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

VE-钙粘蛋白修饰和结合伴侣调节内皮连接 (B01)

• 批准号: 394431129
• 金额: --
• 依托单位: Max-Planck-Institut für molekulare Biomedizin
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2018
• 资助国家: 德国
• 起止时间: 2017-12-31 至 2020-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/394431129?language=en
• 关键词: VE; cadherin; modifications; binding; partners

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.

血管通透性的诱导和白细胞进入组织是炎症的标志。VE-钙粘蛋白是一种控制连接完整性的中心粘附分子，其活性受血管内皮蛋白酪氨酸磷酸酶（VE-PTP）调节。在这个建议中，我们要调查的分子机制，使各种酪氨酸残基控制粘附功能的VE-钙粘蛋白在体内。此外，我们将分析VE-钙粘蛋白与VEGFR 2、斑珠蛋白和粘着斑蛋白（通过β-连环蛋白）的相互作用在体内调节内皮连接的相关性。