FGFR2 ligand binding and activation

Stable Identifier
Homo sapiens
Locations in the PathwayBrowser
SVG |   | PPTX  | SBGN
Click the image above or here to open this pathway in the Pathway Browser
Dominant mutations in the fibroblast growth factor receptor 2 (FGFR2) gene have been identified as causes of four phenotypically distinct craniosynostosis syndromes, including Crouzon, Jackson- Weiss, Pfeiffer, and Apert syndromes. FGFR2 binds a number of different FGFs preferentially, as illustrated in this pathway.

FGFR is probably activated by NCAM very differently from the way by which it is activated by FGFs, reflecting the different conditions for NCAM-FGFR and FGF-FGFR interactions. The affinity of FGF for FGFR is approximately 10e6 times higher than that of NCAM for FGFR. Moreover, in the brain NCAM is constantly present on the cell surface at a much higher (micromolar) concentration than FGFs, which only appear transiently in the extracellular environment in the nanomolar range.
Literature References
PubMed ID Title Journal Year
16597617 Receptor specificity of the fibroblast growth factor family. The complete mammalian FGF family.

Ornitz, DM, Umemori, H, Mohammadi, M, Olsen, SK, Ibrahimi, OA, Zhang, X

J Biol Chem 2006
17133345 Differential signal transduction of alternatively spliced FGFR2 variants expressed in human mammary epithelial cells

Ethier, SP, Moffa, AB

J Cell Physiol 2007
16844695 Intracellular retention, degradation, and signaling of glycosylation-deficient FGFR2 and craniosynostosis syndrome-associated FGFR2C278F

Hatch, NE, Hudson, M, Cunningham, ML, Seto, ML, Bothwell, M

J Biol Chem 2006
Event Information
Orthologous Events
Cite Us!