- Catalogue N°
- 855.930.000 - 200µg / 200µl
855.930.005 - 500µg / 500µl
- Target species
- Recognises both natural and recombinant human VEGF165
- Myeloma X63/AG.8653 x Balb/c node cells
- Recombinant human VEGF165
- 200µg or 500µg (Discovery Size also available please enquire)
- Mouse IgG2a Kappa light chain
- Phosphate-buffered saline. Sterile-filtered through 0.22 µm. Carrier and preservative free
- Stable at +2-8°C for 12 months. For longer storage freeze aliquots.
VEGF-A (Vascular Endothelial Growth Factor A) is a dimeric glycoprotein considered to be the main inducer of human blood vessels. It belongs to the VEGF family of related growth factors, along with VEGF-B, -C, -D (also known as FlGF) and PLGF (Placental Growth Factor). VEGF-A plays a crucial role in vasculogenesis, the process by which blood vessels are generated and angiogenesis, the expansion of an existing vascular bed by sprouting of new blood vessels as it acts as a highly specific mitogen for endothelial cells. Angiogenesis typically occurs as a response to a stimulus such as tissue hypoxia or other stress and results in improved perfusion and increased oxygen delivery. Angiogenis is essential during pregnancy and in tissue growth and repair and is also a key underlying process in the pathogenesis of several major human diseases including cancer.
The human VEGF gene (located on chromosome 6) consists of several exons that can be alternatively spliced to encode several protein isoforms, including: VEGF121, VEGF145, VEGF162, VEGF165, VEGF183, VEGF189, and VEGF206. The primary receptor tyrosine kinases (RTKs) for VEGF isoforms are VEGFR1 (Flt-1), VEGFR2 (Flk-1 or KDR), and VEGFR3 (Flt-4). VEGFR2 is the primary receptor responsible for endothelial cell mitogenic and migratory responses to VEGF, while VEGFR1 is thought to function primarily as a decoy receptor during development, and to modulate signaling of VEGFR2 in the adult.
The identification of different isoforms has raised the possibility of more detailed prognostic profiling and follow-up of cancer patients. The development of new agents capable of modifying the function of VEGF has led to the use of novel treatments in both malignant and nonmalignant diseases. VEGF-blocking therapy appears very promising in the treatment of cancer, since it is directed only against migrating and proliferating capillary endothelial cells at a site of angiogenesis. Combination therapy seems more effective, because both the endothelial cell and tumor cell compartments of a tumor are targeted and blocking angiogenesis may decrease the interstitial pressure in tumors, leading to a greater penetration of the cytotoxic drugs.
Version 5 - 06.19
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