VEGFR2 also called KDR or Flk-1, is identified as the receptor for VEGF and VEGFC and an early marker for endothelial cell progenitors, whose expression is restricted to endothelial cells in vivo. VEGFR2 was shown to be the primary signal transducer for angiogenesis and the development of pathological conditions such as cancer and diabetic retinopathy. It has been shown that VEGFR2 is expressed mainly in the endothelial cells, and the expression is upregulated in the tumor vasculature. Thus the inhibition of VEGFR2 activity and its downstream signaling are important targets for the treatment of diseases involving angiogenesis. VEGFR2 transduces the major signals for angiogenesis via its strong tyrosine kinase activity. However, unlike other representative tyrosine kinase receptors, VEGFR2 does not use the Ras pathway as major downstream signaling but rather uses the phospholipase C-protein kinase C pathway to signal mitogen-activated protein (MAP)-kinase activation and DNA synthesis. VEGFR2 is a direct and major signal transducer for pathological angiogenesis, including cancer and diabetic retinopathy, in cooperation with an many other signaling partners, thus, VEGFR2 and its downstream signaling appear to be critical targets for the suppression of these diseases. VEGF and VEGFR2-mediated survival signaling are critical to endothelial cell survival, maintenance of the vasculature and alveolar structure, and regeneration of lung tissue. Reduced VEGF and VEGFR2 expression in emphysematous lungs has been linked to increased endothelial cell death and vascular regression.
Vascular endothelial growth factor receptor 3 (VEGFR3), also known as FLT-4, together with the other two members VEGFR1 (FLT-1) and VEGFR2 (KDR/Flk-1) are receptors for vascular endothelial growth factors (VEGF) and belong to the class III subfamily of receptor tyrosine kinases (RTKs). The VEGFR3 protein is expressed mainly on lymphatic vessels but it is also up-regulated in tumor angiogenesis. Mutations in VEGFR3 have been identified in patients with primary lymphoedema. The VEGF-C/VEGF-D/VEGFR3 signaling pathway may provide a target for antilymphangiogenic therapy in prostate cancer, breast cancer, gastric cancer, lung cancer, non-small cell lung cancer (NSCLC), and so on.
Human Vascular endothelial growth factor receptor 2(KDR, VEGFR-2) is a member of the class III subfamily of receptor tyrosine kinases (RTKs). KDR is involved in a number of fundamental biological processes such as the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. It also plays an essential role in promoting proliferation, survival, migration and differentiation of endothelial cells, reorganization of the actin cytoskeleton. VEGFR2 is identified as the receptor for VEGF and VEGFC and an early marker for endothelial cell progenitors, whose expression is restricted to endothelial cells in vivo.The adaptor protein SHB has been shown to interact with VEGFR2 in receptor tyrosine kinase signaling. In addition, VEGFR2 is able to interact with HIV-1 extracellular Tat protein upon VEGF activation, and seems to enhance angiogenesis in Kaposi's sarcoma lesions. VEGF R2 is thought to be the primary inducer of VEGF-mediated blood vessel growth, while VEGF R3 plays a significant role in VEGF-C and VEGF-D-mediated lymphangiogenesis.
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