Carroll_ChIP_exo
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina Genome Analyzer IIx, Illumina HiSeq 2000
ORGANISM(S): Homo sapiens
SUBMITTER: Gordon Brown
PROVIDER: E-MTAB-1827 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We performed androgen receptor (AR) ChIP-seq after GFP control or FOXA1 over-expression in two AR driven cancer models; LNCaP prostate cancer cell line and MDA-MB-453 molecular apocrine breast cancer cell line.
2014-01-14 | E-MTAB-1749 | biostudies-arrayexpress
Project description:We performed a comparision of AR binding sites as well as the histone modifications H3K27 acetylation and H3K4 monomethylation in the presence and absence of FoxA1 in the molecular apocrine breast cancer cell line, MDA-MB-453. We also probed AP2alpha binding in asynchronous MDA-MB-453 cells.
2014-04-17 | E-MTAB-1694 | biostudies-arrayexpress
Project description:Using a transcriptional network derived from 2000 breast cancer gene expression profiles we identify the master regulators (MRs) of FGFR2 signalling. To validate the identified regulons, we examined whether there was enrichment of TF binding near the transcription start sites (TSS) of genes found in the regulons of a particular MR. For ESR1 and SPDEF, ChIP-seq experiments were performed in MCF-7 cells, while existing data was analysed for FOXA1 (Hurtado et al. Nature Genetics, 43:27–33, 2010) and GATA3 (Theodorou, et al., Genome Res 23: 12-22, 2013). ChIP-seq experiments were performed on three biological replicates per each transcription factor. For each sample, 36bp single-end reads were obtained. Peak regions were identified in all ChIP-seq TF data sets using the peak caller algorithm MACS (Zhang et al., Genome Biology, 9(9):R137, 2008) with default parameters.
2013-07-17 | E-GEOD-48930 | biostudies-arrayexpress
Project description:Breast cancer (BC) is the most common cancer in women worldwide, and is classified in multiple subtypes, including the so called triple-negative BC (TNBC). This is characterized by lack of estrogen receptor alpha (ERα), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/neu), that represent common targets for BC treatment. Their absence limits the number of therapies that may be applied for TNBC treatment, suggesting the need to identify novel therapeutic targets against this disease. Several studies reported that the beta ER subtype (ERβ) is expressed in a sizeable fraction of TNBCs where its presence correlates with improved patient outcome. We evaluated ERβ expression in TNBC tissues by immunohistochemistry using two validated antibodies, demonstrating presence of this protein in 28% of samples. To investigate, in this context, the role of this estrogen receptor in TNBC biology, ERβ-expressing cell lines, representing different TNBC subtypes, were generated. Cellular and functional assays confirmed the antiproliferative activity of ERβ in TNBCs. Interaction proteomics revealed in BC nuclei the presence of several protein complexes associated with this receptor involved in chromatin remodeling, miRNA maturation and mRNA transcription. Transcriptome analyses pointed out tumor subtype-specific signaling pathways deregulation. Interestingly, among these the cholesterol biosynthesis pathway was commonly downregulated in all cell lines tested. Global analyses of ERβ binding to the genome showed its recruitment to regulatory sites of Sterol Regulatory Element-Binding Protein 1 (SREBP1), indicating a direct regulation of this pathway by the receptor. These findings suggest that drugs targeting components of cholesterol biosynthesis pathway may be new potential therapeutic options for TNBC treatment.
2019-12-02 | E-MTAB-8056 | biostudies-arrayexpress
Project description:The aim of this project is to locate the precise binding of the ONECUT1 transcription factor. NOTE: This study was updated on 7th May 2014. All samples, experiments, runs and files were replaced. This was due to an incorrect reagent being used in the earlier version.
2014-05-10 | E-MTAB-2060 | biostudies-arrayexpress
Project description:Metabolic dysfunction-associated steatotic liver disease is the most prevalent liver disease and affects a quarter of the global population. Estrogens are associated to safeguard the liver from metabolic diseases. We fed male mice a control or high-fat diet for 13 weeks which induced fatty liver. We injected a subset of male mice fed a high-fat diet with four different estrogen receptor (ER) agonists for the last three weeks of the high-fat diet, activating ERalpha or ERbeta. Livers were collected and crosslinked using formaldehyde. ChIP-seq against H3K27ac (Abcam #4729, 5ug per IP) or H3K4me3 (Merck 05-1339, 5ug per IP) was performed, followed by library preparation and sequencing on an Illumina NextSeq 500 instrument. RNA-seq of the same individual mice was performed and is accessible under E-MTAB-11833. The mouse identification column ('Sample' followed by number) can be used to match the individual mice between the experiments.
2024-02-22 | E-MTAB-11929 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-07-17 | E-GEOD-48931 | biostudies-arrayexpress
Project description:The Estrogen Receptor alpha (ERa) is the key transcriptional regulator in luminal breast cancer and the main target for adjuvant treatment. Luminal gene signatures are dictated by the transcriptional capacities of ERa, which are a direct consequence of the receptors binding preference at specific sites on the chromatin. The identification of ERa binding signatures on a genome-wide level has greatly enhanced our understanding of Estrogen Receptor biology in cell lines, but the technique has its limitations with respect its applicability in limit amounts of tumor tissue. Here, we present a refinement of the ChIP-seq procedures to enable transcription factor mapping on limited amounts of tissue culture cells and illustrate the applicability of this refined technology by mapping the ERa genome-wide chromatin binding landscape in core needle biopsy material from primary breast tumors.
2013-04-01 | E-MTAB-1534 | biostudies-arrayexpress
Project description:Background: The androgen receptor (AR) is a tumor suppressor in estrogen receptor (ER) positive breast cancer, a role sustained in some ER negative breast cancers. Key factors dictating AR genomic activity in a breast context are largely unknown. Herein, we employed an unbiased chromatin immunoprecipitation-based proteomic technique to identify endogenous AR interacting co-regulatory proteins in ER positive and negative models of breast cancer to gain new insight into mechanisms of AR signaling in this disease. Results: The DNA-binding factor GATA3 is identified and validated as a novel AR interacting protein in breast cancer cells irrespective of ER status. AR activation by the natural ligand 5α-dihydrotestosterone (DHT) increases nuclear AR-GATA3 interactions, resulting in AR-dependent enrichment of GATA3 chromatin binding at a sub-set of genomic loci. Silencing GATA3 reduces but does not prevent AR DNA binding and transactivation of genes associated with AR/GATA3 co-occupied loci, indicating a co-regulatory role for GATA3 in AR signaling. DHT-induced AR/GATA3 binding coincides with upregulation of luminal differentiation genes, including EHF and KDM4B, established master regulators of a breast epithelial cell lineage. These findings are validated in a patient-derived xenograft model of breast cancer. Interaction between AR and GATA3 is also associated with AR-mediated growth inhibition in ER positive and ER negative breast cancer.
2024-01-30 | PXD047997 | Pride
Project description:We performed an evolutionary comparison of the binding of the TF CTCF in human, chimpanzee, gorilla, orang-utan, macaque, baboon and marmoset using lymphoblastoid cell lines (LCLs). We also probes YY1 binding in human, chimpanzee, orang-utan and baboon LCLs as well as human and mouse liver.
2013-11-20 | E-MTAB-1511 | biostudies-arrayexpress