Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SET1B facilitates activation of the hypoxia response through site-specific histone methylation [ChIP-seq_1]

ABSTRACT: SET1B facilitates activation of the hypoxia response through site-specific histone methylation [ChIP-seq_1]

PROVIDER: PRJNA667729 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12781720_1.fastq.gz	Fastqsanger.gz
	SRR12781720_2.fastq.gz	Fastqsanger.gz
	SRR12781721_1.fastq.gz	Fastqsanger.gz
	SRR12781721_2.fastq.gz	Fastqsanger.gz
	SRR12781722_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

SET1B facilitates activation of the hypoxia response through site-specific histone methylation [ChIP-seq_1]

Project description:Hypoxia-inducible transcription factors (HIFs) are fundamental to the cellular adaptation to low oxygen levels but how they interact with chromatin and efficiently activate their target genes is unclear. Using genome-wide mutagenesis in human cancer cells, we define genes required for HIF transcriptional activation, and identify a requirement for the Histone 3 lysine 4 (H3K4) methyltransferase SET1B. Loss of SET1B leads to a selective reduction in HIF transcriptional activity in hypoxia, with SET1B driving expression of genes involved in angiogenesis rather than glycolysis, resulting in impaired tumour establishment in SET1B deficient xenografts. Mechanistically, we show that SET1B is itself oxygen regulated, accumulates on chromatin in hypoxia, and is recruited to HIF target genes through HIF-1a. Accordingly, we show that the hypoxic induction of H3K4me3 at specific HIF targets is both HIF and SET1B dependent, and when impaired, decreases promotor acetylation and gene expression. Together, these findings reveal SET1B as a determinant of site-specific histone methylation and provide insight into how HIF target genes are differentially regulated.

2021-04-30 | GSE159128 | GEO

SET1B facilitates activation of the hypoxia response through site-specific histone methylation

2021-05-04 | GSE169087 | GEO

SET1B facilitates activation of the hypoxia response through site-specific histone methylation [ChIP-seq_2]

2021-04-30 | GSE169040 | GEO

SET1B facilitates activation of the hypoxia response through site-specific histone methylation

Project description:SET1B facilitates activation of the hypoxia response through site-specific histone methylation

| PRJNA714950 | ENA

SET1B facilitates activation of the hypoxia response through site-specific histone methylation

Project description:SET1B facilitates activation of the hypoxia response through site-specific histone methylation

| PRJNA715190 | ENA

SET1B facilitates activation of the hypoxia response through site-specific histone methylation [ChIP-seq_2]

Project description:SET1B facilitates activation of the hypoxia response through site-specific histone methylation [ChIP-seq_2]

| PRJNA714954 | ENA

Mapping SET1B Chromatin Interactions with DamID using DamMapper, a Comprehensive Snakemake Workflow

Project description:Background DNA adenine methyltransferase identification followed by sequencing (DamID-seq) is a powerful method used to map genome-wide chromatin-protein interactions. However, the bioinformatic analysis of DamID-seq data presents significant challenges due to the inherent complexities of the data and a notable lack of comprehensive software solutions for data-processing and downstream analysis. Results To address these challenges, we present a comprehensive bioinformatic workflow for DamID-seq data analysis, DamMapper, using the Snakemake workflow management system. Key features include straightforward processing of multiple biological replicates, visualisation of quality control figures, such as a correlation heatmaps and principal component analysis (PCA) plotting, and robust code quality maintained through continuous integration (CI). Reproducibility is ensured across diverse computational environments, including cloud computing and high-performance computing (HPC) clusters, through the implementation of software environments (Conda) and containerisation (Docker/Apptainer). We validated this workflow using a previously published DamID-seq dataset and Furthermore, we apply it to analyse novel datasets for proteins involved in the hypoxia response, specifically the transcription factor HIF-1α and the histone methyltransferase SET1B. This application reveals a strong concordance between our HIF-1α DamID-seq results and ChIP-seq data, and importantly, provides the first genome-wide DNA binding map for SET1B. Conclusions This work provides a validated, reproducible, and feature-rich workflow that overcomes common hurdles in DamID-seq data analysis. By streamlining the processing and ensuring robustness, DamMapper facilitates reliable analysis and enables new biological discoveries, as demonstrated by the characterization of SET1B binding sites. The workflow is available under the MIT license at: https://github.com/niekwit/damid-seq.

2025-08-21 | GSE296995 | GEO

SET1B facilitates activation of the hypoxia response through site-specific histone methylation

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

2021-04-30 | GSE169041 | GEO

The HIF complex recruits the histone methyltransferase SET1B to activate specific hypoxia-inducible genes.

Project description:Hypoxia-inducible transcription factors (HIFs) are fundamental to cellular adaptation to low oxygen levels, but it is unclear how they interact with chromatin and activate their target genes. Here, we use genome-wide mutagenesis to identify genes involved in HIF transcriptional activity, and define a requirement for the histone H3 lysine 4 (H3K4) methyltransferase SET1B. SET1B loss leads to a selective reduction in transcriptional activation of HIF target genes, resulting in impaired cell growth, angiogenesis and tumor establishment in SET1B-deficient xenografts. Mechanistically, we show that SET1B accumulates on chromatin in hypoxia, and is recruited to HIF target genes by the HIF complex. The selective induction of H3K4 trimethylation at HIF target loci is both HIF- and SET1B-dependent and, when impaired, correlates with decreased promoter acetylation and gene expression. Together, these findings show SET1B as a determinant of site-specific histone methylation and provide insight into how HIF target genes are differentially regulated.

| S-EPMC7611696 | biostudies-literature

Hypoxia-enhanced Derivation of iPSCs from Human Dental Pulp Cells

Project description:Hypoxia enhances the reprogramming efficiency of human dermal fibroblasts to become induced pluripotent stem cells (iPSCs). Because we showed previously that the hypoxia facilitates the isolation and maintenance of human dental pulp cells (DPCs), we examined here whether it promotes the reprogramming of DPCs to become iPSCs. To investigate the effect of oxygen concentration on global gene expression, we compared DPCs cultured for 6 days under hypoxia and normoxia.

2013-09-03 | E-GEOD-45872 | biostudies-arrayexpress

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