VEGFR2/CD309 antibody

Catalog No. ABIN2745581

This Mouse Monoclonal antibody specifically detects VEGFR2/CD309 in WB, IHC, ELISA and FACS. It exhibits reactivity toward Human.

Quick Overview for VEGFR2/CD309 antibody (ABIN2745581)

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

Reactivity: Human

Host: Mouse

Clonality: Monoclonal

Conjugate: This VEGFR2/CD309 antibody is un-conjugated

Application: Western Blotting (WB), Immunohistochemistry (IHC), ELISA, Flow Cytometry (FACS)

Clone: EIC

Product Details anti-VEGFR2/CD309 Antibody

Specificity: The antibody will detect native human VEGFR-2/KDR in ELISA experiments and on the surface of different human cell types.

Cross-Reactivity: Human

Purification: Protein G purified.

Immunogen: Recombinant human soluble extracellular VEGFR-2.

Isotype: IgG1

Application Details

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

Restrictions: For Research Use only

Handling

Format: Lyophilized

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

Concentration: Lot specific

Buffer: Lyophilized.

Storage: 4 °C,-20 °C

Storage Comment: Short Term Storage: +4°C
Long Term Storage: -20°C
Stable for at least 6 months after receipt when stored at -20°C.

Expiry Date: 6 months

Target Details for VEGFR2/CD309

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

Alternative Name: VEGFR-2/KDR

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 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.

UniProt: P35968

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