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

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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.