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

ABSTRACT: Epigenome analysis of HELLS in liver cancer

PROVIDER: PRJNA875419 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Epigenome analysis of HELLS in liver cancer [methylation]

Project description:Epigenome analysis of HELLS in liver cancer [methylation]

| PRJNA875945 | ENA

HELLS knockdown or overexpression in liver cancer cells

Project description:HELLS knockdown or overexpression in liver cancer cells

| PRJNA875943 | ENA

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

Project description:The activating E2F-transcription factors are best known for their dependence on the Retinoblastoma protein and their role in cellular proliferation. E2F3 is uniquely amplified in specific human tumours where its expression is inversely correlated with the survival of patients. Here, E2F3 interaction partners were identified by mass spectrometric analysis. We show that the SNF2-like HELLS interacts with E2F3 in vivo and cooperates with its oncogenic functions. Depletion of HELLS severely perturbs the induction of E2F-target genes, hinders cell cycle re-entry and growth. Using chromatin immmunoprecipitation coupled to sequencing we identified genome-wide targets of HELLS and E2F3. Our analysis revealed that HELLS binds near promoters of active genes, including the trithorax-related MLL1, and co-regulates E2F3-dependent genes. Our analysis is the first to link HELLS with E2F-controlled processes that are critical to establish a proliferative tumour circuitry. Strikingly, just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours. Our work reveals that HELLS is important for E2F3 in tumour cell proliferation.

2011-12-19 | GSE33791 | GEO

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

2011-12-19 | E-GEOD-33791 | biostudies-arrayexpress

Epigenome analysis of cirrhosis and dysplastic liver samples

Project description:Epigenome analysis of cirrhosis and dysplastic liver samples

| PRJNA663577 | ENA

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Tumors from Rb1/p107 DKO and Rb1/p107/Hells TKO mice were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE143732 | GEO

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Retinae from Rb1/p107 DKO and Rb1/p107/Hells TKO mice at postnatal day 21 were analyzed for gene expression using RNA-seq.

2020-03-09 | GSE144427 | GEO

Chromatin accessibility analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells P21 retinae

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Retinae from Rb1/p107 DKO and Rb1/p107/Hells TKO mice at postnatal day 21 were analyzed for gene expression using ATAC-seq.

2020-03-09 | GSE144428 | GEO

Epigenome analysis of primary cervical cancer and normal

Project description:Epigenome analysis of primary cervical cancer and normal

| PRJNA871279 | ENA

PRDM9 activity depends on HELLS and promotes 5-Hydroxymethylcytosine enrichment

Project description:Meiotic recombination starts with the formation of DNA double-strand breaks (DSBs) at specific genomic locations that correspond to PRDM9-binding sites. The molecular steps occurring from PRDM9 binding to DSB formation are unknown. Using proteomic approaches to find PRDM9 partners, we identified HELLS, a member of the SNF2-like family of chromatin remodelers. Upon functional analyses during mouse male meiosis, we demonstrated that HELLS is required for PRDM9 binding and DSB activity at PRDM9 sites. However, HELLS is not required for DSB activity at PRDM9-independent sites. HELLS is also essential for 5-hydroxymethylcytosine (5hmC) enrichment at PRDM9 sites. Analyses of 5hmC in mice deficient for SPO11, which catalyzes DSB formation, and in PRDM9 methyltransferase deficient mice reveal that 5hmC is triggered at DSB-prone sites upon PRDM9 binding and histone modification, but independent of DSB activity. These findings highlight the complex regulation of the chromatin and epigenetic environments at PRDM9-specified hotspots.

2020-11-19 | GSE145768 | 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