Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene Expression Analyisis of T-ALL LOUCY cell lines treated with ETV6 siRNA vs. scramble control siRNA

ABSTRACT: Transcriptional effects of ETV6 inactivation in immature T-ALL were investigated by gene expression analysis upon siRNA-mediated knockdown of ETV6 in LOUCY cells, a T-ALL cell line with a transcriptional program highly related to that of immature T-ALLs. Gene Set Enrichment Analysis (GSEA) of the ETV6 knockdown signature showed a significant enrichment in genes characteristically upregulated in ETV6 mutant immature T-ALLs including HOXA13, PRDM16, PTEN and CD33. 4 samples were analyzed: two biological replicates for each experimental group.

ORGANISM(S): Homo sapiens

SUBMITTER: Alberto Ambesi-Impiombato

PROVIDER: E-GEOD-33820 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Gene Expression Analyisis of T-ALL LOUCY cell lines treated with ETV6 siRNA vs. scramble control siRNA

Project description:Transcriptional effects of ETV6 inactivation in immature T-ALL were investigated by gene expression analysis upon siRNA-mediated knockdown of ETV6 in LOUCY cells, a T-ALL cell line with a transcriptional program highly related to that of immature T-ALLs. Gene Set Enrichment Analysis (GSEA) of the ETV6 knockdown signature showed a significant enrichment in genes characteristically upregulated in ETV6 mutant immature T-ALLs including HOXA13, PRDM16, PTEN and CD33.

2011-11-24 | GSE33820 | GEO

Identification of ETV6 bound protein by affinity purification of ETV6-HA fusion protein in REH cells

Project description:To determine the protein partners of ETV6, we expressed ETV6 and HA-tagged ETV6 in Reh pre-B leukemic cells. Anti-HA magnetic beads were used for affinity purification of ETV6-HA (and ETV6 control) from the nuclear and cytoplasmic fraction. Following purification on-beads digest and LC-MS/MS experiments were performed at the Proteomics platform of the CHU de Quebec Research Center, Quebec, Canada.

2022-01-26 | PXD031001 | Pride

Gene expression analysis of Early immature and Late mature T-ALL cell lines

Project description:Early immature T-cell acute lymphoblastic leukemias (T-ALLs) account for about 5-10% of pediatric T-ALLs and are associated with poor prognosis. However, the genetic defects that drive the biology of these tumors remain largely unknown. Analysis of microarray gene expression signatures in adult T-ALL demonstrated a high prevalence of early immature leukemias and revealed a close relationship between these tumors and myeloid leukemias. Consistently, adult immature T- ALLs showed characteristic mutations in myeloid specific oncogenes and tumor suppressors including IDH1, IDH2, DNMT3A, FLT3 and NRAS. Moreover, we identified ETV6 mutations as a novel genetic lesion uniquely present in immature adult T-ALL. All together, our results demonstrate that early immature adult T- ALL represents a heterogeneous category of leukemias characterized by the presence of overlapping myeloid and T-ALL characteristics and highlight the role of ETV6 mutations in these tumors.

2013-06-18 | GSE48046 | GEO

Gene expression analysis of Early immature and Late mature T-ALL cell lines

2013-06-18 | E-GEOD-48046 | biostudies-arrayexpress

ChIP-seq in the cell line NALM-6 for RUNX1 and ETV6-RUNX1 to assess competition between the two proteins for DNA binding

Project description:RUNX1 and ETV6-RUNX1 possess the same DNA-binding runt domain and are therefore expected to bind to canonical RUNX motifs. As the ETV6-RUNX1 fusion arises in the context of native RUNX1 expression, and since RUNX1 is retained or amplified in B-ALL, the two proteins are likely to compete for the same target sites. To assess this, we performed RUNX1 ChIP-seq in the presence of exogenous ETV6-RUNX1 (or non DNA binding ETV6-RUNX1-R139G) and the reciprocal experiment: ETV6-RUNX1 ChIP (using a V5 tag) in the presence of exogenous RUNX1 or vector control.

2022-10-31 | E-MTAB-12209 | biostudies-arrayexpress

RNA-seq as a global measure of the similarity between human pluripotent stem cell and fetal liver derived B cell hierarchies

Project description:Evidence suggests childhood acute lymphoblastic leukemia (cALL) arises in early human development. Existing models of pre-leukemic initiation using the ETV6-RUNX1 fusion do not recapitulate human disease, highlighting the need for a developmentally relevant human model system. A human pluripotent stem cell (hPSC) model genome was engineered to express ETV6-RUNX1 from the endogenous ETV6 promoter. RNA-seq data from sorted hematopoietic progenitors identified according to surface markers.

