VEGFR2/CD309 antibody (C-Term)

Catalog No. ABIN616031

Product Details anti-VEGFR2/CD309 Antibody

Target: VEGFR2/CD309 (VEGFR2) (VEGF Receptor 2 (VEGFR2))

Binding Specificity: C-Term

Reactivity: Human, Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This VEGFR2/CD309 antibody is un-conjugated

Application: Western Blotting (WB)

Specificity: This antibody detects endogenous sVEGFR-2/Flk-1.

Cross-Reactivity (Details): Species reactivity (tested):Human, Mouse.

Purification: Protein A Chromatography

Immunogen: Peptide of the C-terminal end of native Mouse soluble VEGFR-2/Flk-1 (GMEASLGDRIAMP).

Isotype: IgG

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Reconstitution: Centrifuge vial prior to opening. Restore in sterile water to a concentration of 0.1-1.0 mg/mL.

Buffer: PBS, pH 7.2

Handling Advice: Avoid repeated freezing and thawing.

Storage: 4 °C/-20 °C

Storage Comment: 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.

Target Details for VEGFR2/CD309

Target: VEGFR2/CD309 (VEGFR2) (VEGF Receptor 2 (VEGFR2))

Alternative Name: CD309 / VEGFR-2 / Flk-1 (VEGFR2 Products)

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: FLK1, KDR, Kinase NYK, Kinase insert domain receptor, Protein-tyrosine kinase receptor Flk-1, VEGF Receptor 2, VEGFR2, Vascular endothelial growth factor receptor 2

Gene ID: 10090

UniProt: P35918

Pathways: RTK Signaling, Glycosaminoglycan Metabolic Process, Signaling Events mediated by VEGFR1 and VEGFR2, Growth Factor Binding, Regulation of long-term Neuronal Synaptic Plasticity, VEGF Signaling