anti-SRY (Sex Determining Region Y)-Box 17 (SOX17) Antibodies

Human SRY (Sex Determining Region Y)-Box 17 (SOX17) interaction partners

1. The Sox17-Notch1-Hes1 pathway is critical for maintaining the undifferentiated state of IAHCs.

2. Case-control analyses reveal significant overrepresentation of rare variants in ATP13A3, AQP1 and SOX17, and provide independent validation of a critical role for GDF2 in heritable pulmonary arterial hypertension.

3. These data strongly implicate SOX17 as a new risk gene contributing to Pulmonary arterial hypertension-congenital heart disease.

4. This study showed that 1 of 4 SNPs located near the SOX17 gene, rs1072737, was statistically associated with intracranial aneurysm (IA) formation in a Korean population. The MAF of this variant (minor allele, C) showed a highly ethnic difference between Korean and European populations. Two SNPs rs10958409 and rs9298506 showed statistically significant associations with increased IA risk in the current meta-analysis.

5. The combination of methylated SOX17 with cytology better predicted neoplastic grade than cytology alone

6. SOX17 acts as a tumor suppressor in cholangiocarcinoma and its genetic, molecular and/or pharmacological restoration may represent a new promising therapeutic strategy.

7. Our results suggest that decreasing SOX17 levels may promote EC development and progression, and that by downregulating MAML3 expression and Wnt signaling, SOX17 acts as a tumor suppressor that may improve outcome in patients with EC.

8. SOX2 repression in TCam-2 cells can be abrogated by recruitment of the constitutively expressed H3K27 demethylase UTX to the SOX2 promoter through retinoid signaling, leading to expression of neuronal and other lineage genes. SOX17 has been shown to initiate human PGC specification, with its target PRDM1 suppressing mesendodermal genes

9. Dedifferentiation of fibroblasts to CD34(+) progenitor cells gives rise to endothelial cells and erythroblasts in a SOX17-dependent manner.

10. Study extracted and analyzed the experimentally validated 3D models of SOX17-HMG domain and beta-catenin; the molecular level disturbance in the two essential human proteins upon M76A and G103R mutation of SOX17, which further hampers the cell signaling phenomena for the human cytological developments beginning from gastrulation and endoderm formation.

11. SOX17 promoter is highly methylated in primary tumors and in corresponding plasma samples both in operable and advanced non-small cell lung cancer.

12. The definitive endoderm and foregut endoderm differentiation capabilities of Wnt pathway-modulated cells were determined based on the expression levels of the endodermal transcription factors SOX17 and FOXA2 and those of the transcription activator GATA4 and the alpha-fetoprotein (AFP) gene, respectively.

13. Knockdown of OCT4 during differentiation inhibits mesendoderm formation and removal of the H3K27me3 mark from the SOX17 promoter, suggesting that OCT4 acts to induce removal of the Polycomb2 complex.

14. high expression of the Sox17 associated pathway in medium and small arteries indicates that Brain arteriovenous malformation vessels are intrinsically active

15. SOX17 demethylation induced miR-371-5p expression and consequently suppressed its direct target SOX2. A novel mechanism of the SOX17/miR-371-5p/SOX2 axis is involved in the regulation of EMT, stemness and metastasis.

16. Decreased expression of SOX17 is associated with tumor progression in breast cancer.

17. In this study, oligodendroglioma patients with 1p/19q LOH and Sox17 protein expression had a better prognosis.

18. SOX17 might play a role in the development of Ovarian Cancer, and may be a therapeutic target in OC.

19. Decreased Sox17 expression is correlated with melanoma progression, an unfavorable survival of melanoma patients and is an independent molecular prognostic factor for melanoma.

20. Possible association of SOX-17 and RBBP8 with brain arteriovenous malformations, genes involved in cell cycle progression, deserves further investigation

Zebrafish SRY (Sex Determining Region Y)-Box 17 (SOX17) interaction partners

1. Targeted knockdown of Sox17 and Chd in dorsal forerunner cells led to aberrant Left-Right (L-R) asymmetry establishment, as visualized by the expression of southpaw and lefty, and heart and pancreas placement in the embryo.

2. knockout of dusp4 revealed a specific loss of sox17, establishing a new class of endoderm specification defect

3. Results describe sox17 cis-regulatory elements, and examine the specific input predictions of the gene regulatory networks.

Mouse (Murine) SRY (Sex Determining Region Y)-Box 17 (SOX17) interaction partners

1. 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.

2. SOX17 regulates uterine epithelial-stromal cross-talk acting via a distal enhancer upstream of Ihh

3. Enforced expression of Sox17 increases expression of morphogenesis genes and promotes integration of transplanted converted cells into injured vessels.

4. 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.

5. 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.

6. SOX-17 transcription factor is indispensable in developmental angiogenesis and as a positive feedback regulator of VEGF signaling.

7. findings indicate the role of Sry-related HMG box gene-17 (Sox17) in uterine receptivity to embryo implantation.

8. 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

9. Sox17 inhibition of Runx1 and Gata2 maintains endothelial fate in endothelial-to-haematopoietic transition

10. Sox17 deficiency in mouse can induce intracranial aneurysm under hypertensive conditions, suggesting Sox17 deficiency as a potential genetic factor for IA formation.

11. These results identify a novel role for Sox17 in adult liver as a modulator of the metabolic adaptation to fasting.

12. 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.

13. Hhex and Cer1 are indispensable components of the Sox17 pathway for cardiopoiesis.

14. A regulatory network, incluing Sox17 and the retinoic acid receptor, controls nephrocan expression and midgut patterning.

15. 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.

16. SoxF proteins, especially Sox17, contribute to the maintenance of cell clusters containing hematopoietic stem cells in the midgestation aorta-gonad-mesonephros region

17. Sox17 is a component of the complex signaling network that orchestrates arterial/venous specification.

18. Sox17 is required for normal formation of the pulmonary vasculature and postnatal cardiovascular homeostasis.

19. This study demonstrate that Sox17 expression is highest in newly generated oligodendrocytes under pathological conditions and could be used as a marker of oligodendrocyte regeneration.

20. Expression of Kras(G12D) and SOX17 in mice induces development of metaplasias with a biliary phenotype containing tuft cells. Expression of SOX17 induces pancreatitis and promotes Kras(G12D)-induced tumorigenesis in mice.