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Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [ChIP-seq]

ABSTRACT: Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithelial cell types including those lining the respiratory system. Disruption of the airway epithelium is central to many lung diseases, and a network of transcription factors coordinates its normal function. EHF can act as a transcriptional activator or a repressor, though its targets in lung epithelial cells are largely uncharacterized. Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq), showed that the majority of EHF binding sites in lung epithelial cells are intergenic or intronic and coincide with putative enhancers, marked by specific histone modifications. EHF occupies many genomic sites that are close to genes involved in intercellular and cell-matrix adhesion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63398 | GEO | 2014/12/23

SECONDARY ACCESSION(S): PRJNA267665

REPOSITORIES: GEO

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Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [ChIP-seq]

Project description:Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithelial cell types including those lining the respiratory system. Disruption of the airway epithelium is central to many lung diseases, and a network of transcription factors coordinates its normal function. EHF can act as a transcriptional activator or a repressor, though its targets in lung epithelial cells are largely uncharacterized. Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq), showed that the majority of EHF binding sites in lung epithelial cells are intergenic or intronic and coincide with putative enhancers, marked by specific histone modifications. EHF occupies many genomic sites that are close to genes involved in intercellular and cell-matrix adhesion. Examination of EHF binding plus two histone modifications in Calu-3 cells. There are two replicates of the EHF ChIP-seq plus an input sample (control). There is one replicate each of the two histone modifications, plus a second input sample (control).

2014-12-23 | E-GEOD-63398 | biostudies-arrayexpress

Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [DNAse-seq]

Project description:Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithelial cell types including those lining the respiratory system. Disruption of the airway epithelium is central to many lung diseases, and a network of transcription factors coordinates its normal function. EHF can act as a transcriptional activator or a repressor, though its targets in lung epithelial cells are largely uncharacterized. Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq), showed that the majority of EHF binding sites in lung epithelial cells are intergenic or intronic and coincide with putative enhancers, marked by specific histone modifications and increased DNase hypersensitivity. Examination of open chromatin region in Calu-3 cells with 1 replicate

2014-12-23 | E-GEOD-63399 | biostudies-arrayexpress

Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [DNAse-seq]

2014-12-23 | GSE63399 | GEO

Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [RNA-seq]

Project description:Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithelial cell types including those lining the respiratory system. Disruption of the airway epithelium is central to many lung diseases, and a network of transcription factors coordinates its normal function. EHF can act as a transcriptional activator or a repressor, though its targets in lung epithelial cells are largely uncharacterized. RNA-seq after EHF depletion or overexpression showed significant alterations in the expression of genes involved in response to wounding. EHF knockdown also targeted genes in pathways of epithelial development and differentiation and locomotory behavior. mRNA profiles from Calu-3 cells treated with negative control (NC) or EHF siRNA, in quintuplicate. mRNA profiles from 3 pcDNA (empty vector control) clones and 3 pcDNA-EHF overexpression A549 clones, 3-4 replicates each.

2014-12-23 | E-GEOD-63397 | biostudies-arrayexpress

Ets homologous factor regulates pathways controlling response to injury in Calu-3 airway epithelial cells [RNA-seq]

2014-12-23 | GSE63397 | GEO

Ets homologous factor has critical roles in epithelial dysfunction in airway disease [ChIP-seq]

Project description:Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithelial cell types including those lining the respiratory system. Disruption of the airway epithelium is central to many lung diseases, and a network of transcription factors coordinates its normal function. EHF can act as a transcriptional activator or a repressor. Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq), showed that EHF binding sites in lung epithelial cells are enriched at promoters and coincide with putative enhancers, marked by specific histone modifications. Using EHF ChIP-seq and RNA-seq after EHF depletion, we show its targets in HBE cells are enriched for genes involved in degradation of misfolded proteins, inflammation, and wound repair.

2017-05-22 | GSE85401 | GEO

Ets homologous factor has critical roles in epithelial dysfunction in airway disease [RNA-seq]

2017-05-22 | GSE85402 | GEO

Coordinate regulation of ELF5 and EHF at the chr11p13 modifier region

Project description:E74-like factor 5 (ELF5) and ETS-homologous factor (EHF) are epithelial selective ETS family transcription factors (TFs) encoded by genes at chr11p13, a region associated with cystic fibrosis (CF) lung disease severity. EHF controls many key processes in lung epithelial function so its regulatory mechanisms are important. Using CRISPR/Cas9 technology, we removed three cis-regulatory elements (CREs) from the chr11p13 region in airway epithelial cells. Deletion of two enhancers and one CRE within a stretch enhancer at the EHF locus caused subtle changes in chromatin architecture, and though EHF expression did not change, ELF5 abundance increased. ELF5 is normally very low in airway cells so we next examined cell types that express more ELF5 (LNCaP and T47D). ATAC-seq experiments in these lines revealed novel peaks of open chromatin (potential CREs) at the 5’ end of chr11p13 that were associated with an expressed ELF5 gene. Furthermore, 4C-seq assays identified direct interactions between the active ELF5 promoter and sites within the EHF locus, suggesting coordinate regulation between these TFs. ChIP-seq for ELF5 in T47D cells revealed ELF5 occupancy within EHF introns 1 and 6 and siRNA-mediated depletion of ELF5 repressed EHF expression. These results define a new role for ELF5 in lung epithelial biology.

2021-05-11 | GSE131084 | GEO

Genome-wide occupancy of FLAG-ERG and FLAG-EHF in RWPE1 cells

Project description:We compared the genome occupancy for FLAG-tagged versions of the ETS factors ERG and EHF in the normal prostate epithelial cell line RWPE1. Our in vitro binding studies support a model whereby oncogenic ETS factors like ERG bind cooperativly with AP1 factors at closly spaced ETS-AP1 sites, while certain non-oncogenic factors like EHF bind anti-cooperatively with AP1 at the same sites. ETS and AP1 binding motifs were enriched in both ChIP datasets, but the ERG-FLAG bound reginos contained a much higher percentage of ETS-AP1 sites spaced in close proximity, consistent with our in vitro binding data.

2018-05-10 | GSE114241 | GEO

Analysis of ETS gene expression patterns uncovers novel ETS mediated gene silencing pathways in prostate cancers

Project description:Deregulated expression of ETS transcription factors with oncogenic and tumor suppressor function occurs frequently in prostate cancer leading to profound alterations of the cancer transcriptome. By integrating genomic and functional studies we identified key targets of the aberrantly expressed ETS factors, ERG and ESE3. Altered expression of ETS factors led to the induction of the polycomb group protein EZH2 and silencing of the tumor suppressor Nkx3.1. Nkx3.1 was controlled by ERG and ESE3 both directly via binding to ETS binding sites in the gene promoter and indirectly via EZH2-induced histone H3K27 methylation. This may represent a general mechanism linking aberrantly expressed ETS with deregulation of epigenetic pathways and global reprogramming of the prostate epithelial cell transcriptome in prostate tumorigenesis. Keywords: prostate cancer, gene expression profiling, ETS genes

2010-05-25 | GSE14206 | GEO

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