VEGF Polyclonal Antibody
SKU: E-AB-93319-200
VEGF Polyclonal Antibody
| SKU # | E-AB-93319 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Applications | WB, IF |
Product Details
| Isotype | IgG |
| Host | Rabbit |
| Reactivity | Human, Mouse |
| Applications | WB, IF |
| Clonality | Polyclonal |
| Immunogen | A synthetic peptide of human VEGF |
| Abbre | VEGF |
| Synonyms | MVCD1, VEGF, VPF, vascular endothelial growth factor A, VEGFA |
| Swissprot | |
| Calculated MW | 15-27 kDa/34-45 kDa |
| Observed MW | 17 kDa/45 kDa |
| Cellular Localization | Secreted |
| Concentration | 1 mg/mL |
| Buffer | Phosphate buffered solution, pH 7.4, containing 0.05% stabilizer and 50% glycerol. |
| Purification Method | Affinity purification |
| Research Areas | Cancer, Cardiovascular, Metabolism, Developmental Biology, Signal Transduction |
| Conjugation | Unconjugated |
| Storage | Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles. |
| Shipping | The product is shipped with ice pack,upon receipt,store it immediately at the temperature recommended. |
Related Reagents
| Applications | Recommended Dilution |
| WB | 1:500-1:2000 |
| IF | 1:50-1:200 |
Background
This gene is a member of the PDGF/VEGF growth factor family. It encodes a heparin-binding protein, which exists as a disulfide-linked homodimer. This growth factor induces proliferation and migration of vascular endothelial cells, and is essential for both physiological and pathological angiogenesis. Disruption of this gene in mice resulted in abnormal embryonic blood vessel formation. This gene is upregulated in many known tumors and its expression is correlated with tumor stage and progression. Elevated levels of this protein are found in patients with POEMS syndrome, also known as Crow-Fukase syndrome. Allelic variants of this gene have been associated with microvascular complications of diabetes 1 (MVCD1) and atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been described. There is also evidence for alternative translation initiation from upstream non-AUG (CUG) codons resulting in additional isoforms. A recent study showed that a C-terminally extended isoform is produced by use of an alternative in-frame translation termination codon via a stop codon readthrough mechanism, and that this isoform is antiangiogenic. Expression of some isoforms derived from the AUG start codon is regulated by a small upstream open reading frame, which is located within an internal ribosome entry site.