KDR是致癌基因，编码蛋白是激酶结构域受体（一种受体酪氨酸激酶），VEGFR2或Flk-1，是血管内皮生长因子（VEGF）的酪氨酸激酶受体，在血管生成中起关键作用。在缺氧条件下，缺氧诱导因子1（HIF1）蛋白稳定导致KDR和VEGF的上调。VEGF与KDR的结合通过受体二聚化和自身磷酸化，磷脂酶C（PLC-γ）的激活和通过蛋白激酶C（PKC）和RAF / MEK / ERK的下游信号传导刺激血管生成。KDR的突变在肿瘤中是罕见的，并且KDR活性的改变通常通过KDR扩增和随后的过表达发生，最常见于皮肤癌

KDR (kinase domain receptor), also known as VEGFR2 or Flk-1, is a tyrosine kinase receptor for vascular endothelial growth factor (VEGF) and plays a key role in angiogenesis. In hypoxic conditions, hypoxia-inducible factor 1 (HIF1) protein stabilization leads to upregulation of KDR and VEGF. Binding of VEGF to KDR results in stimulation of angiogenesis via receptor dimerization and autophosphorylation, activation of phospholipase C (PLC-gamma) and downstream signaling via protein kinase C (PKC) and RAF/MEK/ERK. Mutations of KDR are rare in tumors, and alterations of KDR activity typically occur via KDR amplification and subsequent overexpression. Most therapies blocking KDR signaling target the angiogenesis pathway in general, such as bevacizumab, an antibody that targets VEGF-A.

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