Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA201508 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of transcriptional profiles of human umbilical vein endothelial cells (HUVECs) expressing wild-type vs. VM-causative mutant forms of TIE2/TEK. The effects of the most common Venous Malformation-causative mutations in the endothelial cell tyrosine kinase receptor: R849W and L914F, were tested. 743 genes were differentially expressed across the four groups. The 80 genes distinguishing between L914F and wild-type TIE2-expressing HUVECs were analyzed in greater detail. 3 batches each of: non-transfected, and wild-type TIE2, R849W-TIE2, and L914F-TIE2 overexpressing HUVECs were compared by exon-array profiling.
2013-06-04 | E-GEOD-46684 | biostudies-arrayexpress
Project description:Comparison of transcriptional profiles of human umbilical vein endothelial cells (HUVECs) expressing wild-type vs. VM-causative mutant forms of TIE2/TEK. The effects of the most common Venous Malformation-causative mutations in the endothelial cell tyrosine kinase receptor: R849W and L914F, were tested. 743 genes were differentially expressed across the four groups. The 80 genes distinguishing between L914F and wild-type TIE2-expressing HUVECs were analyzed in greater detail.
2013-06-04 | GSE46684 | GEO
Project description:Venous Malformation: from causative TIE2 mutations to murine model and targeted therapy
| PRJEB9698 | ENA
Project description:This research aimed to investigate the aberrant expression of circRNA, messenger RNA, and microRNA in orbital venous malformation. A competitive endogenous RNA network was constructed to elucidate their potential roles in orbital venous malformation.
2022-07-06 | GSE158793 | GEO
Project description:This research aimed to investigate the aberrant expression of circRNA, messenger RNA, and microRNA in orbital venous malformation. A competitive endogenous RNA network was constructed to elucidate their potential roles in orbital venous malformation.
2022-07-06 | GSE158791 | GEO
Project description:Proteomics and high connotation functional gene screening (HCS) were used to screen key functional genes that play important roles in the pathogenesis of venous malformation.
2022-02-16 | PXD028848 | Pride
Project description:To identify the miRNA expressing profiles of TIE2 expressing Monocytes (TEMs), we have employed the Agilent Human miRNA 8×60K (Design ID:046064) microarray. Human peripheral blood mononuclear cells (PBMCs) in venous blood from healthy donors were isolated by Lymphoprep (Axis-Shield, Norway). Human monocytes in PBMCs, identified as cells that expressed CD14, were enriched by positive immunomagnetic selection using anti-CD14 MicroBeads (Miltenyi, Germany). TEMs (TIE2+CD14+) and TIE2-Monocytes (Tie2-CD14+) were then isolated by FACS-sorting (Aria II, BD Biosciences) using FITC-conjugated anti-CD14 (BD Biosciences, USA) and APC-conjugated anti-TIE2 (R&D System, USA) antibodies.Three TEMs samples together with their paried TIE2-Monocytes were detected.
2017-05-19 | GSE68322 | GEO
Project description:The role of endothelial dysfunction in tubulointerstitial fibrosis associated with chronic kidney disease (CKD) is not well understood. In this study, we demonstrate that the activation of the endothelial tyrosine kinase TIE2 alleviates renal pathology in experimental CKD in mice. TIE2 activation was achieved using a human angiopoietin-2 (ANGPT2)-binding and TIE2-activating antibody (ABTAA), or through adult-induced endothelial-specific knockout of the vascular endothelial protein tyrosine phosphatase gene (Veptp). Both methods significantly protected CKD mice from endothelial dysfunction, peritubular capillary loss, tubular epithelial injury, and tubulointerstitial fibrosis. Conversely, silencing TIE2 through adult-induced endothelial-specific knockout of the Tie2 gene exacerbated CKD pathology. Additionally, we found that endothelial dysfunction promotes renal fibrosis not through endothelial-to-mesenchymal transition as previously expected, but by inducing the expression of pro-fibrotic PDGFB in tubular epithelial cells, a process that is inhibited by TIE2 activation. Our findings suggest that TIE2 activation via ABTAA warrants investigation in human CKD, where there is a significant unmet medical need.
2025-08-26 | GSE306281 | GEO
Project description:Akt is a robust oncogene that plays key roles in the development and progression of many cancers, including glioma. We evaluated the differential propensities of the Akt isoforms toward progression in the well-characterized RCAs/Ntv-a mouse model of PDGFB-driven low grade glioma. A constitutively active myristoylated form of Akt1 did not induce high-grade glioma (HGG). In stark contrast, Akt2 and Akt3 showed strong progression potential with 78% and 97% of tumors diagnosed as HGG, respectively. We further revealed that significant variations in polarity and hydropathy values among the Akt isoforms in both the pleckstrin homology domain (P domain) and regulatory domain (R domain) were critical in mediating glioma progression. Gene expression profiles from representative Akt-derived tumors indicated dominant and distinct roles for Akt3, consisting primarily of DNA repair pathways. TCGA data from human GBM closely reflected the DNA repair function, as Akt3 was significantly correlated with a 76 gene signature DNA repair panel. Consistently, compared to Akt1 and Akt2 overexpression models, Akt3-expressing human GBM cells had enhanced activation of DNA repair proteins, leading to increased DNA repair and subsequent resistance to radiation and temozolomide. Given the wide range of Akt3-amplified cancers, Akt3 may represent a key resistance factor. 5 different experimental conditions were compared (including GFP, PDGFB, PDGFB in conjunciton with Akt1, Akt2, or Akt3) with 3 mice per treatment
2015-02-24 | E-GEOD-66177 | biostudies-arrayexpress