Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic and transcriptional profiling of triple negative breast cancer

ABSTRACT: The human HCC1806 cell line is frequently used as a preclinical model for triple negative breast cancer (TNBC). Given that dysregulated epigenetic mechanisms are involved in cancer pathogenesis, emerging therapeutic strategies target chromatin regulators, such as histone deacetylases. A comprehensive understanding of the epigenome and transcription profiling in HCC1806 provides the framework for evaluating efficacy and molecular mechanisms of epigenetic therapies. Thus, to study the interplay of transcription and chromatin in the HCC1806 preclinical model, we performed nascent transcription profiling using Precision Run-On coupled to sequencing (PRO-seq). Additionally, we mapped the genome-wide locations for RNA polymerase II (Pol II), CTCF, the histone variant H2A.Z, and 7 histone modifications using ChIP-exo. ChIP-exonuclease (ChIP-exo) is a refined version of ChIP-seq with near base pair precision mapping of protein-DNA interactions. In this Data Descriptor, we present detailed information on experimental design, data generation, quality control analysis, and data validation. We discuss how these data lay the foundation for future analysis to understand the relationship between the nascent transcription and chromatin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE118033 | GEO | 2018/09/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ChIP-seq and ChIP-exo profiling of Pol II, H2A.Z, and H3K4me3 in human K562 cells

Project description:The human K562 chronic myeloid leukemia cell line has long served as an experimental paradigm for functional genomic studies. To systematically and functionally annotate the human genome, the ENCODE consortium generated hundreds of functional genomic data sets, such as ChIP-seq. While ChIP-seq analyses have provided tremendous insights into gene regulation, spatiotemporal insights were limited by a resolution of several hundred base pairs. ChIP-exonuclease (ChIP-exo) is a refined version of ChIP-seq that overcomes this limitation by providing higher precision mapping of protein-DNA interactions. To study the interplay of transcription initiation and chromatin, we profiled the genome-wide locations for RNA-polymerase II (Pol II), the histone variant H2A.Z, and the histone modification H3K4me3 using ChIP-seq and ChIP-exo.

2017-12-20 | GSE108323 | GEO

FOXA2 controls the anti-oxidant response in FH-deficient cells independent of NRF2

Project description:Hereditary Leiomyomatosis and renal cell cancer is caused by fumarate hydratase loss of heterozygosity and subsequence accumulation of fumarate. Fumarate is known to activate the anti-oxidant response and is key for cellular survival. Fumarate succinates KEAP1 which releases NRF2 to activate the antioxidant response. The role of fumarate on the global regulatory chromatin landscape is less understood. Here, by integrating chromatin accessibility and histone ChIP-seq profiles, we identify complex transcription factor networks involved in the highly remodelled chromatin landscape of FH-deficient cells. We implicate FOXA2 in the maintenance of FH-deficient cells by regulating anti-oxidant response genes and subsequent metabolic output, independent of NRF2. These results identify new redox and amino acid metabolism regulators and provide new avenues for therapeutic intervention.

2022-06-01 | ST002199 | MetabolomicsWorkbench

Enhancer Mapping in Chronic Lymphocytic Leukemia

Project description:<p>In this study we profile the epigenomic enhancer landscapes of CLL B cells (CD19+/CD5+) harvested from peripheral blood of patients from our Center. Included are results of ChIPseq profiling using chromatin immunoprecipitation of the enhancer histone mark H3K27ac (acetylated lysine 27 on histone H3), and open chromatin profiles using ATAC-seq (assay for transposase accessible chromatin). These profiles are used to define the global enhancer and super enhancer landscape of CLL B cells, and to derive active transcription factor networks associated with this disease. Also included are H3K27ac ChIP-seq and ATAC-seq datasets for non-CLL B cells obtained from the peripheral blood of normal adult donors.</p>

| phs001704 | dbGaP

Brg1 Modulates Enhancer Activation and Polycomb-mediated Repression in Mesoderm Differentiation [ChIP-exo]

Project description:We investigated the genome-wide occupancy changes in normal and Brg1-deleted mesoderm differentiation of mouse embryonic stem cells of chromatin regulators and histone modifications. ChIP exo for BRG1 in 2 conditions: Day4 THF (Control) and Day4 4OHT (Brg1-deleted). 1-2 replicates per condition.

2015-03-01 | E-GEOD-63976 | biostudies-arrayexpress

High mobility group protein-mediated transcription requires DNA damage marker γ-H2AX

Project description:The eukaryotic genome is organized into chromatins, the physiological template for DNA-dependent processes including replication, recombination, repair, and transcription. Chromatin-mediated transcription regulation involves DNA methylation, chromatin remodeling, and histone modifications. However, chromatin also contains non-histone chromatin-associated proteins, of which the high-mobility group (HMG) proteins are the most abundant. Although it is known that HMG proteins induce structural changes of chromatin, the processes underlying transcription regulation by HMG proteins are poorly understood. Here we decipher the molecular mechanism of transcription regulation mediated by the HMG AT-hook 2 protein (HMGA2). We combined proteomic, ChIP-seq, and transcriptome data to show that HMGA2-induced transcription requires phosphorylation of the histone variant H2AX at S139 (H2AXS139ph; γ-H2AX) mediated by the protein kinase ataxia telangiectasia mutated (ATM). Furthermore, we demonstrate the biological relevance of this mechanism within the context of TGFβ1 signaling. The interplay between HMGA2, ATM, and H2AX is a novel mechanism of transcription initiation. Our results link H2AXS139ph to transcription, assigning a new function for this DNA damage marker. Controlled chromatin opening during transcription may involve intermediates with DNA breaks that may require mechanisms that ensure the integrity of the genome.

