| http://purl.uniprot.org/citations/17008323 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17008323 | http://www.w3.org/2000/01/rdf-schema#comment | "Ginsenoside-Rg1, the most prevalent active constituent of ginseng, is a potent proangiogenic factor of vascular endothelial cells. This suggests that Rg1 may be a new modality for angiotherapy. Rg1 can activate the glucocorticoid receptor (GR). However, the regulatory steps downstream from GR that promote Rg1-induced angiogenesis have not been elucidated. Here we showed for the first time that Rg1 was a potent stimulator of vascular endothelial growth factor (VEGF) expression in human umbilical vein endothelial cells, and importantly this induction was mediated through a phosphatidylinositol 3-kinase (PI3K)/Akt and beta-catenin/T-cell factor-dependent pathway via the GR. Rg1 stimulation resulted in an increase in the level of beta-catenin, culminating its nuclear accumulation, and subsequent activation of VEGF expression. Transfection of a stable form of beta-catenin (S37A) or the use of a glycogen synthase kinase 3beta inhibitor to stabilize beta-catenin induced VEGF synthesis, whereas small interfering RNA-mediated down-regulation of beta-catenin did not, confirming that the effect was beta-catenin-specific. Using a luciferase reporter gene assay, we observed that Rg1 increased T-cell factor/lymphoid enhancer factor transcriptional activity. These events were mediated via a PI3K-dependent phosphorylation of the inhibitory Ser9 residue of glycogen synthase kinase 3beta. In addition, the GR antagonist RU486 was able to inhibit Rg1-induced PI3K/Akt and beta-catenin activation. These findings provide new insights into the mechanism responsible for Rg1 functions."xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m606698200"xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/author | "Wong A.S."xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/author | "Leung K.W."xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/author | "Wong R.N."xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/author | "Pon Y.L."xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/pages | "36280-36288"xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/title | "Ginsenoside-Rg1 induces vascular endothelial growth factor expression through the glucocorticoid receptor-related phosphatidylinositol 3-kinase/Akt and beta-catenin/T-cell factor-dependent pathway in human endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://purl.uniprot.org/core/volume | "281"xsd:string |
| http://purl.uniprot.org/citations/17008323 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17008323 |
| http://purl.uniprot.org/citations/17008323 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17008323 |
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| http://purl.uniprot.org/uniprot/#_A2A2V4-mappedCitation-17008323 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17008323 |
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| http://purl.uniprot.org/uniprot/#_P49841-mappedCitation-17008323 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17008323 |