Mouse VEGFR-2/Flk-1 (native), soluble

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Size5 µg
Price150 €
SourceInsect cells
Purity Confirmation> 95% by SDS-PAGE & visualized by silver stain
Length [aa]654
N Terminal SequenceASVGLPGDFL
Biological ActivityMeasured by its ability to inhibit the VEGF165-induced proliferation in human umbilical vein endothelial (HUVE) cells.
Species ReactivityMouse
Buffer25 mM MES, 100 mM NaCl; pH 5.5
ReconstitutionThe lyophilized mouse sFlk-1 is soluble in water and most aqueous buffers; it should be reconstituted in water or PBS to a concentration of not lower than 100µg/ml.
Stability and StorageThe material is stable for greater than six months at -20° C to -70° C. After the first thawing it is recommended to aliquote the material, because repeated freeze-thaw cycles will decrease the activity. Store at 4 °C not longer than 2 days.
Synonymssoluble vascular endothelial growth factor receptor-2; Kdr; Flk1; Ly73; Flk-1; VEGF receptor 2; VEGFR-2; sVEGFR-2
DescriptionDisruption 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 to our knowledge 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. Recombinant human esKDR generated by alternative splicing consist of the first 6 Ig-like loops followed by the unique C-terminal end: GMEASLGDRIAMP.
Uniprot IDP35918
Protein RefSeqACJ66293.1
mRNA RefSeqEU884114

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