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E-GEOD-59089

ABSTRACT: RNA-seq transcriptional profiling in primary human erythroid progenitor cells upon shRNA-mediated knockdown of PRC2 core subunits

OTHER RELATED OMICS DATASETS IN: PRJNA254355PRJNA254352PRJNA254354

PROVIDER: E-GEOD-59089 | ExpressionAtlas | 2019-05-14

REPOSITORIES: ExpressionAtlas

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Homo sapiens

Project description:RNA-seq transcriptional profiling in primary human erythroid progenitor cells upon shRNA-mediated knockdown of PRC2 core subunits

| PRJNA254355 | ENA

HDAC1 and HDAC2 in fetal hemoglobin induction

Project description:This SuperSeries is composed of the following subset Series: GSE22366: Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples GSE22367: Primary human erythroid progenitor cells SAHA treatment samples GSE22368: Primary human erythroid progenitor cells NK57 treatment samples Refer to individual Series

2010-07-29 | E-GEOD-22369 | biostudies-arrayexpress

RNA-seq transcriptional profiling in primary human erythroid progenitor cells upon shRNA-mediated knockdown of PRC2 core subunits

Project description:Polycomb Repressive Complex 2 (PRC2) plays crucial roles in transcriptional regulation and stem cell development. However, the context-specific functions associated with alternative subunits remain largely unexplored. Here we show that the related enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. We examine the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and reveal the existence of an EZH1-SUZ12 sub-complex lacking EED. We provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains in the absence of H3K27me3, and positively regulate gene expression. Loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets. Moreover, we demonstrate that an erythroid-specific enhancer mediates transcriptional activation of EZH1, and a switch from GATA2 to GATA1 controls the developmental EZH1/2 switch by differential association with EZH1 enhancers during erythropoiesis. Thus, the lineage- and developmental stage-specific regulation of PRC2 expression and subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions during blood stem cell specification. Transcriptional profiling in primary human fetal liver proerythroblasts upon lentiviral shRNA-mediated knockdown of EZH1, EZH2, EED, or SUZ12 by RNA-seq analysis.

2015-01-01 | E-GEOD-59089 | biostudies-arrayexpress

Homo sapiens

Project description:Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples

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Bachmann2011 - Division of labor by dual feedback regulators controls JAK2/STAT5 signaling over broad ligand range

Project description:This is a dynamic pathway model examining the roles of of the two transcriptional negative feedback regulators of the suppressor of cytokine signaling (SOCS) family, CIS and SOCS3, in JAK/STAT5 signaling, within the context of primary erythroid progenitor cells.

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Homo sapiens

Project description:ChIP-seq analysis of PRC2 core subunits in primary human erythroid progenitor cells

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Global transcriptional changes in U87MG glioblastoma cells upon shRNA-mediated TRIM52 knockdown

Project description:Global transcriptional changes in U87MG glioblastoma cells upon shRNA-mediated TRIM52 knockdown

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RNA-seq transcriptonal profiling in human primary adult erythroid progenitor cells (ProEs) after shRNA-mediated depletion of TFAM and PHB2 expression

Project description:The developing erythroid cells require highly coordinated gene expression and metabolism. By comparing the proteomic and transcriptomic changes in human hematopoietic stem/progenitor cells (HSPCs) and lineage-committed erythroid progenitors (ProEs), and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Two principal mitochondrial factors TFAM and PHB2 are tightly regulated at the protein level and indispensable for mitochondria and erythropoiesis. To determine the role of TFAM and PHB2 in mitochondrial function during erythroid development, we employed shRNA-mediated depeltion of TFAM and PHB2 expression in differentiating erythroid cells, and performed RNA-seq transcriptional profiling analysis.

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

Project description:Reactivation of fetal hemoglobin expression by down-regulation of BCL11A is a promising treatment of -hemoglobinopathies. A detailed understanding of BCL11A-mediated repression of -globin gene (HBG1/2) transcription is lacking, as studies to date used perturbations by shRNA or CRISPR/Cas9 gene editing. We leveraged the dTAG PROTAC platform to acutely deplete BCL11A protein in erythroid cells and examined consequences by PRO-seq, proteomics, chromatin accessibility, and histone profiling. Among ≤ 31 genes repressed by BCL11A, HBG1/2 and HBZ show the most abundant and progressive changes in transcription and chromatin accessibility upon BCL11A loss. Transcriptional changes at HBG1/2 were detected in < 2h. Robust HBG1/2 reactivation upon acute BCL11A-depletion occurred without loss of promoter 5methylcytosine (5mC). Using targeted protein degradation, we establish a hierarchy of gene reactivation at BCL11A targets, in which nascent transcription is followed by increased chromatin accessibility, and both are uncoupled from promoter DNA methylation at the HBG1/2 loci

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

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