_2.fastq.gz	Fastqsanger.gz
	SRR21628617_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

Project description:Post-translational modifications (PTMs) on histones play essential roles in cell fate decisions during development. However, how these PTMs are recognized and coordinated remains to be fully illuminated. Here, we show that BRPF1, a multi-histone binding module protein, is essential to maintain pluripotency in human embryonic stem cells (ESCs). BRPF1, H3K4me3 and H3K23ac substantially co-occupy the active and stemness genes in hESCs. BRPF1 deletion impairs H3K23ac and leads to pluripotency exit and closed chromatin accessibility on stemness genes. Deletion of the N terminal or PHD-zinc knuckle-PHD (PZP) modules completely impairs BRPF1 to maintain hESC pluripotency while PWWP module deletion only partially impact its functions. Together, we reveal that the multi-histone binding module protein, BRPF1 co-ordinates the crosstalk between different histone modifications to maintain the pluripotency in hESCs.

2022-12-21 | GSE213694 | GEO

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ChIP-seq]

2022-12-21 | GSE213692 | GEO

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ATAC-seq]

2022-12-21 | GSE213690 | GEO

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency

| PRJNA882072 | ENA

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ChIP-seq]

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ChIP-seq]

| PRJNA882079 | ENA

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

| PRJNA882080 | ENA

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency

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

2022-12-21 | GSE213695 | GEO

RNA-Seq analysis of wild-type and Brpf1-null fetal liver LSK cells

Project description:To compare the impact of hematopoietic-specific Brpf1 gene inactivation, LSK (Lin-Sca1+cKit1+) cells were sorted from wild-type and Brpf1-null fetal liver cells for RNA-Seq.

2016-08-10 | GSE83483 | GEO

Change in H3K4me3 in Suz12(Bgal/Bgal) ESCs, and over Spinal Motor Neuron differentiation (ChIP-Seq)

Project description:Suz12(Bgal/Bgal) ESCs express a truncated form of Suz12 fused to Beta-galactosidase. These cells maintain a reduced level of H3K27me3 despite this mutation to a core component of PRC2, unlike Eed-/- ESCs whose H3K27me3 is ablated. This data shows the concomitant changes in H3K4me3 levels in these cells. An ESC line mutant in Suz12, a core component of Polycomb Repressive Complex 2, was assessed for H3K4me3 by ChIP-seq, as compared to a wild type ESC line, as well as both lines subjected to in vitro differentiation down the Spinal Motor Neuron pathway.

2014-11-17 | E-GEOD-61248 | biostudies-arrayexpress

brpf1 knockdown reduces inhibitory neurotransmission and regulates gene expression of GABAergic interneurons derived from MGE

Project description:Our research is to investigate the role of Brpf1 in the development and function of GABAergic interneurons. To test this, we used mouse primary in vitro cultured GABAergic interneurons derived from medial ganglionic eminence (MGE) and utilized AAV-shBrpf1 virus to knockdown Brpf1. We performed mRNA-seq on the total RNA extracted from the infected neurons .We found that most of the up-regulated genes after Brpf1 knockdown were involved in processes such as protein binding, gene negative transcription, ubiquitination, and inflammation by mRNA-seq. We found that many genes related to neuronal calcium, potassium ion transport and neurotransmitter release changed after Brpf1 was knockdown.Our results demonstrate the key role of Brpf1 in related gene expression of GABAergic interneurons, and provide new lights on the underlying neurobiological mechanisms of BRPF1 mutations that cause mental retardation in children or adolescents.

2021-02-23 | GSE157903 | 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