Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

ABSTRACT: Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

PROVIDER: PRJNA492482 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7889904.fastq.gz	Fastqsanger.gz
	SRR7889905.fastq.gz	Fastqsanger.gz
	SRR7889906.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

Project description:Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

| PRJNA487797 | ENA

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization [ATAC-seq]

Project description:Metastasis is the leading cause of cancer mortality. Chromatin remodeling is crucial for metastasis formation, laying the ground for the cellular reprogramming necessary to drive metastasis. However, little is known about the nature of this remodeling and its regulation. Here, we show that metastasis-inducing pathways regulate histone chaperones to reduce canonical histone incorporation into chromatin, triggering deposition of H3.3 variant at the promoters of poor-prognosis genes and metastasis-inducing transcription factors. This specific incorporation of H3.3 into chromatin is both necessary and sufficient for the induction of aggressive traits that allow for metastasis formation. Together, our data clearly show histone variant H3.3 as a major regulator of cell fate during tumorigenesis, and histone chaperones as valuable therapeutic targets for invasive carcinomas.

2019-09-03 | GSE132046 | GEO

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization [ATAC-seq]

Project description:Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization [ATAC-seq]

| PRJNA545714 | ENA

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

Project description:Carcinomas can acquire metastatic potential by undergoing a cellular program referred to as epithelial-to-mesenchymal transition (EMT). During EMT, the genome undergoes major epigenetic changes required for the expression of genes that promote cell motility, invasiveness, and survival under stress. While recent data point to a crucial role of chromatin remodeling in this process, little is known about the nature of this remodeling and the signals that trigger it. Here we show that metastasis-inducing pathways regulate histone chaperones to reduce canonical histone incorporation into chromatin. This triggers deposition of H3.3 to the promoters of EMT-inducing transcription factors and poor prognosis genes, a phenomenon that is sufficient and necessary for the induction of EMT and metastasis. Together, we have discovered histone H3.3 variant as a major regulator of cell fate during tumorigenesis and histone chaperones as valuable therapeutic targets for metastatic disease.

2019-09-02 | GSE119030 | GEO

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

2019-09-03 | GSE120313 | GEO

Dynamic Incorporation of Histone H3 Variants into Chromatin Is Essential for Acquisition of Aggressive Traits and Metastatic Colonization.

Project description:Metastasis is the leading cause of cancer mortality. Chromatin remodeling provides the foundation for the cellular reprogramming necessary to drive metastasis. However, little is known about the nature of this remodeling and its regulation. Here, we show that metastasis-inducing pathways regulate histone chaperones to reduce canonical histone incorporation into chromatin, triggering deposition of H3.3 variant at the promoters of poor-prognosis genes and metastasis-inducing transcription factors. This specific incorporation of H3.3 into chromatin is both necessary and sufficient for the induction of aggressive traits that allow for metastasis formation. Together, our data clearly show incorporation of histone variant H3.3 into chromatin as a major regulator of cell fate during tumorigenesis, and histone chaperones as valuable therapeutic targets for invasive carcinomas.

| S-EPMC6801101 | biostudies-literature

Dynamic incorporation of histone H3 variants into chromatin is essential for acquisition of aggressive traits and metastatic colonization

Project description:Reductive dimethylation based binary quantification of histone proteins from control (EGFP) and ERK2 (D319N) overexpressing MCF10A cells.

2019-08-13 | MSV000084205 | MassIVE

Chromatin-remodeling factor OsINO80 regulate H2A.Z incorporation [anti-H2A.Z & H3 ChIP-seq]

Project description:Chromatin-remodeling factor OsINO80 regulate H2A.Z incorporation [anti-H2A.Z & H3 ChIP-seq]

| PRJNA753508 | ENA

H3 Acetylation promotes H2A.Z incorporation into chromatin through SWR1 recruitment to stimulate expression.

Project description:H3 Acetylation promotes H2A.Z incorporation into chromatin through SWR1 recruitment to stimulate expression.

| PRJNA1256866 | ENA

H3 Acetylation promotes H2A.Z incorporation into chromatin through SWR1 recruitment to stimulate expression.

Project description:Following DNA replication, canonical H2A in eukaryotes is frequently replaced by histone variants, such as the conserved H2A.Z. Chromatin remodelers like the SWR1 complex facilitate this process, substituting the H2A histone with H2A.Z in an ATP-dependent manner. However, the precise mechanisms that recruit SWR1 to specific loci remain partially studied. In this study, we investigate the role of H3 acetylation in mediating the incorporation of H2A.Z into the chromatin to promote gene expression. Our results show that artificially induced hyperacetylation is associated with higher levels of H2A.Z and a decrease in H2A.W (HTA6 and HTA7). This phenomenon is also observed in histone deacetylases HDA6 and HDA9 defective backgrounds. Moreover, H2A.Z is required for the phenotype observed in hda6-1 and hda9-1

2025-05-02 | GSE295962 | 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