VEGF-A (Isoform 164) Mouse Protein
Specifications
| Product Data | |
| Species | Mouse |
|---|---|
| Expression Host | Insect |
| Predicted MW | 48 kDa |
| Purity | >95% > 95%, by SDS-PAGE and visualised by silver stain. |
| Presentation State | Purified |
| Buffer | Presentation State: Purified State: Lyophilized without stabilizer. |
| Bioactivity | Biological: The ED50 for stimulation of 3H-thymidine incorporation and cell proliferation by human umbilical vein endothelial cells for VEGF164 has been determined to be in the range of 1-2 ng/ml. Specific: 1 x 10e6 units/mg |
| Endotoxin | < 0.1 ng/µg of VEGF |
| Reconstitution Method | Restore in PBS or medium containing at least 0.1% human or bovine serum albumin to a concentration not lower than 50 µg/ml. |
| Preparation | Lyophilized without stabilizer. |
| Protein Description | Recombinant Murine VEGF164 is produced as a homodimer consisting of 164 amino acid residues. |
| Storage | Store VEGF164 Lyophilized at -20°C to -70°C. Reconstituted VEGF164 should be stored in working aliquots at -20°C. Avoid repeated freeze-thaw cycles! |
| Stability | Shelf life: One year from despatch. |
| Shipping | Ambient |
| Reference Data | |
| RefSeq | NP_001020421 |
| Locus ID | 22339 |
| UniProt ID | Q00731 |
| Cytogenetics | 17 22.79 cM |
| Synonyms | VEGFA, VEGF, VPF, Vascular endothelial growth factor A, Vascular permeability factor |
| Summary | 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. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. 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.provided by RefSeq, Nov 2015 |
| Protein Categories | Cytokines, Endocrine and metabolic diseases, Growth Factors, Intracellular Proteins, Membrane Proteins, Nervous system Diseases, Secreated Proteins |
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