Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenome analysis of HELLS in liver cancer [methylation]

ABSTRACT: Epigenome analysis of HELLS in liver cancer [methylation]

PROVIDER: PRJNA875945 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Epigenome analysis of HELLS in liver cancer

Project description:Epigenome analysis of HELLS in liver cancer

| PRJNA875419 | ENA

Epigenome analysis of HELLS in liver cancer [methylation]

Project description:Genome wide DNA methylation profiling of shControl and shHELLS in HepG2. The Illumina Infinium MethylationEPIC BeadChip kits was used to obtain DNA methylation profiles.

2025-04-09 | GSE212556 | GEO

HELLS knockdown or overexpression in liver cancer cells

Project description:Transcriptome analysis after loss or gain of HELLS in HepG2.

2025-04-09 | GSE212554 | GEO

HELLS knockdown or overexpression in liver cancer cells

Project description:HELLS knockdown or overexpression in liver cancer cells

| PRJNA875943 | ENA

Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by enzymatic-methyl sequencing

Project description:We are interested in deciphering the mechanism by which DNA methylation in late B cell differentiation affects humoral immune response. We were using enzymatic-methyl sequencing (EM-seq) and chose to study a very rare immunodeficiency called ICF type 4, where a point mutation in a gene encoding the protein HELLS causes a lack of both circulating antibodies and memory B cells in human. HELLS is a chromatin remodeler, that allows for DNA methylation to occur.

2023-07-27 | E-MTAB-12609 | biostudies-arrayexpress

Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by single-cell RNA sequencing

Project description:We are interested in deciphering the mechanism by which DNA methylation in late B cell differentiation affects humoral immune response. We chose to study a very rare immunodeficiency called ICF type 4, where a point mutation in a gene encoding the protein HELLS causes a lack of both circulating antibodies and memory B cells in human. HELLS is a chromatin remodeler, that allows for DNA methylation to occur. Using a Hells conditional knock-out in B cells, we measured the kinetics of the immune B cell response, following immunization with NP-CGG, and show a lack of memory and plasma cells accompanied by a defect in germinal center maintenance, but not by its formation. Single cell RNAseq of cell sorted naive, germinal center B cells and memory B cells at day 7 and day 14 post NP-immunization helped us better characterize the phenotype.

2023-07-25 | E-MTAB-12499 | biostudies-arrayexpress

Epigenome analysis of HELLS in liver cancer

Project description:Genome wide H3K9me3 profiling of shControl and shHELLS in HepG2 Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for H3K9me3 in HepG2

2025-04-09 | GSE212429 | GEO

The ZBTB24-CDCA7-HELLS axis suppresses the totipotent 2C-like reprogramming by maintaining Dux methylation and repression

Project description:Two-cell-like cells (2CLCs), a rare population (~0.5%) in murine embryonic stem cell (mESC) cultures, are in a transient totipotent-like state resembling that of 2C-stage embryos, and their discovery and characterization have greatly facilitated the study of early developmental events, such as zygotic genome activation. However, the molecular determinants governing 2C-like reprogramming remains to be elucidated. Here, we show that ZBTB24, CDCA7 and HELLS, components of a molecular pathway that is involved in the pathogenesis of immunodeficiency, centromeric instability and facial anomalies (ICF) syndrome, function as negative regulators of 2C-like reprogramming by maintaining DNA methylation of the Dux cluster, a master inducer of the 2C-like state. Disruption of the ZBTB24-CDCA7-HELLS axis results in Dux hypomethylation and derepression, leading to dramatic upregulation of 2C-specific genes, which can be reversed by site-specific re-methylation in the Dux promoter. We also provide evidence that CDCA7 is enriched at the Dux cluster and recruits the CDCA7-HELLS chromatin remodeling complex to constitutive heterochromatin. Our study uncovers a key role for the ZBTB24-CDCA7-HELLS axis in safeguarding the mESC state by suppressing the 2C-like reprogramming.

2025-04-08 | GSE290522 | GEO

The ZBTB24-CDCA7-HELLS axis suppresses the totipotent 2C-like cell reprogramming by maintaining Dux methylation and repression

2025-03-28 | GSE280752 | GEO

The ZBTB24-CDCA7-HELLS axis suppresses the totipotent 2C-like cell reprogramming by maintaining Dux methylation and repression

Project description:Two-cell-like cells (2CLCs), a rare population (~0.5%) in murine embryonic stem cell (mESC) cultures, are in a transient totipotent-like state resembling that of 2C-stage embryos, and their discovery and characterization have greatly facilitated the study of early developmental events, such as zygotic genome activation. However, the molecular determinants governing 2C-like reprogramming remain to be elucidated. Here, we show that ZBTB24, CDCA7 and HELLS, components of a molecular pathway that is involved in the pathogenesis of immunodeficiency, centromeric instability and facial anomalies (ICF) syndrome, function as negative regulators of 2C-like reprogramming by maintaining DNA methylation of the Dux cluster, a master inducer of the 2C-like state. Disruption of the ZBTB24-CDCA7-HELLS axis results in Dux hypomethylation and derepression, leading to dramatic upregulation of 2C-specific genes, which can be reversed by site-specific re-methylation in the Dux promoter. We also provide evidence that CDCA7 is enriched at the Dux cluster and recruits the CDCA7-HELLS chromatin remodelling complex to constitutive heterochromatin. Our study uncovers a key role for the ZBTB24-CDCA7-HELLS axis in safeguarding the mESC state by suppressing the 2C-like reprogramming.

2025-03-28 | GSE279787 | 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