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ECSM2,一种内皮细胞特异性的 VE-cadherin 结合蛋白,具有一个酪氨酸磷酸化位点,对细胞迁移至关重要。

ECSM2, an endothelial specific VE-cadherin binding protein, has a tyrosine phosphorylation site essential to cell migration.

机构信息

Department of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, PR China; Department of Laboratory, The first Clinical Medical School, China Three Gorges University, Yichang 443000, PR China.

Department of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, PR China.

出版信息

Gene. 2018 Jul 1;662:131-138. doi: 10.1016/j.gene.2018.04.013. Epub 2018 Apr 10.

Abstract

Endothelial cell-specific molecule 2 (ECSM2) is a transmembrane protein located in cell-cell junction of endothelial cells (EC). ECSM2 was determined to play an important role in vascular development, EC migration, apoptosis and proliferation, however, no functional domains were determined in intracellular and extracellular region of ECSM2. In current work, functional domains of ECSM2, the relationship of ECSM2 with other endothelial specific protein such as VE-cadherin and the role of ECSM2 in neovascular diseases were determined. It was shown that the 54th amino acid residue of ECSM2 extracellular domain was a tyrosine phosphorylation site, whose mutation led to the loss of EGF-induced tyrosine phosphorylation and inhibition of cell migration. In primary human umbilical vein endothelial cells, ECSM2 bound with VE-cadherin and VEGF stimulation enhanced their binding. In hepatocellular carcinoma, ECSM2 expression was increased, as compared with para-cancerous tissue. This data firstly revealed the functional sites of ECSM2, the crosstalk between ECSM2 and other endothelial cell specific molecules, the expression of ECSM2 in tissues of angiogenesis diseases, thus providing understanding about ECSM2 in depth.

摘要

内皮细胞特异分子 2(ECSM2)是一种位于内皮细胞(EC)细胞-细胞连接处的跨膜蛋白。已经确定 ECSM2 在血管发育、EC 迁移、凋亡和增殖中发挥重要作用,然而,在 ECSM2 的细胞内和细胞外区域没有确定功能域。在当前的工作中,确定了 ECSM2 的功能域、ECSM2 与其他内皮特异性蛋白(如 VE-cadherin)的关系以及 ECSM2 在新生血管疾病中的作用。结果表明,ECSM2 细胞外结构域的第 54 个氨基酸残基是酪氨酸磷酸化位点,其突变导致 EGF 诱导的酪氨酸磷酸化丧失和细胞迁移抑制。在原代人脐静脉内皮细胞中,ECSM2 与 VE-cadherin 结合,并且 VEGF 刺激增强了它们的结合。在肝癌中,与癌旁组织相比,ECSM2 的表达增加。该数据首次揭示了 ECSM2 的功能位点、ECSM2 与其他内皮细胞特异性分子之间的串扰、ECSM2 在血管生成疾病组织中的表达,从而深入了解 ECSM2。

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