Detects rat VEGF in direct ELISAs and Western blots. In direct ELISAs, approximately 20% cross-reactivity with recombinant human (rh) VEGF165 and rhVEGF121 is observed and less than 2% cross-reactivity with rhVEGF-B, recombinant mouse (rm) VEGF-B, rhVEGF-C, rhVEGF-D, and rmVEGF-D is observed.
Polyclonal Goat IgG
Mouse myeloma cell line NS0-derived recombinant rat VEGF164 Ala27-Arg190 Accession # AAL07526
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied as a 0.2 µm filtered solution in PBS.
<0.10 EU per 1 μg of the antibody by the LAL method.
Measured by its ability to neutralize VEGF164-induced proliferation in HUVEC human umbilical vein endothelial cells. The Neutralization Dose (ND50) is typically 0.2-0.6 µg/mL in the presence of 20 ng/mL Recombinant Rat VEGF164.
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
VEGF164 in Rat Kidney. VEGF164 was detected in perfusion fixed frozen sections of rat kidney using 15 µg/mL Goat Anti-Rat VEGF164 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF564) overnight at 4 °C. Tissue was stained with the Anti-Goat HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS008) and counterstained with hematoxylin (blue). View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections.
Cell Proliferation Induced by VEGF164 and Neutralization by Rat VEGF Antibody. Recombinant Rat VEGF164 (Catalog # 564-RV) stimulates proliferation in HUVEC human umbilical vein endothelial cells in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Rat VEGF164 (20 ng/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Rat VEGF 164 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF564). The ND50 is typically 0.2-0.6 µg/mL.
Preparation and Storage
Reconstitute at 0.2 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
Vascular endothelial growth factor (VEGF or VEGF-A), also known as vascular permeability factor (VPF), is a potent mediator of both angiogenesis and vasculogenesis in the fetus and adult. It is a member of the PDGF family that is characterized by a cysteine-knot structure formed by eight conserved cysteine residues. Alternately spliced isoforms of 121, 145, 165, 183, 189, and 206 amino acids (aa) have been identified in humans, with 120, 164, and 188 aa isoforms found in rat and mouse. Isoforms other than VEGF120 and VEGF121 contain basic heparin-binding regions and are not freely diffusible. Rat VEGF164 shares 97% aa sequence identity with corresponding regions of mouse, 88% with human and bovine, 89% with porcine and canine, and 90% with feline and equine VEGF, respectively. VEGF binds the type I transmembrane receptor tyrosine kinases VEGF R1 (also called Flt-1) and VEGF R2 (Flk-1/KDR) on endothelial cells. Although affinity is highest for binding to VEGF R1, VEGF R2 appears to be the primary mediator of VEGF angiogenic activity. Human VEGF165 binds the semaphorin receptor, neuropilin-1 and promotes complex formation with VEGF R2. VEGF is required during embryogenesis to regulate the proliferation, migration, and survival of endothelial cells. In adults, VEGF functions mainly in wound healing and the female reproductive cycle. Pathologically, it is involved in tumor angiogenesis and vascular leakage. Circulating VEGF levels correlate with disease activity in autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus. VEGF is induced by hypoxia and cytokines such as IL-1, IL-6, IL-8, oncostatin M, and TNF-alpha.
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The data collected includes not only links to publications in PubMed,
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