Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

ABSTRACT: H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

PROVIDER: PRJNA417235 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

Project description:H3K27Ac ChIP-seq in MCF7 Y537S ER mutant cells RNAseq analysis of MCF7 Y537S ER mutant cells treated with veh and THZ1

2018-02-15 | GSE106552 | GEO

Knockdown of GRHL2 affects active enhancers (H3K27ac sites) enriched for ER binding

Project description:Differential ChIP-Seq data monitoring changes in active enhancer marks (H3K27ac sites) after treatment with siGRHL2 in MCF7 and T47D breast cancer models. Comparing sites altered by treatment with siGRHL2 after 48hours revealed these sites to be enriched for Estrogen Receptor (ER) binding.

2018-12-07 | GSE123475 | 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

ER ChiP-Seq Mcf7 10nM E2

Project description:ER ChiP-Seq Mcf7 10nM E2

| PRJNA480204 | ENA

Bulk and single cell RNA-seq of MCF7 and MCF7 TDP2-KO cells treated with/without estrogen

Project description:To investigate the function of tyrosyl-DNA phosphodiesterase 2 (TDP2) in estrogen receptor (ER) positive breast cancer, we perfomed bulk and single-cell RNA-seq on MCF7 and MCF7 TDP2-KO cells treated with/without estrogen .

2024-04-17 | GSE225423 | GEO

Gene expression profiles of BxPC-3, MiaPaCa-2 and PANC-1 cell lines treated with DMSO and THZ1 respectively

Project description:By screening an epigenetic-related compound library, we identified THZ1, a covalent inhibitor of CDK7, as a promising candidate. Multiple long-established and patient-derived PDAC cell lines (PDC) were used to validate the efficacy of THZ1 in vitro. In addition, patient-derived xenograft (PDX) models and animal models of PDAC were utilized for examining THZ1 efficacy in vivo. Furthermore, RNA-Seq and H3K27Ac-based Super-Enhancers (SEs) analyses were performed to reveal the molecular mechanism of THZ1 treatment. Lastly, PDAC cell lines with primary or acquired resistance to THZ1 were investigated to explore the potential mechanism of THZ1 susceptibility.

2019-02-01 | GSE121273 | GEO

Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells [MCF7]

Project description:Translating Ribosome Affinity Purification (TRAP) sequencing revealed that human osteogenic cells (FOB1.19) strongly alter the transcriptional profile of ER+ breast cancer cells (MCF7) in 3D coculture system.

2021-04-16 | GSE137270 | GEO

ChIP-Seq analysis of ER binding sites in MCF7 breast cancer cells

Project description:Estrogen Receptor (ER) is a hormonal transcription factor that plays important roles in breast cancer. It functions primarily through binding to the regulatory regions of target genes containing the consensus ERE motifs. In order to identify ER target genes and re-define the ERE motifs we performed ChIP-Seq analysis of ER in MCF7 breast cancer cell line. Applying a novel computational algorithm named Hybrid Motif Sampler (HMS), specifically designed for TFBS motif discovery in ChIP-Seq data, we were able to detect an improved ERE motif and reveal intra-motif dependency especially in neighboring base pairs. MCF7 cells were grown in starving medium (RPMI with 5% FCS) for 3 days prior to the treatment with 10 nM β-estradiol or vehicle control for 45 minutes. ChIP was done using an anti-ER antibody in both the ethl-treated and the E2-treated cells. ChIP-Seq sample prep and sequencing were done following the manufacture's protocol using the Genome Analyzer (Illumina). The read files were analyzed using ethl-treated as control for E2-treated, leading to one final peak file.

2010-02-01 | E-GEOD-19013 | biostudies-arrayexpress

ChIP-Seq analysis of ER binding sites in MCF7 breast cancer cells

2010-02-01 | GSE19013 | GEO

ChIP-seq analysis of MCF7 cells treated with abemaciclib [ER]

Project description:ChIP-seq analysis of MCF7 cells treated with abemaciclib [ER]

| PRJNA548955 | ENA