VEGFA Polyclonal Antibody
Price:
- 宿主： Rabbit
- 反应性： Human;Mouse;Rat
- 应用性： WB;IF
| Verified Samples |
Verified Samples in WB: HeLa, Mouse testis, Mouse brain, Rat brain Verified Samples in IF: HUVEC |
| Dilution | WB 1:500-1:2000, IF 1:50-1:200 |
| Clonality | Polyclonal |
| Isotype | IgG |
| Immunogen | A synthetic peptide of human VEGFA (NP_001165094). |
| Abbre | VEGFA |
| Synonyms | L VEGFA, MVCD1, VEGF, VEGF A, VEGFA, VPF |
| Swissprot | |
| Calculated MW | 15-27 kDa/34-45 kDa |
| Observed MW | 16 kDa/35 kDa |
| Cellular Localization | Secreted. VEGF121 is acidic and freely secreted. VEGF165 is more basic, has heparin-binding properties and, although a signicant proportion remains cell-associated, most is freely secreted. VEGF189 is very basic, it is cell-associated after secretion and is bound avidly by heparin and the extracellular matrix, although it may be released as a soluble form by heparin, heparinase or plasmin. |
| Concentration | 1 mg/mL |
| Storage | Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles. |
| Buffer | PBS with 0.02% sodium azide, 50% glycerol, pH 7.3. |
| Purification Method | Affinity purification |
| Research Areas | Cancer, Cardiovascular, Metabolism, Developmental Biology, Signal Transduction |
| Conjugation | Unconjugated |
| 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. |
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