The rapid protocol (RP) PathScan^® RP Total FGF Receptor 2 Sandwich ELISA Kit is a solid phase sandwich enzyme-linked immunosorbent assay (ELISA) that detects endogenous levels of FGF Receptor 2 protein in a reduced assay time of 1.5 hours. Incubation of cell lysates and detection antibody on the coated microwell plate forms a sandwich with FGF Receptor 2 in a single step. The plate is then extensively washed and TMB reagent is added for signal development. The magnitude of absorbance for the developed color is proportional to the quantity of FGF Receptor 2 protein. Learn more about your ELISA kit options here.

*Antibodies in this kit are custom formulations specific to kit.

The PathScan^® RP Total FGF Receptor 2 Sandwich ELISA Kit detects endogenous levels of FGF Receptor 2 protein. The kit sensitivity is shown in Figure 1. This kit detects proteins from the indicated species, as determined through in-house testing, but may also detect homologous proteins from other species.

Fibroblast growth factors (FGFs) produce mitogenic and angiogenic effects in target cells by signaling through cell surface receptor tyrosine kinases. There are four members of the FGF receptor family: FGFR1 (flg), FGFR2 (bek, KGFR), FGFR3, and FGFR4. Each receptor contains an extracellular ligand-binding domain, a transmembrane domain, and a cytoplasmic kinase domain (1). Following ligand binding and dimerization, the receptors are phosphorylated at specific tyrosine residues (2). Seven tyrosine residues in the cytoplasmic tail of FGFR1 can be phosphorylated: Tyr463, 583, 585, 653, 654, 730, and 766. Tyr653 and Tyr654 are important for catalytic activity of activated FGFR and are essential for signaling (3). The other phosphorylated tyrosine residues may provide docking sites for downstream signaling components, such as Crk and PLCγ (4,5).

FGFR2 has several splicing isoforms, with ligand specificity largely determined by alternative splicing of exons 8 (IIIb) and 9 (IIIc). Alternative splicing is cell type specific, resulting in isoforms showing various tissue distribution and biological activities (6,7). Research studies have shown that mutations in the corresponding FGFR2 gene cause syndromes characterized by facial and limb defects, including LADD Syndrome, Crouzon Syndrome, Beare-Stevenson Cutis Gyrata Syndrome, Pfeiffer Syndrome, Apert Syndrome, and Jackson-Weiss Syndrome (8-10). Investigators have also observed mutations and altered expression of FGFR2 in cases of gastric, endometrial, and breast cancer (11).