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Single cell expression profiling of the mouse Sox17-null myocardium at E8.5

ABSTRACT: To understand the function of Sox17 in the precursor cells of the mouse endocardium amd the effect in the develoiping heart tube, single cell expression profiling of the Sox17-null endocardium and myocardium were performed.

ORGANISM(S): Mus musculus

PROVIDER: GSE125322 | GEO | 2019/02/12

REPOSITORIES: GEO

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Single cell expression profiling of the mouse Sox17-null endocardium at E8.5

Project description:To understand the function of Sox17 in the precursor cells of the mouse endocardium and the effect in the develoiping heart tube, single cell expression profiling of the Sox17-null endocardium and myocardium were performed.

2019-02-12 | GSE125321 | GEO

Single cell expression profiling of the mouse Sox17-null endocardium and myocardium at E8.5

Project description:Single cell expression profiling of the mouse Sox17-null endocardium and myocardium at E8.5

| PRJNA515853 | ENA

Single cell expression profiling of the mouse Sox17-null myocardium at E8.5

Project description:Single cell expression profiling of the mouse Sox17-null myocardium at E8.5

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Single cell expression profiling of the mouse Sox17-null endocardium at E8.5

Project description:Single cell expression profiling of the mouse Sox17-null endocardium at E8.5

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Single cell expression profiling of the mouse Sox17-null endocardium and myocardium at E8.5

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

2019-02-12 | GSE125323 | GEO

Effects of the Sox17 ∆50 mutation on SOX17 function in mouse embryonic liver development

2024-10-31 | E-MTAB-13982 | biostudies-arrayexpress

Effects of the Sox17∆50/GFP mutation on SOX17 function in mouse embryonic liver development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals, crossed them to a Sox17GFPCre (a Sox17 null allele), and surveyed how this mutation affected Sox17 expression. Livers were isolated from E12.5 Sox17∆50/GFPCRe compound heterozygous and Sox17+/+ embryos (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.

2024-10-31 | E-MTAB-13983 | biostudies-arrayexpress

Effects of the Sox17∆50 mutation on SOX17 function in mouse embryonic biliary development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals and surveyed how this mutation altered Sox17 expression. EPCAM+/CXCR4+ endodermal cells were isolated from E10.5 Sox17∆50/∆50 and Sox17+/+ embryos (n = 1 of each genotype). Posterior foregut and midgut regions of embryos were dissected by removal of embryonic head, heart, tail, limb buds, posterior and dorsal body trunk. Sox17+/+ and Sox17Δ50/Δ50 cell samples were labelled with barcodes from 3'CellPlex Kit (10X Genomics) and subsequently pooled together for single isolation, library preparation and sequencing.

2024-10-31 | E-MTAB-14000 | biostudies-arrayexpress

Transcriptional regulation of Sox17 in HUVEC

Project description:We identified Sox17 as a novel angiogenic transcription factor in the context of tumor. Our data revealed that Sox17 promotes tumor angiogenesis and tumor vessel abnormality. We found that Sox17 is specifically expressed in tumor endothelial cells within tumors. Our study elucidates a novel transcriptional regulation for tumor angiogenesis Control HUVECs vs. Sox17 knockdown HUVECs. Biological replicates: 3 control replicates, 3 transfected replicates.

2012-12-17 | E-GEOD-37395 | biostudies-arrayexpress

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVEC), there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induces cell cycle programming, proliferative and anti-apoptotic phenotypes, a process mediated by the activation of E2F Transcription Factor 1 (E2F1) signaling. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-03-15 | GSE192649 | GEO

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