Vascular Endothelial Growth Factor Receptor-2; KDR; FLK-1 |
Monoclonal Antibody |
3(4H3) |
Mouse IgG1 |
Recombinant human soluble extracellular VEGFR-2. |
Flow Cytometry: (2-5μg/ml)Western Blot: (2-5μg/ml)Optimal conditions must be determined individually for each application. |
Human |
The antibody will detect native human VEGFR-2/KDR in ELISA experiments and on the surface of different human cell types. |
Protein G purified. |
Protein G purified. |
Lyophilized. |
Centrifuge vial prior to opening. Reconstitute with sterile water to a concentration of 0.1-1.0mg/ml. |
BLUE ICE |
+4°C |
-20°C |
After opening, prepare aliquots and store at -20°C.Avoid freeze/thaw cycles. |
Stable for at least 6 months after receipt when stored at -20°C. |
Download PDF |
Download PDF |
Disruption of the precise balance of positive and negative molecular regulators of blood and lymphatic vessel growth can lead to myriad diseases. Although dozens of natural inhibitors of hemangiogenesis have been identified, an endogenous selective inhibitor of lymphatic vessel growth has not been previously described. A splice variant of the gene encoding vascular endothelial growth factor receptor-2 (VEGFR-2) that encodes a secreted form of the protein, designated endogenous soluble VEGFR-2 (esVEGFR-2/KDR) has been described. The endogenous soluble esKDR inhibits developmental and reparative lymphangiogenesis by blocking VEGF-C function. Tissue-specific loss of esKDR in mice induced, at birth, spontaneous lymphatic invasion of the normally alymphatic cornea and hyperplasia of skin lymphatics without affecting blood vasculature. Administration of esKDR inhibited lymphangiogenesis but not hemangiogenesis induced by corneal suture injury or transplantation, enhanced corneal allograft survival and suppressed lymphangioma cellular proliferation. Naturally occurring esKDR thus acts as a molecular uncoupler of blood and lymphatic vessels; modulation of esKDR might have therapeutic effects in treating lymphatic vascular malformations, transplantation rejection and, potentially, tumor lymphangiogenesis and lymphedema.
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