Wallez Yann, Vilgrain Isabelle, Huber Philippe
Laboratoire de Développement et Vieillissement de l'Endothélium, Université Joseph Fourier, Grenoble, France.
Trends Cardiovasc Med. 2006 Feb;16(2):55-9. doi: 10.1016/j.tcm.2005.11.008.
Because angiogenesis is a key step in a number of pathologic processes, including tumor growth and atherosclerosis, many research studies have investigated the regulatory signals active at various stages of vascular invasion. The differential activities of the endothelial junction protein vascular endothelial (VE)-cadherin reflect the versatile behavior of endothelial cells between vascular quiescence and angiogenesis. VE-cadherin function and signaling are deeply modified in proliferating cells, and this conversion is accompanied by phosphorylation of the protein on tyrosine residues and enhanced transcription of its gene. Recent advances in the complex interplay between protein tyrosine kinases and phosphatases regulating VE-cadherin phosphorylation and function are discussed in this review.
由于血管生成是包括肿瘤生长和动脉粥样硬化在内的许多病理过程中的关键步骤,许多研究都对血管侵袭各个阶段活跃的调节信号进行了调查。内皮连接蛋白血管内皮(VE)-钙黏蛋白的不同活性反映了内皮细胞在血管静止和血管生成之间的多样行为。VE-钙黏蛋白的功能和信号传导在增殖细胞中会发生深刻改变,这种转变伴随着该蛋白酪氨酸残基的磷酸化及其基因转录的增强。本文综述了调节VE-钙黏蛋白磷酸化和功能的蛋白酪氨酸激酶与磷酸酶之间复杂相互作用的最新进展。