VEGFR2/CD309 Antikörper

Produktnummer ABIN2745581

Dieses Maus Monoklonal-Antikörper erkennt spezifisch VEGFR2/CD309 in WB, IHC, ELISA und FACS. Er zeigt eine Reaktivität gegenüber Human.

Kurzübersicht für VEGFR2/CD309 Antikörper (ABIN2745581)

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

Reaktivität: Human

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser VEGFR2/CD309 Antikörper ist unkonjugiert

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

Klon: EIC

Produktdetails anti-VEGFR2/CD309 Antikörper

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

Kreuzreaktivität: Human

Aufreinigung: Protein G purified.

Immunogen: Recombinant human soluble extracellular VEGFR-2.

Isotyp: IgG1

Anwendungsinformationen

Applikationshinweise: Optimal working dilution should be determined by the investigator.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Lyophilized

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

Konzentration: Lot specific

Buffer: Lyophilized.

Lagerung: 4 °C,-20 °C

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

Haltbarkeit: 6 months

Details zu VEGFR2/CD309

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

Andere Bezeichnung: VEGFR-2/KDR

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