Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression of two Ewing sarcoma cell lines (A-673, EW-22), transduced with inducible shRNAs against GLRX3

ABSTRACT: Gene expression of two Ewing sarcoma cell lines (A-673, EW-22), transduced with inducible shRNAs against GLRX3

PROVIDER: PRJNA1102875 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression of two Ewing sarcoma cell lines (A-673, EW-22), transduced with inducible shRNAs against GLRX3

Project description:This dataset comprises transcriptome data of two Ewing sarcoma cell lines (A-673 and EW-22) after knockdown of the gene GLRX3 10 samples were normalized (log2) with Affymetrix Expression Console Software (v1.4) using SST-RMA algorithm. Gene expression data were annotated at gene level with the Affymetrix library for Clariom D arrays (human).

2024-12-03 | GSE264510 | GEO

Gene expression of two Ewing sarcoma cell lines (A-673, ES7), transduced with inducible shControl or two different shRNA against RRM2

Project description:This dataset comprises transcriptome data of two Ewing sarcoma cell lines (A-673 and ES7) after knockdown of the gene RRM2

2021-08-03 | GSE166415 | GEO

Gene expression of two Ewing sarcoma cell lines (A-673, ES7), treated with triapine (3-AP) or vehicle (DMSO)

Project description:This dataset comprises transcriptome data of two Ewing sarcoma cell lines (A-673, ES7) after treatment with triapine (3-AP) or vehicle (DMSO) for 72h.

2021-08-03 | GSE166419 | GEO

Gene expression of two Ewing sarcoma cell lines (A-673, ES7), transduced with inducible shControl or two different shRNA against RRM2

Project description:Gene expression of two Ewing sarcoma cell lines (A-673, ES7), transduced with inducible shControl or two different shRNA against RRM2

| PRJNA700851 | ENA

Genome-wide chromatin analysis of Ewing sarcoma (ChIP-seq)

Project description:We show that EWS-FLI1, an aberrant transcription factor responsible for the pathogenesis of Ewing sarcoma, reprograms gene regulatory circuits by directly inducing or directly repressing enhancers. At GGAA repeats, which lack regulatory potential in other cell types and are not evolutionarily conserved, EWS- FLI1 multimers potently induce chromatin opening, recruit p300 and WDR5, and create de novo enhancers. GGAA repeat enhancers can loop to physically interact with target promoters, as demonstrated by chromosome conformation capture assays. Conversely, EWS-FLI1 inactivates conserved enhancers containing canonical ETS motifs by displacing wild-type ETS transcription factors and abrogating p300 recruitment. ChIP-seq for of 4 histone modifications (H3K27ac, H3K4me1, H3K4me3 and H3K27me3), FLI1, p300, WDR5, ELF1 and GABPA in primary Ewing sarcomas, Ewing sarcoma cell lines (A673 and SKMNC cells), and mesenchymal stem cells (MSC). EWS-FLI1 was knocked down in Ewing sarcoma cell lines with lentiviral shRNAs (shFLI1 and shGFP control). EWS-FLI1 was expressed in MSCs with lentiviral expression vectors (pLIV EWSFLI1 or pLIV empty vector control). * Raw data not provided for the MSC and Primary Ewing sarcoma samples. *

2014-10-30 | E-GEOD-61944 | biostudies-arrayexpress

Effect of the NuRD subunit CHD4 on DNA accessibility in Ewing sarcoma cells [ATAC-seq]

Project description:We established Ewing sarcoma cells (SKNMC) stably expressing two doxycycline-inducible shRNAs targeting the NuRD component CHD4 to study its influence on DNA accessibility.

2023-11-07 | GSE224002 | GEO

MicroRNA-seq of MDA-MB-231 cells transduced with anti-ELOVL5 and control shRNAs

Project description:MiRNA isoforms (isomiRs) are single stranded small RNAs originating from the same pri-miRNA hairpin as a result of cleavage by Drosha and Dicer enzymes. Variations at the 5’-end of a miRNA alter the seed region of the molecule, thus affecting the targetome of the miRNA. MDA-MB-231 cells were transduced with shRNAs against ELOVL5 and luciferase genes. Small RNA sequencing was used to study the cleavage profiles of shRNAs.

2021-05-03 | GSE173709 | GEO

Genome-wide chromatin analysis of Ewing sarcoma (RNA-seq)

Project description:We show that EWS-FLI1, an aberrant transcription factor responsible for the pathogenesis of Ewing sarcoma, reprograms gene regulatory circuits by directly inducing or directly repressing enhancers. At GGAA repeats, which lack regulatory potential in other cell types and are not evolutionarily conserved, EWS- FLI1 multimers potently induce chromatin opening, recruit p300 and WDR5, and create de novo enhancers. GGAA repeat enhancers can loop to physically interact with target promoters, as demonstrated by chromosome conformation capture assays. Conversely, EWS-FLI1 inactivates conserved enhancers containing canonical ETS motifs by displacing wild-type ETS transcription factors and abrogating p300 recruitment. Ewing sarcoma cell lines (A673 and SKNMC) were analyzed by RNA-seq. EWS-FLI1 was depleted by infection with lentiviral shRNAs (shFLI1 and shGFP control).

2014-10-30 | E-GEOD-61950 | biostudies-arrayexpress

Effect of CHD4 and EWS-FLI1 knockdown on gene expression of Ewing sarcoma cells.

Project description:We established Ewing sarcoma cells (SKNMC) stably expressing doxycycline-inducible shRNAs targeting the NuRD component CHD4 or the fusion transcription factor EWS-FLI1 to study their influence in gene expression regulation.

2023-11-07 | GSE224004 | GEO

Ewing Sarcoma

Project description:This SuperSeries is composed of the following subset Series: GSE36857: Goldengate Methylation analysis: Ewing Sarcoma GSE36858: 5- AZA treatment of EWS cell lines Refer to individual Series

2012-09-01 | E-GEOD-36859 | 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