Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIPseq of DDX3X, DDX54, ER and H3K4me3 in human MCF7 cells

ABSTRACT: ChIPseq of DDX3X, DDX54, ER and H3K4me3 in human MCF7 cells

PROVIDER: PRJEB23458 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2195860.fastq.gz	Fastqsanger.gz
	ERR2195870.fastq.gz	Fastqsanger.gz
	ERR2195861.fastq.gz	Fastqsanger.gz
	ERR2195871.fastq.gz	Fastqsanger.gz
	ERR2195862.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

ChIPseq of DDX3X, DDX54, ERalpha and H3K4me3 in human breast cancer MCF7 cells

Project description:We aimed to investigate the chromatin binding activity of DDX3X and DDX54 RNA helicases in human ER -dependent breast cancer MCF7 cells. We run a parallel chromatin binding profiling of ER ChIP-seq. H3K4me3 profiling was used as a quality control of the ChIP-seq procedure.

2019-11-14 | E-MTAB-6211 | biostudies-arrayexpress

Expression profiling of DDX3X and DDX54 knockdown in MCF7 cells

Project description:We performed RNA-seq to observe the gene expression changes in cells following siRNA-mediated knockdown of DDX3X and DDX54 RNA helicases in human breast cancer MCF7 cells. Two siRNAs were used to target each RNA helicase and scramble siRNA-treated MCF7 cells were used as controls.

2018-11-21 | E-MTAB-6235 | biostudies-arrayexpress

iCLIP of DDX3X and DDX54 in human breast cancer MCF7 cells

Project description:Individual nucleotide resolution cross-linking immunoprecipitation (iCLIP) detects protein-RNA binding sites at a single nucleotide resolution. We aimed to identify the transcripts directly bound to DDX3X and DDX54 in human breast cancer MCF7 cells and to characterize the site of interaction at a single nucleotide resolution.

2018-11-21 | E-MTAB-6230 | biostudies-arrayexpress

iCLIP of DDX3X and DDX54 in human MCF7 cells

Project description:iCLIP of DDX3X and DDX54 in human MCF7 cells

| PRJEB23553 | ENA

Expression profiling of DDX3X and DDX54 knockdown in MCF7 cells

Project description:Expression profiling of DDX3X and DDX54 knockdown in MCF7 cells

| PRJEB23554 | ENA

Histone ChIPSeq of H3K79me2 before and after EPZ004777 treatment in MCF7 breast cancer cells

Project description:Histone ChIPSeq of H3K79me2 before and after EPZ treatment in MCF7 breast cancer cells

2019-02-08 | E-MTAB-6889 | biostudies-arrayexpress

T1DGC H3K4me3 ChIPseq

Project description:T1DGC H3K4me3 ChIPseq

| PRJNA398437 | ENA

Inhibiting DDX3X triggers tumor-intrinsic type I interferon response and enhances anti-tumor immunity

Project description:Accumulating evidence has shown that cellular double-stranded RNAs (dsRNAs) induce antiviral innate immune responses in human normal and malignant cancer cells. However, it is not fully understood how endogenous ‘self’ dsRNA homeostasis is regulated in the cell. Here, we show that an RNA-binding protein, DEAD-box RNA helicase 3X (DDX3X), prevents the aberrant accumulation of cellular dsRNAs. Loss of DDX3X induces dsRNA sensor-mediated type I interferon signaling and innate immune response in breast cancer cells due to abnormal cytoplasmic accumulation of dsRNAs. Dual depletion of DDX3X and a dsRNA-editing protein, ADAR1 synergistically activates the cytosolic dsRNA pathway in breast cancer cell. Moreover, inhibiting DDX3X enhances the antitumor activity by increasing tumor intrinsic-type I interferon response, antigen presentation, and tumor-infiltration of cytotoxic T cells as well as dendritic cells in breast tumors, which may lead to the development of breast cancer therapy by targeting DDX3X in combination with immune checkpoint blockade. To assess the impact of DDX3X on the gene expression in the breast cancer, we stably depleted DDX3X in breast cancer MCF7 cells using a short hairpin RNA (shRNA)-mediated knockdown, and performed a genome-wide transcriptome analysis using a next-generation RNA deep sequencing.

2020-09-03 | GSE157323 | GEO

Medulloblastoma associated DDX3X mutants restore malignant potential of medulloblastoma cells decreased upon the loss of DDX3X expression

Project description:DDX3X is an ATP-dependent RNA helicase. Missense mutations in DDX3X gene are known to occur in WNT, SHH subgroup medulloblastomas. The role of DDX3X in medulloblastoma biology was studied by downregulating its expression in a SHH subgroup Daoy medulloblastoma cell line. DDX3X knockdown resulted in considerable reduction in proliferation, clonogenic potential and anchorage-independent growth of the medulloblastoma cells. Transcriptome analysis was performed to delineate the molecular mechanism underlying reduction in the malignant potential of the medulloblastoma cells upon DDX3X knockdown. Exogenous expression of three DDX3X missense mutants in the DDX3X knockdown cells could restore the malignant potential of the medulloblastoma cells.

2023-03-31 | GSE201967 | GEO

ER-RIME in wt-MCF7 and MCF7-LTED

Project description:Wild type (wt) MCF7 cells, modelling breast cancer at primary diagnosis, were cultured in phenol red-free RPMI supplemented with 10% FBS and 1nM estradiol (E2). Long-term oestrogen deprived (LTED) cell lines, which model resistance to endocrine therapy, were cultured in phenol red-free RPMI in the absence of exogenous E2 and supplemented with 10% dextran charcoal-stripped bovine serum (DCC). Samples were harvested at baseline and at the point of resistance (LTED). In order to do comparative analysis in the ER-interactome of wt-MCF7 and MCF7-LTED cells, ER-RIME (rapid immunoprecipitation mass spectrometry of endogenous proteins) was conducted in these cells.

2020-07-13 | PXD004648 | Pride

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