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The role of Erg in B cell development (ChIP-Seq)

ABSTRACT: ChIP-seq of B-cell progenitors and Rag1CreT/+;ErgΔ/Δ thymocytes for Erg transcription factor

ORGANISM(S): Mus musculus

PROVIDER: GSE132853 | GEO | 2020/04/14

REPOSITORIES: GEO

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Hi-C profiling of B-cell progenitors from Erg KO and WT mice

Project description:Hi-C was used to examine long range chromatin interactions in B cell progenitors in the presence and absence of the Erg transcription factor. Specifically, OP9 cultured B220+ B-cell progenitors derived from the bone marrow of Rag1CreT/+;ErgΔ/Δ mice and from Rag1CreT/+ and Rag1Cre+/+;Erg fl/fl control mice were isolated and DNA interactions were profiled by in situ Hi-C.

2020-04-14 | GSE133246 | GEO

The role of Erg in B cell development (ChIP-Seq)

Project description:The role of Erg in B cell development (ChIP-Seq)

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The transcription factor ERG regulates super-enhancers in endothelial cells [ERG ChIP-seq]

Project description:The transcription factor ERG regulates super-enhancers in endothelial cells [ERG ChIP-seq]

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ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning

Project description:Precise vascular patterning is critical for normal growth and development. The ERG transcription factor drives Delta like ligand 4 (DLL4)/Notch signalling and is thought to act as pivotal regulators of endothelial cell (EC) dynamics and developmental angiogenesis. However, molecular regulation of ERG activity remains obscure. Using a series of EC specific Focal Adhesion Kinase (FAK)-knockout (KO) and point-mutant FAK-knockin mice, we show that loss of ECFAK, its kinase activity or phosphorylation at FAK-Y397, but not FAK-Y861, reduces ERG and DLL4 expression levels together with concomitant aberrations in vascular patterning. Rapid Immunoprecipitation Mass Spectrometry of Endogenous Proteins identified that endothelial nuclear-FAK interacts with the de-ubiquitinase USP9x and the ubiquitin ligase TRIM25 enzymes. Further in silico analysis corroborates that ERG interacts with USP9x and TRIM25. Moreover, ERG levels are reduced in FAKKO ECs via a ubiquitin-mediated post-translational modification programme involving USP9x and TRIM25. Re-expression of ERG in vivo and in vitro rescues the aberrant vessel sprouting defects observed in the absence of ECFAK. Our findings identify ECFAK as a regulator of retinal vascular patterning by controlling ERG protein degradation via TRIM25/USP9x.

2022-07-05 | PXD033447 | Pride

ERG promotes the maintenance of hematopoietic stem cells by restricting their differentiation

2015-09-21 | GSE69873 | GEO

Oncofusion protein AML1-ETO targets ERG factor binding sites in AML

Project description:ERG has been identified as an essential factor for the function and maintenance of adult hematopoietic stem cells and high ERG expression is a negative prognostic marker for treatment outcome in AML. The molecular function of ERG and its interplay with other factors is however largely unknown. Here we demonstrate that ERG has cell type specific distributions in normal CD34+ myeloid progenitors and in AML cells and identify ERG as a potential pioneering protein for binding of oncofusion protein complexes. In addition, we identify H3 acetylation as the epigenetic mark preferentially associated with ERG binding. This intimate connection between ERG binding and H3 acetylation implies that one of the molecular strategies of the oncofusion proteins PML-RARa and AML1-ETO could involve the targeting of histone deacetylase activities to ETS factor bound hematopoietic regulatory sites. Examination of AML1-ETO, RUNX1, CBFb, HEB, FLI1 and ERG binding sites (ChIP-seq) in leukemic and normal hematopoietic cells, association with chromatin modifications and expression (RNA-seq) analysis of an AML1-ETO expressing cell line (SKNO-1)

2012-09-18 | E-GEOD-23730 | biostudies-arrayexpress

ERG promotes the maintenance of hematopoietic stem cells by restricting their differentiation

Project description:To investigate the role of the transcription factor ERG in hematopoiesis we generated Erg heterozygous knockout and conditional Erg knockout mice. We found that several hematopoietic cell types were decreased in these mice. To define Erg downstream target genes in hematopoietic stem cells, we sorted Lineage-, Sca-1+, c-kit+, CD150+, CD48- cells from Erg +/- mice for gene expression analysis. To define Erg downstream target genes in hematopoietic progenitors, we sorted multipotent progenitors (Lineage-, Sca-1+, c-kit+, CD150-) from Erg -/- mice for gene expression analysis. We generated Erg heterozygous knockout mice and provide 3 replicates for wild type (Erg +/+) populations of stem cells (HSC) and 3 replicates for Erg +/- mices. We also generated a conditional Erg knockout mice. We provide 3 replicates for Erg fl/fl and 3 replicates for Erg (-/-) mice.

2015-09-21 | E-GEOD-69873 | biostudies-arrayexpress

Staphylococcal Nuclease and Tudor Domain Containing protein SND1 interacts with ERG and plays a critical role in prostate cancer in vivo

Project description:ERG is a transcriptional factor, which is recombined with promoter of TMPRSS2 and prominently overexpressed in half of human prostate cancers. The mechanisms of ERG-mediated oncogenesis are not completely understood. We performed an unbiased Mass Spectrometry screen for ERG-binding proteins and found that ERG binds to MTDH/SND1 protein complex in prostate cancer cells. We determined that ERG binds to the SND1/MTDH protein complex via SND1 and this interaction plays a critical role in ERG-mediated cancer.

2023-03-22 | PXD036882 | Pride

High ERG expression in human HSPCs promotes progenitor but not stem cell proliferation and molecular signatures that are enriched in high ERG leukemia.

Project description:ERG is an Ets-transcription factor required for normal blood stem cell development. High ERG expression in acute myeloid leukemia (AML) and acute T-cell lymphoblastic leukemia (T-ALL) is associated with a stem cell signature and poor prognosis. In murine over-expression models, human ERG is a potent oncogene that induces both T-ALL and AML. However the functional and molecular consequences of high ERG expression in normal hematopoietic stem/progenitors (HSPCs), and how this contributes to leukemia development, are unknown. Here we show that retroviral transduction of ERG into human CD34+ cells and maintenance of ERG at levels present in high ERG AML results in altered myeloid and T cell differentiation and an increase in the self-renewal capacity of transduced progenitors but not the more primitive stem cell compartment. Integrated analysis of genome-wide expression in high ERG CD34+ and ERG binding profiles in HSPCs revealed that these functional characteristics were accompanied by an expression signature that was enriched in normal HSCs, high ERG AMLs, early T-cell precursor (ETP)-ALLs and leukemic stem cell signatures associated with poor clinical outcome. The proliferative advantage of high ERG progenitors may provide a cellular context for the acquisition and propagation of mutations that contribute to the pathogenesis of leukaemia. RNA sequencing in ERG overexpressing human CD34+ cells

2014-10-31 | E-GEOD-53665 | biostudies-arrayexpress

Promotion and maintenance of leukemia by ERG Thymocytes No.2

Project description:Thymocytes from mice transplanted with bone marrow cells infected with retrivirus for ERG were compared with control thymocytes regarding to gene expression. Mutations in Notch1 gene were not detected in the thymocytes.

2011-04-16 | E-MEXP-2988 | biostudies-arrayexpress

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