VEGFR2
Vascular Endothelial Growth Factor Receptor 2 (VEGFR2), also known as KDR (Kinase Insert Domain Receptor) or Flk-1 (Fetal Liver Kinase-1), is a protein that in humans is encoded by the KDR gene. VEGFR2 is a central component of the Vascular Endothelial Growth Factor (VEGF) signaling pathway, playing a key role in angiogenesis, the process by which new blood vessels form from pre-existing vessels. This receptor is predominantly expressed on the surface of endothelial cells and has been implicated in the regulation of cell proliferation, migration, and survival.
Structure[edit | edit source]
VEGFR2 is a type III receptor tyrosine kinase (RTK) that consists of seven immunoglobulin-like domains in its extracellular region, a single transmembrane helix, and a cytoplasmic domain that contains a split kinase domain. Upon binding to its ligand, VEGF, VEGFR2 undergoes dimerization and autophosphorylation, activating its kinase activity, which in turn triggers a cascade of downstream signaling pathways.
Function[edit | edit source]
The primary function of VEGFR2 is to mediate the response to VEGF, which is a potent angiogenic factor. This involves the stimulation of endothelial cell proliferation, migration, and survival, as well as increased vascular permeability. VEGFR2 signaling is crucial for both physiological and pathological angiogenesis, including wound healing, development, and cancer progression.
Clinical Significance[edit | edit source]
Given its pivotal role in angiogenesis, VEGFR2 is a significant target in cancer therapy. Inhibitors of VEGFR2, such as sunitinib, sorafenib, and bevacizumab, have been developed and approved for the treatment of various malignancies. These agents work by blocking the angiogenic signals, thereby inhibiting tumor growth and metastasis.
Research[edit | edit source]
Research on VEGFR2 has also extended into other areas, including the study of its role in diabetic retinopathy, a condition characterized by the proliferation of retinal blood vessels, and in cardiovascular diseases, where angiogenesis may contribute to the repair of damaged heart tissue.
See Also[edit | edit source]
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