CST, 5874SC, Rat Vascular Endothelial Growth Factor-164 (rVEGF164 )

Growth Factors and Cytokines for studying VEGF rat in the research area. Product Usage Information Reconstitution: With carrier: Add sterile PBS or PBS containing 1% bovine or human serum albumin or 5-10% FBS to a final rVEGF164 concentration of greater than 50 μg/ml. Solubilize for 30 minutes at room temperature with occasional gentle vortexing. Carrier free: Add sterile PBS or PBS containing protein to minimize absorption of rVEGF164 to surfaces. Solubilize for 30 minutes at room temperature with occasional gentle vortexing. Stock rVEGF164 should be greater than 50 μg/ml. Formulation With carrier: Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.2 containing 20 μg BSA per 1 μg rVEGF 164 . Carrier free: Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.2. Storage Stable in lyophilized state at -20°C for 1 year after receipt. Sterile stock solutions reconstituted with carrier protein are stable at 4°C for 2 months and at -20°C for 6 months. Avoid repeated freeze-thaw cycles. Maintain sterility. Storage at -20°C should be in a manual defrost freezer. Source / Purification Recombinant rat VEGF (rVEGF ) Ala27-Arg190 (Accession #NP_001103803) was expressed in human 293 cells at Cell Signaling Technology. Background VEGF is one of many splice variants of the VEGF-A gene, and is one amino acid shorter than its human counterpart, VEGF (1, 2). VEGF is produced by a number of cells including endothelial cells, macrophages, and T cells (1, 2). VEGF is involved in angiogenesis, vascular endothelial cell survival, growth, migration, and vascular permeability (1,2). Gene expression is induced by hypoxia, inflammatory cytokines, and oncogenes (1, 2). VEGF binds to heparan sulfate and is retained on the cell surface and in the extracellular matrix (1-3). VEGFR1 and VEGFR2 are the receptor tyrosine kinases for VEGF (2). NRP-1 and NRP-2 may function as co-receptors and enhance VEGFR2 signaling (2-3). Binding of VEGF to VEGFR1 and VEGFR2 leads to activation of the PI3K/AKT, p38 MAPK, FAK, and Paxillin (2).