Human Neuropilin-1 ELISA Kit

Product details

The Human Neuropilin-1 Enzyme-Linked Immunosorbent Assay (ELISA) kit (ab213813) is designed for the quantitative detection of Human Neuropilin-1 in cell culture supernatants, cell lysates, tissue homogenates, serum and plasma (heparin, EDTA).

The ELISA kit is based on standard sandwich enzyme-linked immunosorbent assay technology. A polyconal antibody from goat specific for Neuropilin-1 has been pre-coated onto 96-well plates. Standards (Expression system for standard: NSO; Immunogen sequence: F22-K644) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for Neuropilin-1 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 Neuropilin-1 amount of sample captured in plate.

NRP1 (Neuropilin 1) also known as NP1, NRP, BDCA4 or VEGF165R, is a membrane-bound co-receptor to a tyrosine kinase receptor for both vascular endothelial growth factor (VEGF) and semaphorin family members. NRP1 plays versatile roles in angiogenesis, axon guidance, cell survival, migration and invasion. By somatic cell hybrid analysis, the NRP1 gene was mapped to chromosome 10. NRP1 bounds PGF1 with lower affinity. NRP1-mediated interactions are a necessary element in the initiation of the primary immune response and offer another example, like that of agrin, of a molecule shared by neurologic and immunologic synapses. After T-cell contact with DC, T-cell NRP1 colocalized with CD3 in the immunologic synapse and, sometimes, also at the opposite pole of the T cell. Soluble NRP1 interacts in a homophilic fashion with NRP1 on both DC and T cells, and this binding can be inhibited by blocking antibodies to NRP1. Furthermore, selective NRP1 inhibition in this model suppressed neovascular formation substantially.