Baf250A, Brd9 and Baf180 knockdown impact on myoblast transcriptome
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ABSTRACT:
PROVIDER: PRJNA756240 | ENA |
REPOSITORIES: ENA
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Project description:We performed RNA-seq to investigate global changes in gene expression in proliferating myoblasts transduced with either the scramble, Baf250A, Brd9 or Baf180 shRNAs. This study revelaed that the Baf250-containing BAF complex and the Brd9-containing ncBAF complex contribute to myoblast proliferation but the Baf180-containing PBAF subfamily does not.
2022-03-04 | GSE182421 | GEO
Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+ cells. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOCS3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.
2019-05-02 | GSE129437 | GEO
Project description:Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown
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Project description:Transcriptional profiling of mouse myoblast cells comparing control vs. Mybbp1a knockdown. Stable clones of C2C12 cells harboring control or Mybbp1a-targeting shRNA were established and further pooled for analysis. Goal was to determine, based on the effects of Mybbp1a depletion on global gene expression, candidate downstream target genes of Mybbp1a, a putative transcriptional co-repressor. Two-condition experiment, control vs. Mybbp1a knockdown C2C12 cells (mixed stable clones). Biological replicates: 2.
2011-08-09 | E-GEOD-31319 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse myoblast cells comparing control vs. Mybbp1a knockdown. Stable clones of C2C12 cells harboring control or Mybbp1a-targeting shRNA were established and further pooled for analysis. Goal was to determine, based on the effects of Mybbp1a depletion on global gene expression, candidate downstream target genes of Mybbp1a, a putative transcriptional co-repressor.
2011-08-10 | GSE31319 | GEO
Project description:Impact of HypERrlnc Knockdown on the human pericyte transcriptome
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Project description:RNAseq was performed on the cells with GABPA knockdown, the cells with GPD1L knockdown, the cells with BRD9 knockdown and the control cells.
2022-05-18 | GSE165728 | GEO
Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer stem cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOC3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.
2019-11-11 | PXD013245 | Pride
Project description:BRD9 was identified in a genome-wide screen for genes regulating the response to interferon (IFN) in a A549 based reporter cell line. Subsequent experiments determined an involvement of BRD9 in the transcriptional regulation of Interferon-stimulated genes (ISGs) expression following stimulation with IFN-a2. The aim of this proximity-labelling experiments was to gain a more mechanistic understanding of BRD9 recruitment during the IFN signal transduction using A549 cells stably transduced with BRD9-TurboID and mCherry-TurboID fusion proteins. The BRD9 interactome in the absence of IFN- a2 was determined. We found that following IFN-a2 treatment, STAT2 significantly associates with BRD9-TurboID.
2021-08-17 | PXD026926 | Pride
Project description:Bromodomain containing protein 9 (BRD9), a member of the non-canonical BRG1/BRM-associated factor (ncBAF) chromatin remodeling complex, has been implicated as a synthetic lethal target in AML but its function in normal human hematopoiesis is unknown. In hematopoietic stem and progenitor cells (HSPC) genomic or chemical inhibition of BRD9 led to a proliferative disadvantage and loss of stem cells in vitro. Human HSPCs with reduced BRD9 protein levels produced lower numbers of immature mixed multipotent GEMM colonies in semi-solid media. In lineage-promoting culture conditions, cells with reduced BRD9 levels failed to differentiate into the megakaryocytic lineage and showed delayed differentiation into erythroid cells but enhanced terminal myeloid differentiation. HSPCs with BRD9 knock down (KD) had reduced long-term multilineage engraftment in a xenotransplantation assay. An increased number of downregulated genes in RNAseq analysis after BRD9 KD coupled with a gain in chromatin accessibility at the promoters of several repressive transcription factors (TF) suggest that BRD9 functions in the maintenance of active transcription during HSC differentiation. In particular, the hematopoietic master regulator GATA1 was identified as one of the core TFs regulating the gene networks modulated by BRD9 loss in HSPCs. BRD9 inhibition reduced a GATA1-luciferase reporter signal, further suggesting a role for BRD9 in regulating GATA1 activity. BRD9 is therefore an additional example of epigenetic regulation of human hematopoiesis.
2024-05-01 | GSE264030 | GEO