Biosynthesis and expression of VE-cadherin is regulated by the PI3K/mTOR signaling pathway
| Autor: | Christian Zuppinger, Melinda Oroszlán, Michael Bieri, Paul Mohacsi |
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| Rok vydání: | 2009 |
| Předmět: |
Immunology
Biology mTORC2 Adherens junction Mice Phosphatidylinositol 3-Kinases Antigens CD Animals Humans Enzyme Inhibitors Molecular Biology Cells Cultured PI3K/AKT/mTOR pathway S1PR1 Phosphoinositide-3 Kinase Inhibitors Mice Knockout TOR Serine-Threonine Kinases RPTOR Endothelial Cells Cadherins Cell biology Vascular endothelial growth factor B Vascular endothelial growth factor A Vascular endothelial growth factor C Cancer research Protein Kinases Signal Transduction |
| Zdroj: | Molecular Immunology. 46:866-872 |
| ISSN: | 0161-5890 |
| DOI: | 10.1016/j.molimm.2008.09.011 |
| Popis: | Vascular endothelial (VE)-cadherin is an essential protein of adherens junctions of endothelial cells and plays a pivotal role in vascular homeostasis. Mammalian target of rapamycin complex 2 (mTORC2) deficient mice display defects in fetal vascular development. Blocking mTOR or the upstream kinase phosphoinositide 3-kinase (PI3K) led to a dose-dependently decrease of the VE-cadherin mRNA and protein expression. Immunofluorescent staining showed a strongly decreased expression of VE-cadherin at the interface of human umbilical endothelial cells (HUVECs) followed by intercellular gap formation. Herewith, we demonstrated that the expression of VE-cadherin is dependent on mTOR and PI3K signaling. |
| Databáze: | OpenAIRE |
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