VE-cadherin modifications and binding partners regulate endothelial junctions (B01)

血管通透性的诱导和白细胞进入组织是炎症的特征。VE-钙粘蛋白是一种控制连接完整性的中枢黏附分子，其活性受血管内皮蛋白酪氨酸磷酸酶(VE-PTP)的调节。在这项建议中，我们想要研究体内各种酪氨酸残基控制VE-钙粘附素黏附功能的分子机制。此外，我们还将分析VE-钙粘蛋白与血管内皮细胞生长因子2、白蛋白和纽蛋白(通过-连环蛋白)在体内调节内皮连接的相互作用的相关性。

The induction of vascular permeability and the entry of leukocytes into tissue are hallmarks of inflammation. VE-cadherin is a central adhesion molecule that that controls junction integrity and whose its activity is regulated by the vascular endothelial protein tyrosine phosphatase (VE-PTP). In this proposal we want to investigate the molecular mechanisms whereby various tyrosine residues control the adhesive function of VE-cadherin in vivo. In addition, we will analyze the relevance of the interaction of VE-cadherin with VEGFR2, with plakoglobin and with vinculin (via -catenin) for the regulation of endothelial junctions in vivo.