Immunohistochemistry (formalin fixed paraffin embedded, rodent tissues only): use at a concentration of 5 - 10μg / ml for 30 min at RT. Staining of formalin fixed tissues requires boiling tissue sections in 10mM Tris-HCl, pH 10.0, for 10 - 20 min followed by cooling at RT for 20 min.Neutralising (Int J Oncology, 8:505-511): assay dependent. Optimal dilutions / concentrations should be determined by the end user. Staining of formalin fixed tissues requires boiling tissue sections in 10mM Tris-HCl, pH 10.0, for 10 - 20 min followed by cooling at RT for 20 min.
Store as concentrated solution. Centrifuge briefly prior to opening vial. Store at 4ºC. DO NOT FREEZE.
Concentration
0.2 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
Human recombinant VEGF 165.
Purification
Protein A purified
Conjugation
Unconjugated
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
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. [provided by RefSeq, Nov 2015]
