Cell Signaling Technology

Product Pathways - Tyrosine Kinase/ Adaptors

FGF Receptor 2 Antibody #3116

Applications Reactivity MW (kDa) Source
W H (M) (R) 145 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

FGF Receptor 2 Antibody detects endogenous levels of total FGF receptor 2 protein. It does not cross-react with other FGF receptor family members.

Source / Purification

Polyclonal antibodies are produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to the sequence around Pro38 of human FGF receptor 2. Antibodies are purified by protein A and peptide affinity chrmatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using FGF Receptor 2 Antibody.

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: FGFR-1 (flg), FGFR-2 (bek, KGFR), FGFR-3 and FGFR-4. 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 FGFR-1 can be phosphorylated: Tyr463, Tyr583, Tyr585, Tyr653, Tyr654, Tyr730 and Tyr766. Tyrosines 653 and 654 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).

FGFR-2 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). Mutations in the corresponding FGFR-2 gene cause syndromes characterized by facial and limb defects, including LADD Syndrome, Crouzon Syndrome, Beare-Stevenson Cutis Grata Syndrome, Pfieffer Syndrome, Apert Syndrome and Jackson-Weiss Syndrome. Mutations and altered expression of FGFR-2 may also be seen in cases of gastric, endometrial and breast cancer (8).

  1. Powers, C.J. et al. (2000) Endocr Relat Cancer 7, 165-97.
  2. Reilly, J.F. et al. (2000) J Biol Chem 275, 7771-8.
  3. Mohammadi, M. et al. (1996) Mol Cell Biol 16, 977-89.
  4. Mohammadi, M. et al. (1991) Mol Cell Biol 11, 5068-78.
  5. Larsson, H. et al. (1999) J Biol Chem 274, 25726-34.
  6. Muh, S.J. et al. (2002) J Biol Chem 277, 50143-54.
  7. Coutts, J.C. and Gallagher, J.T. (1995) Immunol Cell Biol 73, 584-9.
  8. Eswarakumar, V.P. et al. (2005) Cytokine Growth Factor Rev 16, 139-49.

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