VEGF-A (E9X8Q) Rabbit mAb #50661
- WB
- IP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 16, 20, 23, 26 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:200 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
VEGF-A (E9X8Q) Rabbit mAb recognizes endogenous levels of total VEGF-A protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of human VEGF-A protein.
Background
Vascular endothelial growth factor-A (VEGF-A; formerly VEGF) belongs to the VEGF/PDGF family of growth factors that play a critical role in promoting vascular development. VEGF-A is primarily known for its function in promoting angiogenesis, the process by which new blood vessels are sprouted from pre-existing blood vessels. VEGF-A has eight isoforms, derived from differentially spliced mRNA variants encoded by the VEGF-A gene (1). All isoforms contain a conserved receptor binding domain, but differ in their C-terminal domains that regulate binding to components in the extracellular matrix. VEGF-A is secreted by multiple cell types, including fibroblasts, macrophages, and some tumor cells (1). Binding of VEGF-A to its cognate receptors (VEGFR2 and to a lesser extent VEGFR1) on the endothelial cell surface activates the receptor and initiates downstream signaling, resulting in endothelial cell proliferation, survival, migration, and changes to vascular permeability, all crucial processes for angiogenesis (3). Tumor cells have been shown to respond to hypoxia by increasing VEGF-A mRNA expression. Increased secretion of VEGF-A in the tumor microenvironment stimulates angiogenesis to further promote tumor progression (4). In addition to promoting tumor angiogenesis, VEGF-A has also been shown to play an important role in normal tissue development, tissue regeneration, tumor cell proliferation, neovascular eye diseases, and cancer immunity (2,5). For this reason, targeting angiogenesis via the VEGF-A pathway has been a major focus in cancer therapeutics research.
- Peach, C.J. et al. (2018) Int J Mol Sci 19, 1264. doi: 10.3390/ijms19041264.
- Goel, H.L. and Mercurio, A.M. (2013) Nat Rev Cancer 13, 871-82.
- Karaman, S. et al. (2018) Development 145, dev151019. doi: 10.1242/dev.151019.
- Levy, A.P. et al. (1997) Kidney Int 51, 575-8.
- Apte, R.S. et al. (2019) Cell 176, 1248-1264.
Limited Uses
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