2020-12-15 | PXD016586 | Pride

Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells [ChIP-seq]

Project description:We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, and assessed its consequences on histone modification by ChIP-seq,and compared this to changes in nascent transcription, DNA methylation, Protein expression and chromatin accessibility.

2022-07-19 | GSE194342 | GEO

A high-resolution view of transcription and chromatin states across distinct metabolic states in budding yeast

Project description:Under continuous, glucose-limited conditions, budding yeast exhibit robust metabolic cycles associated with major oscillations of gene expression and metabolic state. However, how such fluctuations might be coordinately linked to changes in chromatin status is less well understood. Here, we examine the correlated genome-wide transcription and chromatin states across the yeast metabolic cycle (YMC) at unprecedented temporal resolution, revealing a "just in time supply chain" by which specific cellular processes such as ribosome biogenesis are coordinated in time with remarkable precision. We identify distinct chromatin and splicing patterns associated with different gene categories and determine the relative timing of chromatin modifications to maximal transcription. Additionally, we interrogate chromatin modifier occupancy and observe subtly distinct spatial and temporal patterns compared to the modifications themselves. Furthermore, we identify multiple lysine mutants in H3 or H4 tails that disrupt metabolic cycling, supporting a potentially cooperative role of histone modifications in the YMC. 16 time points RNA-seq and ChIP-seq of 8 histone marks over one metabolic cycle, 14 time points ChIP-seq of 3 chromatin modifiers over one metabolic cycle

2014-08-31 | E-GEOD-52339 | biostudies-arrayexpress

Histone H3.3 lysine 9 and 27 control repressive chromatin states at cryptic cis-regulatory elements and bivalent promoters in mouse embryonic stem cells

Project description:Histone modifications are associated with distinct transcriptional states, but it is unclear whether they instruct gene expression. To investigate this, we mutated histone H3.3 K9 and K27 residues in mouse embryonic stem cells (mESCs). Here, we find that H3.3K9 is essential for controlling specific distal intergenic regions and for proper H3K27me3 deposition at promoters. The H3.3K9A mutation resulted in decreased H3K9me3 at regions encompassing endogenous retroviruses and induced a gain of H3K27ac and nascent transcription. These changes in the chromatin environment unleashed cryptic enhancers, resulting in the activation of distinctive transcriptional programs and culminating in protein expression normally restricted to specialized immune cell types. The H3.3K27A mutant disrupted deposition and spreading of the repressive H3K27me3 mark, particularly impacting bivalent genes with higher basal level of H3.3 at promoters. Therefore, H3.3K9 and K27 crucially orchestrate repressive chromatin states at cis-regulatory elements and bivalent promoters, respectively, and instruct proper transcription in mESCs.

2024-06-24 | MSV000095134 | MassIVE

Dynamic enhancer landscape in postmitotic motor neurons

Project description:Generic spinal motor neuron identity is specified by cooperative binding of selector transcription factors to motor neuron specific enhancers. Whether these enhancers remain active to maintain the motor neuron expression program following downregulation of selector factors in maturing motor neurons remains unknown. We demonstrate that enhancers established by selector genes are highly transient during motor neuron differentiation. The chromatin immunoprecipitation-exonuclease (ChIP-exo) assay reveals that Isl1 is anchored to nascent motor neuron enhancers through protein-protein interaction. Stage-specific recruitment of transcription factors correlates with active enhancer marks. The majority of genes contain distinct early and late enhancers suggesting that the motor neuron expression program is maintained by a dynamic regulatory landscape.

2016-12-05 | GSE79561 | GEO

Characterizing protein-DNA binding event subtypes in ChIP-exo data

Project description:Regulatory proteins associate with the genome either by directly binding cognate DNA motifs or via protein-protein interactions with other regulators. Each genomic recruitment mechanism may be associated with distinct motifs, and may also result in distinct characteristic patterns in high-resolution protein-DNA binding assays. For example, the ChIP-exo protocol precisely characterizes protein-DNA crosslinking patterns by combining chromatin immunoprecipitation (ChIP) with 5’ to 3’ exonuclease digestion. Since different regulatory complexes will result in different protein-DNA crosslinking signatures, analysis of ChIP-exo sequencing tag patterns should enable detection of multiple protein-DNA binding modes for a given regulatory protein. However, current ChIP-exo analysis methods either treat all binding events as being of a uniform type, or rely on the presence of DNA motifs to cluster binding events into subtypes. To systematically detect multiple protein-DNA interaction modes in a single ChIP-exo experiment, we introduce the ChIP-exo mixture model (ChExMix). ChExMix probabilistically models the genomic locations and subtype membership of protein-DNA binding events using both ChIP-exo tag enrichment patterns and DNA sequence information, thus offering a principled and robust approach to characterizing binding subtypes in ChIP-exo data. We demonstrate that ChExMix achieves accurate detection and classification of binding event subtypes using in silico mixed ChIP-exo data. We further demonstrate the unique analysis abilities of ChExMix using a collection of ChIP-exo experiments that profile the binding of key transcription factors in MCF-7 cells. In these data, ChExMix detects cooperative binding interactions between FoxA1, ERalpha, and CTCF, thus demonstrating that ChExMix can effectively stratify ChIP-exo binding events into biologically meaningful subtypes.

2018-02-13 | GSE110502 | GEO

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