VEGF Receptor 2 (KDR) (esKDR) Rabbit Polyclonal Antibody
Other products for "KDR"
Specifications
Product Data | |
Applications | IF, WB |
Recommended Dilution | Western blot: 1-5 μg/ml. Immunofluorescence/Immunohistochemistry: 1-5 µg/ml. |
Reactivities | Human |
Host | Rabbit |
Isotype | IgG |
Clonality | Polyclonal |
Immunogen | Peptide consisting of the unique C-terminal end of esKDR: CGRETILDHSAEAVGMP |
Specificity | This antibody detects CD309 / VEGFR-2 / Flk-1. This poyclonal antibody directed against the unique C-terminal end of the endogenous sKDR (CGRETILDHSAEAVGMP) recognizing solely the endogenous form but not sKDR (D7) and sKDR (D7)-Fc consisting of the full extraplasmatic domain. The endogenous sKDR generated by alternative splicing consists of the first 6 Ig-like loops with a unique c-terminal end. |
Formulation | PBS, pH 7.2 State: Purified State: Lyophilized purified IgG fraction |
Reconstitution Method | Restore in sterile water to a concentration of 0.1-1.0 mg/ml. |
Purification | Protein A Chromatography |
Storage | Store lyophilized at 2-8°C for 6 months or at -20°C long term. After reconstitution store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C long term. Avoid repeated freezing and thawing. |
Stability | Shelf life: one year from despatch. |
Gene Name | Homo sapiens kinase insert domain receptor (a type III receptor tyrosine kinase) (KDR) |
Database Link | |
Background | 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 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: CGRETILDHSAEAVGMP. |
Synonyms | VEGFR2, FLK1, KDR, VEGF Receptor 2 |
Reference Data | |
Protein Families | Druggable Genome, ES Cell Differentiation/IPS, Protein Kinase, Transmembrane |
Protein Pathways | Cytokine-cytokine receptor interaction, Endocytosis, Focal adhesion, VEGF signaling pathway |
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