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Probing Hemogenic Precursors with Endoglin Regulatory Elements uncovers LRP2 as a Regulator of Hematopoiesis

ABSTRACT: Different combinations of Endoglin tissue specific enhancers define hemangioblast and hemogenic endothelium cell fractions

ORGANISM(S): Mus musculus

PROVIDER: GSE77390 | GEO | 2016/12/06

SECONDARY ACCESSION(S): PRJNA310206

REPOSITORIES: GEO

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Effect of endoglin loss on embryoid bodies

Project description:Analysis of embryonic sten cell-derived embryoid bodies following endoglin knock out. Loss of endoglin leads to profound reduction of key hematopoietic regulators including SCL, LMO2, Gata2, and TGF-β signaling molecule ALK-1. Results provide insight into molecular mechanisms underlying hemangioblast and primitive hematopoietic development.

2011-05-16 | GSE29300 | GEO

Effect of endoglin loss on embryoid bodies

Project description:Analysis of embryonic sten cell-derived embryoid bodies following endoglin knock out. Loss of endoglin leads to profound reduction of key hematopoietic regulators including SCL, LMO2, Gata2, and TGF-? signaling molecule ALK-1. Results provide insight into molecular mechanisms underlying hemangioblast and primitive hematopoietic development. Total RNA obtained from differentiated day 3 EBs of endoglin knock out ES cells were compared to wild type E14 control ES cells.

2011-05-16 | E-GEOD-29300 | biostudies-arrayexpress

Endoglin Protein Interactome Profiling Identifies TRIM21 and Galectin-3 as New Binding Partners

Project description:Endoglin is a 180-kDa glycoprotein receptor primarily expressed by the vascular endothelium and involved in cardiovascular disease and cancer. Heterozygous mutations in the endoglin gene (ENG) cause Hereditary Hemorrhagic Telangiectasia type 1, a vascular disease that present with nose and gastrointestinal bleeding, skin and mucosa telangiectases, and arteriovenous malformations in internal organs. A circulating form of endoglin (alias soluble endoglin, sEng), proteolytically released from the membrane-bound protein, has been observed in several inflammation-related pathological conditions and appears to contribute to endothelial dysfunction and cancer development through unknown mechanisms. Membrane-bound endoglin is an auxiliary component of the TGF-β receptor complex and the extracellular region of endoglin has been shown to interact with types I and II TGF-β receptors, as well as with BMP9 and BMP10 ligands, both members of the TGF-β family. To search for novel protein interactors, we have screened a microarray containing over 9,000 unique human proteins using recombinant sEng as bait. We find that sEng binds with high affinity, at least, to 22 new proteins. Among these, we have validated the interaction of endoglin with galectin-3, a secreted member of the lectin family with capacity to bind membrane glycoproteins, and with tripartite motif-containing protein 21 (TRIM21), an E3 ubiquitin-protein ligase. Using human endothelial cells and Chinese hamster ovary cells, we showed that endoglin co-immunoprecipitates and co-localizes with galectin-3 or TRIM21. These results open new research avenues on endoglin function and regulation.

2019-09-25 | PXD015402 | Pride

Hemogenic Endothelium transcriptome along the timeline of hESC differentiation

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The hemogenic competence of endothelial progenitors is restricted by Runx1 silencing during embryonic development

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ChIP-on-chip data from human ES cells-derived CD34+CD43+CD45low cells (hemogenic endothelium-like cells) overexpressing 3xFLAG-Sox17-ERT

Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells enhances expansion of hemogenic endothelium-like cells. Human ES cells were differentiated for 6 days in EBs, then CD34+CD43-CD45- endothelial cells were isolated, plated onto OP9 cells, and transduced with the 4OH-tamoxifen (4OHT)-inducible 3×FLAG-tagged Sox17-ERT retrovirus. The cells were seeded on OP9 stromal cells and cultured in the presence of 4OH-tamoxifen. At day 27 of the co-culture with OP9 cells, CD34+CD43+CD45low hemogenic endothelium-like cells overexpressing Sox17-ERT were collected by CD34 magnetic-activated cell sorting (MACS) and subjected to a ChIP-chip analysis.

2012-12-14 | E-GEOD-37528 | biostudies-arrayexpress

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