VEGFR-1 and VEGFR-2: two non-identical twins with a unique physiognomy.
VEGFR-1 and VEGFR-2: two non-identical twins with a unique physiognomy.
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DOI：
10.2741/1839
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发表时间：
2006
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影响因子：
--
通讯作者：
N. Rahimi
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文献类型：
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作者：
N. Rahimi
血管生成包括内皮细胞分化、增殖、迁移和脐带形成，这些过程导致小管形成，形成血管。一组与血管生成有关的生长因子受体是受体酪氨酸激酶的VEGFR家族。VEGFR-1和VEGFR-2是密切相关的受体酪氨酸激酶，具有共同和特异性配体。VEGFR-1是一种激酶受损的RTK，而VEGFR-2是一种高活性的激酶。尽管VEGFR-1和VEGFR-2具有不同的激酶激活潜力，但它们都是正常发育和血管生成所必需的。VEGFR-1通过涉及配体捕获、受体同源和异源二聚化的机制调节血管生成。VEGFR-2在体外刺激多种信号通路和广泛的生物反应。调控VEGFR-2激活的机制、募集信号蛋白的能力以及下调的能力都受到其羧基末端的高度调控。本文综述了最近对VEGFR-1和VEGFR-2激活机制的研究，并重点关注了VEGFR-1和VEGFR-2调节血管生成的信号通路。
Angiogenesis involves endothelial cell differentiation, proliferation, migration and cord formation, which lead to tubulogenesis to form vessels. One group of growth factor receptors implicated in angiogenesis is the VEGFR family of receptor tyrosine kinases. VEGFR-1 and VEGFR-2 are closely related receptor tyrosine kinases and have both common and specific ligands. VEGFR-1 is a kinase-impaired RTK whereas VEGFR-2 is a highly active kinase. Despite their differential kinase activation potentials, both VEGFR-1 and VEGFR-2 are required for normal development and angiogenesis. VEGFR-1 regulates angiogenesis by mechanisms that involve ligand-trapping, receptor homo- and heterodimerization. VEGFR-2 stimulates variety of signaling pathways and broad biological responses in vitro. The mechanisms that govern VEGFR-2 activation, its ability to recruit signaling proteins and to undergo downregulation are highly regulated by its carboxyl terminus. This review highlights recent insights into the mechanism of activation of VEGFR-1 and VEGFR-2, and focuses on the signaling pathways employed by VEGFR-1 and VEGFR-2 that regulate angiogenesis.