VEGFR2/CD309 Antikörper (C-Term)

Produktnummer ABIN616032

Der Kaninchen Polyklonal anti-VEGFR2/CD309 Antikörper (ABIN616032) detektiert spezifisch VEGFR2/CD309 in WB. Dieser Antikörper reagiert spezifisch mit Proben aus Human und Maus.

Kurzübersicht für VEGFR2/CD309 Antikörper (C-Term) (ABIN616032)

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

Reaktivität: Human, Maus

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser VEGFR2/CD309 Antikörper ist unkonjugiert

Applikation: Western Blotting (WB)

Produktdetails anti-VEGFR2/CD309 Antikörper

Bindungsspezifität: C-Term

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

Kreuzreaktivität (Details): Species reactivity (tested):Human, Mouse.

Aufreinigung: Protein A Chromatography

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

Isotyp: IgG

Anwendungsinformationen

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

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

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

Buffer: PBS, pH 7.2

Handhabung: Avoid repeated freezing and thawing.

Lagerung: 4 °C/-20 °C

Informationen zur Lagerung: 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.

Details zu VEGFR2/CD309

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

Andere Bezeichnung: CD309 / VEGFR-2 / Flk-1

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 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

Gen-ID: 10090

UniProt: P35918

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