Human VEGF ELISA Kit

Detection Principle:

This kit uses double antibody sandwich enzyme-linked immunosorbent assay technology. The specific anti human vegfantibody was pre coated on a high affinity enzyme plate. Standards, samples to be tested and biotinylated detection antibodies are added into the wells of enzyme plate. After incubation, the vegfpresent in the samples combines with solid-phase antibodies and detection antibodies to form immune complexes. After washing to remove unbound material, horseradish peroxidase labeled streptavidin (streptavidin HRP) was added. After washing, the chromogenic substrate was added to avoid light for color development. Stop the reaction by adding stop solution, and determine the absorbance value at 450 nmwavelength (reference correction wavelength 540nmor 570nm).

Detection Type: Double antibody sandwich method

Form: pre coated 96orifice plate

Detection Sample Type: cell supernatant, serum, Plasma

Loading Amount: 100ul

Kit Components:

Pre coated 96well plates, standards, vegfdetection antibody, dilution buffer, chromogenic solution (a, b)One copy of washing solution, termination solution, sa-hrp, plate sealing membrane and instructions

Sensitivity: 7.8pg/ml

Detection Range: 31.2 - 2000 pg/ml

Recovery Range: 113-135%

Storage Method: 2-8℃

Standard Curve

Background:

Vascular endothelial growth factor (VEGF or VEGF-A), also known as vascular permeability factor, is A potent regulator of neovascularization and angiogenesis in fetuses and adults. Vascular endothelial growth factor (VEGF) belongs to the PDGF family of proteins, which is characterized by the presence of eight conserved cystine residues in the structure of cystine knots and dimers bound by antiparallel disulfide bonds. After selective cutting and length of the sequence of amino acids, the human expression of different subtypes, including: VEGF121, VEGF145, VEGF165, VEGF183, VEGF189 and VEGF206 and so on. The VEGF165 is a form of expression quantity highest, followed by VEGF121 and VEGF189. "With the exception of VEGF121, all isoforms contain the basic heparin-binding domain and do not diffuse freely." Human VEGF165 and mice and rats corresponding protein amino acid sequence homology of 88%. VEGF is expressed in various cells and tissues, including skeletal muscle cells and cardiomyocytes, hepatocytes, osteoblasts, neutrophils, macrophages, keratinocytes, brown adipocytes, CD34+ stem cells, endothelial cells, fibroblasts, vascular smooth muscle cells, and so on. VEGF expression is induced by hypoxia and cytokines including IL-1, IL-6, IL-8, ONcostatin M and tumor necrosis factor-alpha. And so on. The amount of VEGF expression also varies during development and in adults.

"The dimer of VEGF binds to two related tyrosine kinase receptors, VEGF R1 (also called Flt-1) and VEGF R2 (Flk-1/KDR)." VEGF can also induce homodimer and autophosphorylation of the latter. These receptors possess seven extracellular immunoglobulin domains and a separate intracellular tyrosine receptor domain. Vascular endothelial cells and some other non-endothelial cells express VEGF receptors. Although the highest affinity of VEGF and VEGF R1, but VEGF R2 is regulation of VEGF angiogenic factor. VEGF165 is combined with the arm board (semaporin) receptor protein, neurofilament protein 1 (neuropilin 1), thus promote complex formation with VEGF R2.

VEGF is famous for its participation in angiogenesis. In the process of embryonic development, VEGF regulation of endothelial cell proliferation, migration and survival, and thus control the density of blood vessels, volume; But it does not play a role in the pattern of blood vessel formation. VEGF promotes bone formation through the recruitment of osteoblasts and chondrocytes, and it is also a monocyte chemotactic factor. In the postpartum period, VEGF maintains the integrity of vascular endothelial cells and is a potent mitogen for large/small vascular endothelial cells. In the adult, VEGF mainly in wound repair and female reproductive cycle play a role. VEGF promotes vascular permeability in disease tissues. Therefore, VEGF by extravasation and transfer process of tumor angiogenesis in the tumor. Various therapeutic strategies aimed at blocking VEGF activity are being used to control VEGF-induced tumor angiogenesis. The level of circulating VEGF is associated with the severity of autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus.