Description
This Human Junctional Adhesion Molecule C ELISA Kit is intended for quantitative detection of human JAM-C in cell culture supernates, serum and plasma (heparin, EDTA). Strip well format. Reagents for up to 96 tests.
This human JAM-C ELISA Kit was based on standard sandwich enzyme-linked immune-sorbent assay technology. A monoclonal antibody from mouse specific for JAM-C has been precoated onto 96-well plates. Standards (Expression system for standard: NSO, Immunogen sequence: V32-N241) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for JAM-C is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex was added and unbound conjugates were washed away with PBS or TBS buffer. HRP substrate TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the human Fibronectin amount of sample captured in plate.
The capture antibody is a monoclonal antibody from mouse, the detection antibody is a biotinylated detection polyclonal antibody from goat. Expression system for standard: This gene is mapped to 11q25. Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. The protein encoded by this immunoglobulin superfamily gene member is localized in the tight junctions between high endothelial cells. Unlike other proteins in this family, the this protein is unable to adhere to leukocyte cell lines and only forms weak homotypic interactions. The encoded protein is a member of the junctional adhesion molecule protein family and acts as a receptor for another member of this family. A mutation in an intron of this gene is associated with hemorrhagic destruction of the brain, subependymal calcification, and congenital cataracts. Alternative splicing results in multiple transcript variants