VEGFR2/CD309 anticorps (C-Term)

N° du produit ABIN616032

Cet anticorps anti-VEGFR2/CD309 Polyclonal Lapin (ABIN616032) détecte spécifiquement VEGFR2/CD309 dans WB. L’anticorps est réactif avec des échantillons de Humain et Souris.

Aperçu rapide pour VEGFR2/CD309 anticorps (C-Term) (ABIN616032)

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

Reactivité: Humain, Souris

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp VEGFR2/CD309 est non-conjugé

Application: Western Blotting (WB)

Détail du produit anti-VEGFR2/CD309 anticorps

Épitope: C-Term

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

Réactivité croisée (Details): Species reactivity (tested):Human, Mouse.

Purification: Protein A Chromatography

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

Isotype: IgG

Information d'application

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

Restrictions: For Research Use only

Stockage

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

Conseil sur la manipulation: Avoid repeated freezing and thawing.

Stock: 4 °C/-20 °C

Stockage commentaire: 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.

Détails sur VEGFR2/CD309

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

Autre désignation: CD309 / VEGFR-2 / Flk-1

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 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

ID gène: 10090

UniProt: P35918

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