FGF Receptor 2 (D4L2V) Rabbit mAb (Alexa Fluor® 488 Conjugate) #37374
- F
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Flow Cytometry (Live) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
FGF Receptor 2 (D4L2V) Rabbit mAb (Alexa Fluor® 488 Conjugate) recognizes endogenous levels of total FGFR2 protein and does not cross-react with FGFR1 or FGFR4.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of human FGFR2 protein.
Background
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).
- Powers, C.J. et al. (2000) Endocr Relat Cancer 7, 165-97.
- Reilly, J.F. et al. (2000) J Biol Chem 275, 7771-8.
- Mohammadi, M. et al. (1996) Mol Cell Biol 16, 977-89.
- Mohammadi, M. et al. (1991) Mol Cell Biol 11, 5068-78.
- Larsson, H. et al. (1999) J Biol Chem 274, 25726-34.
- Muh, S.J. et al. (2002) J Biol Chem 277, 50143-54.
- Coutts, J.C. and Gallagher, J.T. (1995) Immunol Cell Biol 73, 584-9.
- Jeftha, A. et al. (2004) J Clin Pediatr Dent 28, 173-6.
- Wilkinson, C.C. et al. (2012) Childs Nerv Syst 28, 1221-6.
- Slavotinek, A. et al. (2009) Am J Med Genet A 149A, 1814-7.
- Katoh, M. (2009) J Invest Dermatol 129, 1861-7.
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