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Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ChIP-seq]

ABSTRACT: Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ChIP-seq]

PROVIDER: PRJNA765350 | ENA |

REPOSITORIES: ENA

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Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis

| PRJNA765349 | ENA

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ATAC-seq]

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ATAC-seq]

| PRJNA765025 | ENA

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [RNA-seq]

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [RNA-seq]

| PRJNA765029 | ENA

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ChIP-seq]

Project description:To determine hemogen function in regulatory elements, ChIPmentation was performed in both WT and hemogen KO K562 cells and H3K27ac enrichment was significantly reduced at both promoters and enhancers in loss of hemogen. To identify direct targets and the regulatory role of hemogen in murine erythroid gene expression, hemogen and BRG1 ChIP-seq was performed in the WT and hemogen KO E14.5 fetal liver cells. Hemogen was found enriched in GATA1/TAL1 binding motifs and equally bind to the promoter and potential enhancer region. Notably, BRG1 occupancy (95%) was almost completely coincident with hemogen binding sites and loss of hemogen greatly impaired the BRG1 occupancy at both erythroid promoters and enhancers.

2022-03-21 | GSE184605 | GEO

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ATAC-seq]

Project description:To determine hemogen function in chromatin accessbility, ATAC Seq was performed in both WT and hemogen KO mouse liver. Loss of hemogen caused generally decresed of chrmoatin accessbility on the hemogen/BRG1 binding promoter and enhancer .

2022-03-21 | GSE184553 | GEO

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [RNA-seq]

Project description:To gain insight into hemogen function during human erythropoiesis, RNA-seq was performed in different type of erythroid cells, such as WT and hemogen KD CD34+ cells, WT and hemogen KD HUDEP2 cells, WT and hemogen KO K562 cells. Notably, depletion of hemogen in these human erythroid cells significantly reduced the expression of genes associated with heme and hemoglobin synthesis, such as ALAS2, HMBS, GYPA, EPOR, and HBB, supporting a positive role of hemogen in erythroid maturation. To further explore hemogen function in mouse embryonic erythropoiesis, RNA-seq was performed in WT and hemogen KO E14.5 fetal liver cells and the data indicated hemogen play a consistently positive role in erythroid maturation-related genes as shown in the human cells, suggested hemogen is conserved activator during the mammalian erythropoiesis.

2022-03-21 | GSE184558 | GEO

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-21 | GSE184606 | GEO

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

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

IPMK physically binds to the SWI/SNF complex and modulates BRG1 occupancy

Project description:Inositol polyphosphate multikinase (IPMK), a key enzyme in the inositol polyphosphate (IP) metabolism, is a pleiotropic signaling factor involved in major biological events, including transcriptional control. In the yeast, IPMK and its IP products promote the activity of the chromatin-remodeling complex SWI/SNF, which plays a critical role in gene expression by regulating chromatin accessibility. However, the direct link between IPMK and chromatin remodelers remains unclear, raising a question on how IPMK contributes to the transcriptional regulation in mammals. By employing unbiased screening approaches and in vivo/in vitro immunoprecipitations, here we demonstrated that mammalian IPMK physically interacts with the SWI/SNF complex by directly binding to SMARCB1, BRG1, and SMARCC1. Furthermore, we identified the specific domains required for the IPMK-SMARCB1 binding. Notably, using the CUT&RUN and ATAC-seq assays, we discovered that IPMK co-localizes with BRG1 and regulates BRG1 localization as well as BRG1-mediated chromatin accessibility in a genome-wide manner in mouse embryonic stem cells. Finally, our mRNA-seq analyses revealed that IPMK and SMARCB1 regulate the expression of a common gene set, validating a functional link between IPMK and the SWI/SNF complex. Together, these findings show that IPMK regulates promoter-targeting of the SWI/SNF complex and thereby contributes to SWI/SNF-meditated chromatin accessibility, transcription, and differentiation.

2022-05-10 | GSE158525 | GEO

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