VEGFR2/CD309 anticorps

N° du produit ABIN2745581

Cet anticorps Souris Monoclonal détecte spécifiquement VEGFR2/CD309 dans WB, IHC, ELISA et FACS. Il présente une réactivité envers Humain.

Aperçu rapide pour VEGFR2/CD309 anticorps (ABIN2745581)

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

Reactivité: Humain

Hôte: Souris

Clonalité: Monoclonal

Conjugué: Cet anticorp VEGFR2/CD309 est non-conjugé

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

Clone: EIC

Détail du produit anti-VEGFR2/CD309 anticorps

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

Réactivité croisée: Humain

Purification: Protein G purified.

Immunogène: Recombinant human soluble extracellular VEGFR-2.

Isotype: IgG1

Information d'application

Indications d'application: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Stockage

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.

Stock: 4 °C,-20 °C

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

Date de péremption: 6 months

Détails sur VEGFR2/CD309

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

Autre désignation: VEGFR-2/KDR

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