Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [ChIP-seq]

ABSTRACT: GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [ChIP-seq]

PROVIDER: PRJNA832810 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18959158_1.fastq.gz	Fastqsanger.gz
	SRR18959158_2.fastq.gz	Fastqsanger.gz
	SRR18959159_1.fastq.gz	Fastqsanger.gz
	SRR18959159_2.fastq.gz	Fastqsanger.gz
	SRR18959160_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.

Project description:GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.

| PRJNA832809 | ENA

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [RNA-seq]

Project description:GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [RNA-seq]

| PRJNA832811 | ENA

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [ChIP-seq]

Project description:In order to identify GATA-3 target genes in T-cell lymphoproliferative neoplasms, we performed GATA-3 ChIP-seq on 3 cutaneous T-cell lymphoma (CTCL) and 4 T-cell acute lymphoblastic leukemia (T-ALL). We have also established cell lines in which GATA-3 was knocked down by shRNA.

2022-04-30 | GSE201743 | GEO

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms [RNA-seq]

2022-04-30 | GSE201742 | GEO

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.

Project description:Neoplasms originating from thymic T-cell progenitors and post-thymic mature T-cell subsets account for a minority of lymphoproliferative neoplasms. These T-cell derived neoplasms, while molecularly and genetically heterogeneous, exploit transcription factors and signaling pathways that are critically important in normal T-cell biology, including those implicated in antigen-, costimulatory-, and cytokine-receptor signaling. The transcription factor GATA-3 regulates the growth and proliferation of both immature and mature T cells and has recently been implicated in T-cell neoplasms, including the most common mature T-cell lymphoma observed in much of the Western world. Here we show that GATA-3 is a proto-oncogene across the spectrum of T-cell neoplasms, including those derived from T-cell progenitors and their mature progeny, and further define the transcriptional programs that are GATA-3 dependent, which include therapeutically targetable gene products. The discovery that p300-dependent acetylation regulates GATA-3 mediated transcription by attenuating DNA binding has novel therapeutic implications. As most patients afflicted with GATA-3 driven T-cell neoplasms will succumb to their disease within a few years of diagnosis, these findings suggest opportunities to improve outcomes for these patients.

| S-EPMC9633835 | biostudies-literature

GATA-3 is a proto-oncogene in T-cell lymphoproliferative neoplasms.

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

2022-04-30 | GSE201744 | GEO

A Drosophila proto-oncogene homolog controls aggression via aminergic neurons

Project description:A Drosophila proto-oncogene homolog controls aggression via aminergic neurons

| PRJNA625242 | ENA

Muschampia proto

Project description:Muschampia proto overview

| PRJNA1182463 | ENA

The proto-oncogene TCL1A deregulates mitotic checkpoint transition and genomic stability in CLL

Project description:The proto-oncogene TCL1A deregulates mitotic checkpoint transition and genomic stability in CLL

| PRJNA791361 | ENA

Activation of proto-oncogenes by disruption of chromosome neighborhoods [5C-Seq]

Project description:Mutations such as gene fusion, translocation and focal amplification are a frequent cause of proto-oncogene activation during tumorigenesis, but such mutations do not explain all cases of proto-oncogene activation. Here we show that disruption of local chromosome conformation can also activate proto-oncogenes in human cells. We mapped chromosome structures in T-cell acute lymphoblastic leukemia (T-ALL), and found that active oncogenes and silent proto-oncogenes generally occur within insulated neighborhoods formed by the looping of two interacting CTCF sites co-occupied by cohesin. Recurrent microdeletions frequently overlap neighborhood boundary sites in T-ALL genomes, and we demonstrate that site-specific perturbation of loop boundaries is sufficient to activate the respective proto-oncogenes in non-malignant cells. We found somatic genomic rearrangements affecting loop boundaries in many cancers. These results suggest that chromosome structural organization is fundamental to identify functional somatic alterations in cancer genomes.

2016-01-23 | GSE77142 | 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