Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATAC-seq of MCF-7 cells post ligand treatment

ABSTRACT: ATAC-seq of MCF-7 cells post ligand treatment

PROVIDER: PRJNA483774 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7629160_1.fastq.gz	Fastqsanger.gz
	SRR7629160_2.fastq.gz	Fastqsanger.gz
	SRR7629161_1.fastq.gz	Fastqsanger.gz
	SRR7629161_2.fastq.gz	Fastqsanger.gz
	SRR7629152_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

ATAC-seq of MCF-7 cells post ligand treatment

Project description:Goal: study the impact of estrogen receptor ligands on chromatin accessibility in MCF-7 cells Methods: Assay for Transposase-Accessible Chromatin using Sequencing (ATAC-Seq) Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), significantly alters chromatin accessibility and partially mimics the effect of natural ligand E2 on chromatin accessibility in MCF-7 breast cells. Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand have very little impact on chromatin accessibility.

2019-07-25 | GSE117940 | GEO

ChIP-seq of ER in MCF-7 cells post ligand treatment

Project description:ChIP-seq of ER in MCF-7 cells post ligand treatment

| PRJNA483772 | ENA

ATAC-seq, ChIP-seq and RNA-seq of breast cancer cell lines post ligand treatment

Project description:ATAC-seq, ChIP-seq and RNA-seq of breast cancer cell lines post ligand treatment

| PRJNA483771 | ENA

RNA-seq of breast cancer cell lines post ligand treatment II

Project description:RNA-seq of breast cancer cell lines post ligand treatment II

| PRJNA529360 | ENA

RNA-seq of breast cancer cell lines post ligand treatment I

Project description:RNA-seq of breast cancer cell lines post ligand treatment I

| PRJNA483773 | ENA

ChIP-seq of ER in MCF-7 cells post ligand treatment

Project description:Goal: study the impact of estrogen receptor (ER) ligands on ER binding to chromatin in MCF-7 cells Methods: ER Chromatin Immunoprecipitation and Sequencing (ChIP-seq) Results: All tested ligands increase binding of ER onto DNA in MCF-7 breast cells. These ligands thus promote an association between ER and DNA, irrespective of their mode of action: selective ER modulator (SERM) 4-OH tamoxifen, and selective ER degraders (SERD) fulvestrant and GDC-0927.

2019-07-25 | GSE117941 | GEO

RNA-seq of HCC1428 LTED breast cancer cell line post ligand treatment

Project description:RNA-seq of HCC1428 LTED breast cancer cell line post ligand treatment

| PRJNA644983 | ENA

RNA-seq of breast cancer cell lines post ligand treatment I

Project description:Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MCF-7, HCC1500, MDA-MB-330, EFM-19, T-47D, BT-474, and CAMA-1). Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand do not induce, or induce very weakly the expression of ER target genes. The effect of GDC-0810 depends on the cellular context.

2019-07-25 | GSE117942 | GEO

ATAC-seq from Nutlin-3a-treated MCF-7 cells

Project description:ATAC-seq from MCF-7 cells treated with Nutlin-3a or DMSO control

2024-09-18 | GSE250017 | GEO

Expression profiling of ligand-stimulated wild type and tamoxifen-resistant MCF-7

Project description:Quantitative phosphoproteome and transcriptome analysis of ligand-stimulated MCF-7 human breast cancer cells was performed to understand the mechanisms of tamoxifen resistance at a systems level. Phosphoproteome data revealed that wild type (WT) cells were more enriched with phospho-proteins than tamoxifen-resistant (TamR) cells after stimulation with ligands. Surprisingly, decreased phosphorylation after ligand perturbation was more common than increased phosphorylation. In particular, 17beta-estradiol (E2) induced down-regulation in WT cells at a very high rate. E2 and the ErbB ligand, heregulin (HRG) induced almost equal numbers of up-regulated phospho-proteins in WT cells. Pathway and motif activity analyses using transcriptome data additionally suggested that deregulated activation of GSK3B?(glycogen synthase kinase 3 beta) and MAPK1/3 signaling might be associated with altered activation of CREB and AP-1 transcription factors in TamR cells and this hypothesis was validated by reporter assays. An examination of clinical samples revealed that, inhibitory phosphorylation of GSK3B at serine 9 was significantly lower in tamoxifen-treated breast cancer patients that eventually had relapses, implying that activation of GSK3B may be associated with the tamoxifen resistant phenotype. Thus, the combined phosphoproteome and transcriptome dataset analyses revealed distinct signal-transcription programs in tumor cells and provided a novel molecular target to understand tamoxifen resistance. The MCF-7 human breast cancer cell line and tamoxifen-resistant MCF-7 cells were stimulated by the growth hormone heregulin (HRG) or 17beta-estradiol (E2) in the presence or absence of tamoxifen. Control was set as non-treated cells.

2010-11-03 | E-GEOD-21618 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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