Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis

ABSTRACT: Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis

PROVIDER: PRJNA1041369 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26852500_1.fastq.gz	Fastqsanger.gz
	SRR26852500_2.fastq.gz	Fastqsanger.gz
	SRR26854300.fastq.gz	Fastqsanger.gz
	SRR26852501_1.fastq.gz	Fastqsanger.gz
	SRR26852501_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 204

Similar Datasets

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (CUT&RUN)

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (CUT&RUN)

| PRJNA1041376 | ENA

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (RNA-Seq)

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (RNA-Seq)

| PRJNA1041375 | ENA

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (Spatial Transcriptomics)

Project description:Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (Spatial Transcriptomics)

| PRJNA1041374 | ENA

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (Spatial Transcriptomics)

Project description:To investigate the role H3K36 methylation in stratifying epithelia

2023-12-01 | GSE247994 | GEO

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (RNA-Seq)

Project description:To investigate the role H3K36 methylation in stratifying epithelia

2023-12-01 | GSE247992 | GEO

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis (CUT&RUN)

Project description:To investigate the role H3K36 methylation in stratifying epithelia

2023-12-01 | GSE247991 | GEO

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis

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

2023-12-01 | GSE247995 | GEO

BMP7 Signaling in TGFb Receptor-2 deficient Stromal Cells Provokes Epithelial Carcinogenesis

Project description:BMP7 Signaling in TGFb Receptor-2 deficient Stromal Cells Provokes Epithelial Carcinogenesis

| PRJNA416879 | ENA

Aberrant DNA Methylation in Dimethylarsinic Acid-induced Rat Bladder Carcinogenesis

Project description:DNA methylation profile in rat bladder carcinogenesis treated with dimethylarsinic acid.

2023-11-06 | GSE243372 | GEO

Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis

Project description:Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis.

2019-03-09 | GSE124370 | 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