2018-02-08 | E-MTAB-6382 | biostudies-arrayexpress

Molecular role of the PAX5-ETV6 oncoprotein in promoting B cell acute lymphoblastic leukemia

2017-02-06 | GSE84987 | GEO

GATA3 acts upstream of FOXA1 in mediating ER binding by shaping enhancer accessibility

Project description:Estrogen Receptor (ESR1) drives growth in the majority of human breast cancers by binding to regulatory elements and inducing transcription events that promote tumor growth. Differences in enhancer occupancy by ESR1, contribute to the diverse expression profiles and clinical outcome observed in breast cancer patients. GATA3 is an ESR1 co-operating transcription factor mutated in breast tumors, however its genomic properties are not fully defined. In order to investigate the composition of enhancers involved in estrogen-induced transcription and the potential role of GATA3, we performed extensive ChIP-sequencing in unstimulated breast cancer cells and following estrogen treatment. We find that GATA3 is pivotal in mediating enhancer accessibility at regulatory regions involved in ESR1-mediated transcription. GATA3 silencing resulted in a global redistribution of co-factors and active histone marks prior to estrogen stimulation. These global genomic changes altered the ESR1 binding profile that subsequently occurred following estrogen, with events exhibiting both loss and gain in binding affinity, implying a GATA3 mediated re-distribution of ESR1 binding. The GATA3-mediated re-distributed ESR1 profile correlated with changes in gene expression, suggestive of its functionality. Chromatin loops at the TFF locus involving ESR1 bound enhancers occurred independently of ESR1 when GATA3 was silenced, indicating that GATA3, when present on the chromatin, may serve as a licensing factor for estrogen- ESR1 mediated interactions between cis-regulatory elements. Together these experiments suggest that GATA3 directly impacts ESR1 enhancer accessibility and may potentially explain the contribution of mutant-GATA3 in the heterogeneity of ESR1+ breast cancer. GATA and ER binding studied by chromatin immunoprecipitation in breast cancer cell lines, with and without estrogen stimulation and by knocking down GATA

2012-11-26 | E-GEOD-40129 | biostudies-arrayexpress

Transcription profiling by array of siRNA transfected HEK293T cells untreated or treated with TNF-alpha to study the effect of siRNA-mediated knockdown of different genes

Project description:HEK293T cells were treated with TNF-alpha for different periods of time to study the effect of siRNA-mediated knockdown of different genes (negative control: Renilla luciferase; positive controls: TNFRSF1A, RelA; gene of interest: CASP4) on TNF-induced gene expression

2012-07-06 | E-MTAB-900 | biostudies-arrayexpress

Molecular role of the PAX5-ETV6 oncoprotein in promoting B cell acute lymphoblastic leukemia

Project description:PAX5 is a tumor suppressor in B-ALL, while the role of PAX5 fusion proteins in B-ALL development is largely unknown. Here we studied the function of PAX5-ETV6 and PAX5- FOXP1 in mice expressing these proteins from the Pax5 locus. Both proteins arrested Blymphopoiesis at the pro-B-to-pre-B cell transition and, contrary to their proposed dominantnegative role, did not interfere with the expression of most Pax5 target genes. Pax5-Etv6, but not Pax5-Foxp1, cooperated with loss of the Cdkna2a/b tumor suppressor in promoting B-ALL development. Regulated Pax5-Etv6 target genes identified in these B-ALLs encode proteins implicated in pre-BCR signaling and migration/adhesion, which could contribute to the proliferation, survival and tissue infiltration of leukemic B-cells. Together with similar observations made in human PAX5-ETV6+ B-ALLs, these data identified PAX5-ETV6 as a potent oncoprotein. 36 samples in total: A) 24 RNA-Seq samples in 5 cell types: pro-B (5 genotypes, 2-4 replicates) large pre-B (2 genotypes, 2 replicates each) small pre-B (1 genotype, 2 replicates) lymph node (1 genotype, 3 replicates) bone marrow (1 genotype, 2 replicates) B) 12 ChIP-Seq samples in 2 cell types: pro-B (H3K27me3, H3K9ac, H3K4me2, H3K4me3, H3K27ac, 1 replicate each; Pax5Etv6 ChIP, Prd ChIP, 2 replicates each; Pax5 ChIP 1 replicate) lymph node (1 genotype, 2 replicates).

2016-07-30 | E-GEOD-84987 | biostudies-arrayexpress

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