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findings provide direct evidence of the crucial roles of sex determining region Y-box 17 (SOX17) in proper formation and maintenance of the marginal zone endoderm region
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Study in a mouse endotoxemia model of inflammatory endothelial injury and human cells demonstrated that endothelial Sox17 expression plays an obligatory role in normalizing the endothelium. Restoration of endothelial integrity is mediated by activation of HIF-1alpha, upregulation of its target Sox17, and subsequent downstream expression of Cyclin E1 which mediates endothelial regeneration.
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Data show that SOX7, SOX17 and SOX18 (SOXF) transcriptional factors are induced during satellite cell specification.
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During early postnatal development, Sox17 overexpression increases the pool of OPCs at the expense of differentiated oligodendrocytes. However, the oligodendroglial cell population, oligodendrocyte progenitor cells (OPCs)proliferation and apoptosis remained unchanged in Sox17 transgenic mice. Sox17 represses the expression of the major myelin genes, resulting in a severe CNS hypomyelination.
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SOX17 regulates uterine epithelial-stromal cross-talk acting via a distal enhancer upstream of Ihh
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Enforced expression of Sox17 increases expression of morphogenesis genes and promotes integration of transplanted converted cells into injured vessels.
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The defective gallbladder contraction positively correlated with the severity of embryonic hepatitis in Sox17(+/-) embryos, suggesting a potential contribution of embryonic cholecystitis and fetal gallbladder contraction in the early pathogenesis of congenital biliary atresia.
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Sox17 disruption in epithelial and stromal compartments led to inhibition of endometrial adenogenesis and a loss of reproductive capacity. Epithelium-specific Sox17 disruption resulted in normal adenogenesis although reproductive capacity remained impaired. Non-epithelial, Sox17-positive cells are necessary for adenogenesis and endometrial glands require Sox17 to properly function.
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SOX-17 transcription factor is indispensable in developmental angiogenesis and as a positive feedback regulator of VEGF signaling.
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findings indicate the role of Sry-related HMG box gene-17 (Sox17) in uterine receptivity to embryo implantation.
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combined deletion of Sox7, Sox17, and Sox18 at the onset of retinal angiogenesis leads to a dense capillary plexus with a nearly complete loss of radial arteries and veins, whereas the presence of a single Sox17 allele largely restores arterial identity
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Sox17 inhibition of Runx1 and Gata2 maintains endothelial fate in endothelial-to-haematopoietic transition
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Sox17 deficiency in mouse can induce intracranial aneurysm under hypertensive conditions, suggesting Sox17 deficiency as a potential genetic factor for IA formation.
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These results identify a novel role for Sox17 in adult liver as a modulator of the metabolic adaptation to fasting.
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the transcription factor SOX17, which is activated in prospective definitive endoderm cells before intercalation, is necessary for gut endoderm morphogenesis and the assembly of the basement membrane that separates gut endoderm from mesoderm.
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Hhex and Cer1 are indispensable components of the Sox17 pathway for cardiopoiesis.
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A regulatory network, incluing Sox17 and the retinoic acid receptor, controls nephrocan expression and midgut patterning.
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Sox17 promotes endothelial migration. It destabilizes endothelial junctions, rearranges the cytoskeleton, and upregulates several genes expressed in tip cells. The Notch pathway regulates Sox17 expression mainly at the post-transcriptional level.
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SoxF proteins, especially Sox17, contribute to the maintenance of cell clusters containing hematopoietic stem cells in the midgestation aorta-gonad-mesonephros region
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Sox17 is a component of the complex signaling network that orchestrates arterial/venous specification.