CD309 / VEGFR-2 / Flk-1 (esFlk1) Rabbit Polyclonal Antibody

CAT#: AP26035PU-N

CD309 / VEGFR-2 / Flk-1 (esFlk1) rabbit polyclonal antibody, Purified

Product Images

Western blot was performed using monoclonal anti-Mouse esFlk-1 (Cat.-No DM3522P) recognizing the soluble as well as the transmembrane form of Flk-1 and poyclonal antibody (Cat.-No AP26035PU) directed against the unique C-terminal end of the endogenous esFl

Specifications

Product Data

• Applications: WB
• Recommended Dilution: Western blot: 1-5 µg/ml.
• Reactivities: Human, Mouse
• Host: Rabbit
• Isotype: IgG
• Clonality: Polyclonal
• Immunogen: Peptide of the C-terminal end of native Mouse soluble VEGFR-2/Flk-1 (GMEASLGDRIAMP).
• Specificity: This antibody detects endogenous sVEGFR-2/Flk-1.
• Formulation: PBS, pH 7.2
  State: Purified
  State: Lyophilized purified IgG fraction
• Reconstitution Method: Centrifuge vial prior to opening. Restore in sterile water to a concentration of 0.1-1.0 mg/ml.
• Purification: Protein A Chromatography
• Conjugation: Unconjugated
• Storage:

  Prior to reconstitution store at 2-8°C.
  Following reconstitution store undiluted at 2-8°C for one month
  or (in aliquots) at -20°C for longer.
  Avoid repeated freezing and thawing.

• Stability: Shelf life: one year from despatch.

• Database Link:
  UniProt ID P35918
• 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 mouse esFlk-1 generated by alternative splicing consists of the first 6 Ig-like loops followed by the unique C-terminal end: GMEASLGDRIAMP.
• Synonyms: VEGFR2, FLK1, KDR, VEGF Receptor 2