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The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [RNA-Seq]

ABSTRACT: Mechanisms regulating gene expression in the airway epithelium underlie its response to the environment. A network of transcription factors (TFs) and architectural proteins, modulate chromatin accessibility and recruit activating or repressive signals. Bromodomain-containing proteins function as TFs or by engaging methyltransferase or acetyltransferase activity to induce chromatin modifications. Here we investigate the role of Bromodomain Containing 8 (BRD8) in coordinating lung epithelial function. Sites of BRD8 occupancy genome-wide were mapped in human lung epithelial cell lines (Calu-3 and 16HBE14o-). CCCTC-Binding Factor (CTCF) was identified as a predicted co-factor of BRD8, based upon motif over-representation under BRD8 ChIP-seq peaks. Following siRNA-mediated depletion of BRD8, differentially expressed genes with peaks of BRD8 occupancy within 20 kb were subject to gene ontology process enrichment analysis. BRD8 targets are enriched for genes involved in the innate immune response and depletion of BRD8 increased the secretion of the antimicrobial peptide beta-defensin 1 and multiple chemokines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE158678 | GEO | 2021/01/29

REPOSITORIES: GEO

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The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [ChIP-seq]

Project description:Mechanisms regulating gene expression in the airway epithelium underlie its response to the environment. A network of transcription factors (TFs) and architectural proteins, modulate chromatin accessibility and recruit activating or repressive signals. Bromodomain-containing proteins function as TFs or by engaging methyltransferase or acetyltransferase activity to induce chromatin modifications. Here we investigate the role of Bromodomain Containing 8 (BRD8) in coordinating lung epithelial function. Sites of BRD8 occupancy genome-wide were mapped in human lung epithelial cell lines (Calu-3 and 16HBE14o-). CCCTC-Binding Factor (CTCF) was identified as a predicted co-factor of BRD8, based upon motif over-representation under BRD8 ChIP-seq peaks. Following siRNA-mediated depletion of BRD8, differentially expressed genes with peaks of BRD8 occupancy within 20 kb were subject to gene ontology process enrichment analysis. BRD8 targets are enriched for genes involved in the innate immune response and depletion of BRD8 increased the secretion of the antimicrobial peptide beta-defensin 1 and multiple chemokines.

2021-01-29 | GSE158686 | GEO

Genomic BRD8-binding sites in human colorectal cancer cells

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Krüppel-Like Factor 5 Regulates Airway Epithelial Cell Identity and Function [CHIP-seq]

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Krüppel-Like Factor 5 Regulates Airway Epithelial Cell Identity and Function [RNA-seq]

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The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells

Project description:The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells

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The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [ChIP-seq]

Project description:The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [ChIP-seq]

| PRJNA666188 | ENA

The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [RNA-Seq]

Project description:The Bromodomain Containing 8 (BRD8) Transcriptional Network in Human Lung Epithelial Cells [RNA-Seq]

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Hematopoietic transcription factors and p300/CBP shape the effects of BET bromodomain inhibition in leukemia [RNA-Seq]

Project description:The bromodomain and extraterminal (BET) protein Brd4 is a validated drug target in leukemia, yet its regulatory function in this disease is not well understood. Here, we show that Brd4 chromatin occupancy in acute myeloid leukemia closely correlates with the hematopoietic transcription factors (TFs) Pu.1, Fli1, Erg, C/EBPα, C/EBPβ, and Myb at nucleosome-depleted enhancer and promoter regions. We provide evidence that these TFs, in conjunction with the lysine acetyltransferase activity of p300/CBP, facilitate Brd4 recruitment to their occupied sites to promote transcriptional activation. Moreover, chemical inhibition of BET bromodomains is found to suppress the functional output each hematopoietic TF, thereby interfering with essential lineage-specific transcriptional circuits in this disease. These findings reveal a chromatin-based signaling cascade comprised of hematopoietic TFs, p300/CBP, and Brd4, which supports leukemia maintenance and is suppressed by BET bromodomain inhibition. PolyA selected RNA-Seq for drug treated or shRNA-expressing MLL-AF9 transformed acute myeloid leukemia cells (RN2)

2015-05-01 | E-GEOD-66068 | biostudies-arrayexpress

Hematopoietic transcription factors and p300/CBP shape the effects of BET bromodomain inhibition in leukemia [ChIP-Seq]

Project description:The bromodomain and extraterminal (BET) protein Brd4 is a validated drug target in leukemia, yet its regulatory function in this disease is not well understood. Here, we show that Brd4 chromatin occupancy in acute myeloid leukemia closely correlates with the hematopoietic transcription factors (TFs) Pu.1, Fli1, Erg, C/EBPα, C/EBPβ, and Myb at nucleosome-depleted enhancer and promoter regions. We provide evidence that these TFs, in conjunction with the lysine acetyltransferase activity of p300/CBP, facilitate Brd4 recruitment to their occupied sites to promote transcriptional activation. Moreover, chemical inhibition of BET bromodomains is found to suppress the functional output each hematopoietic TF, thereby interfering with essential lineage-specific transcriptional circuits in this disease. These findings reveal a chromatin-based signaling cascade comprised of hematopoietic TFs, p300/CBP, and Brd4, which supports leukemia maintenance and is suppressed by BET bromodomain inhibition. ChIP-Seq for regulatory factors of Brd4 in MLL-AF9 transformed acute myeloid leukemia cells (RN2)

2015-05-01 | E-GEOD-66122 | biostudies-arrayexpress

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