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The "tip" and the "stalk" cells compose the two major types of the endothelial cells; the "tip" cell is based at the far end leading the vessel in an outward growing mode and expresses high levels of VEGFR-2, VEGFR-3, and platelet-derived growth factor-B, while the "stalk" cell is located adjacent to tip cell, expressing high levels of VEGFR-1 and proliferating in the lumen of the newly formed vessel.
Cursiefen and colleagues demonstrated that VEGFR-3 is ectopically expressed in the corneal epithelium .
The effect of AD-VEGF-C was confirmed using recombinant human VEGF-C156S protein, which is a selective agonist of VEGFR-3 where the characteristically spaced cysteine residues in the VEGF homology domain (Cys156) are replaced with serine residues.
An indirect ELISA was performed to detect the presence of VEGFR-3 specific autoantibodies in rat sera from control, sham, and BDL groups.
Expression of the vascular endothelial growth factor C receptor VEGFR-3 in lymphatic endothelium of the skin and in vascular tumors.
When the histologic characteristics are not clear, the endothelial origin of the cyst may be established with immunohistochemical techniques to demonstrate reactivity for CD31, CD34, factor VIII, podoplanin (D2-40), or vascular endothelial growth factor receptor 3 (VEGFR-3).
These growth factors exert their activity through activation of three types of receptors: VEGFR-1 (flt-1), VEGFR-2 (flk-1/ KDR), and VEGFR-3 (flt-4) (1, 4, 5).
M2 PHARMA-July 1, 2014-Study shows VEGFR-3, CXCR4 are predictive biomarkers for FLO, FLP therapy in advanced oesophagogastric cancer
The biological effects of VEGF binding to three receptor tyrosine kinases, VEGFR- 1, VEGFR-2, and VEGFR-3 are fairly well known.
The recent discovery of vascular endothelial growth factor-C (VEGF-C) and VEGF receptor-3 (VEGFR-3) involvement in lymphatic vessel development  and specific lymphatic markers has provided new insights into the field of lymphangiogenesis .
The biological functions of VEGF are mediated by its binding to one of the VEGF receptor tyrosine kinases, which include VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1), and VEGFR-3 (Flt-4).
Vascular endothelial growth factor (VEGF)-C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy.
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- VEGF co-regulated chemokine 1
- VEGF in Ischemia for Vascular Angiogenesis
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