Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A carrier-assisted ChIP-seq method for Estrogen Receptor-chromatin interactions from breast cancer core needle biopsy samples

ABSTRACT: 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.

INSTRUMENT(S): Illumina Genome Analyzer II

ORGANISM(S): Homo sapiens

SUBMITTER: Gordon Brown

PROVIDER: E-MTAB-1534 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

ChIP-Seq for RIP140, using the human breast cancer cell line MCF-7 in the absence of hormone or after treatment with Estradiol

Project description:This experiment is designed to assess the role of RIP140 in estrogen receptor-dependent gene expression in MCF7 luminal breast cancer cells. Hormone deprived MCF7 cells were treated for 3 hours with E2 or DMSO control, after which samples were processed for ChIp-seq for RIp140.

2015-03-16 | E-MTAB-2576 | biostudies-arrayexpress

tnni2 Binding Genome Seqences

Project description:ChIP-Seq analysis of the potential accumulated binding sites on whole genome by wild-type tnni2 and tnni2 del175k mutant The primary osteoblasts from Tnni2del175k/175k mice and wild-type littermates (n=3) were cultured for ChIP-Seq. ChIP and construct libraries were performed using the antibody against tnni2 (Santa Cluz Biotechnology) and conducted as previously described above. Illumina HiSeq 2000 is used for sequencing. Raw reads were aligned with the mouse reference 8 using Bowtie software and viewed with the IGV browser.

2013-09-01 | E-GEOD-32166 | biostudies-arrayexpress

An Alternative Splicing Switch Regulates Embryonic Stem Cell Pluripotency and Reprogramming [ChIP-Seq]

Project description:Alternative splicing (AS) is a key process underlying the expansion of proteomic diversity and the regulation of gene expression. However, the contribution of AS to the control of embryonic stem cell (ESC) pluripotency is not well understood. Here, we identify an evolutionarily conserved ESC-specific AS event that changes the DNA binding preference of the forkhead family transcription factor FOXP1. We show that the ESC-specific isoform of FOXP1 stimulates the expression of transcription factor genes required for pluripotency including OCT4, NANOG, NR5A2 and GDF3, while concomitantly repressing genes required for ESC differentiation. Remarkably, this isoform also promotes the maintenance of ESC pluripotency and the efficient reprogramming of somatic cells to induced pluripotent stem cells. These results thus reveal that an AS switch plays a pivotal role in the regulation of pluripotency and functions by controlling critical ESC-specific transcriptional programs. To identify genes potentially directly regulated by FOXP1-ES and FOXP1 in H9 ESCs, we performed chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq). Using an antibody capable of efficiently immunoprecipitating both isoforms, >3400 significant ChIP-Seq peaks were detected across the human genome. To assess if these peaks are sites of FOXP1 and FOXP1-ES occupancy, we determined whether they are significantly enriched in individual PBM-derived 8-mers that bind to either or both isoforms.

2011-09-14 | E-GEOD-31006 | biostudies-arrayexpress

Genome-wide mapping of FOXM1 binding sites

Project description:There are nearly fifty forkhead (FOX) transcription factors encoded in the human genome and due to sharing a common DNA binding domain, they are all thought to bind to similar DNA sequences. It is therefore unclear how these transcription factors are targeted to specific chromatin regions to elicit specific biological effects. Here we used ChIP-seq to investigate the genome-wide chromatin binding mechanisms used by the forkhead transcription factor FOXM1. In keeping with its previous association with cell cycle control, we demonstrate that FOXM1 binds and regulates a group of genes which are mainly involved in controlling late cell cycle events in the G2 and M phases. However, rather than being recruited through canonical RYAAAYA forkhead binding motifs, FOXM1 binding is directed via CHR elements. FOXM1 binds these elements through protein-protein interactions with the MMB transcriptional activator complex. Thus, we have uncovered a novel and unexpected mode of chromatin binding of a FOX transcription factor which allows it to specifically control cell cycle-dependent gene expression. Examination of FOXM1 binding sites in G2/M U2OS cells

2012-11-05 | E-GEOD-38170 | biostudies-arrayexpress

SUMO2 ChIP-seq in the starved U2OS cells

Project description:Chromatin immuno-precipitation using SUMO2 (Life Technologies) antibody in the starved U2OS cell line.

2023-06-01 | E-MTAB-12293 | biostudies-arrayexpress

ChIP-seq of ADNP and TRIM28 in the U2OS cell line (Human Bone Osteosarcoma Epithelial Cells)

Project description:In order to investigate the functions of the zinc finger transcription regulator ZMYM2 and the different types of ZMYM2 binding complex with TRIM28 or ADNP, we generated the ChIP-seq data of ADNP or TRIM28 in U2OS cells.

2023-06-01 | E-MTAB-12292 | biostudies-arrayexpress

SUMO2 ChIP-seq in U2OS cells

Project description:Chromatin immuno-precipitation using SUMO2 (Life Technologies) antibody in U2OS cell line.

2015-08-07 | E-MTAB-3084 | biostudies-arrayexpress

FOXJ3 ChIP-seq in a U2OS stable cell line

Project description:Chromatin immuno-precipitation using anti-Flag (Sigma) antibodies in a U2OS stable cell line. Paired-end R1 and R2 reads are provided, but the processed (mapped) reads are from a single-end (R1 read only) mapping.

2015-12-03 | E-MTAB-3687 | biostudies-arrayexpress

Histone H3K18ac ChIP-seq in U2OS cells

Project description:Chromatin immuno-precipitation using anti-H3K18ac antibodies in U2OS cells.

2016-04-27 | E-MTAB-3695 | biostudies-arrayexpress

ChIP-Seq of BCL11A and SOX2 in lung squamous cell carcinoma (LUSC) LK-2 cell line with or without BCL11A knockdown

Project description:BCL11A is upregulated in lung squamous cell carcinoma (LUSC) but not in lung adenocarcinoma (LUAD). BCL11A interacts with SOX2 at protein level. ChIP-Seq experiment was performed for BCL11A and SOX2 in LUSC LK-2 control or BCL11A-KD cell line in order to identify their role in LUSC pathology.

2018-07-05 | E-MTAB-6958 | 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