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FGF7 — SDC2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: FGF7 → Complex of FGF7-SDC2 (directlyIncreases)
  Evidence: In general, free heparin/HSPGs sequester FGFs in the extracellular environment and act as FGF antagonists. On the contrary, cellassociated HSPGs can directly activate a signal transduction pathway in response to FGF2 [124], promote FGF2 internalization [125,126], and are required for a correct presentation of FGFs to FGFRs, leading to the formation of productive HSPGs/FGF/FGFR ternary complexes [121].

Text-mined interactions from Literome

Bodo et al., Eur J Cell Biol 1999 (Craniofacial Dysostosis) : A regulatory role of fibroblast growth factor in the expression of decorin, biglycan, betaglycan and syndecan in osteoblasts from patients with Crouzon 's syndrome
The et al., Mol Cell 1999 : In contrast to mutants in other HSPG biosynthesis genes, the activity of the HSPG dependent FGF and Wingless signaling pathways are not affected in ttv mutants
Olwin et al., J Cell Biol 1992 : These results suggest that activation of FGF receptors by acidic, basic or Kaposi 's sarcoma FGF requires simultaneous binding to a HSPG and the tyrosine kinase receptor
Quarto et al., J Cell Sci 1994 : It is noteworthy that HSPG binding protects FGF-2 from denaturation and proteolytic degradation, provides a matrix bound or cell-surface reservoir of this factor for the cells and is required for the activation of FGF high-affinity receptors
Coutts et al., Immunol Cell Biol 1995 : The recent discovery of the involvement of heparan sulfate proteoglycans (HSPG) in the activation of fibroblast growth factor receptors ( FGFR ) has led to an intensification of study of this field
Hartmann et al., Curr Biol 1998 : Although a number of growth factors bind cell-surface heparan sulphate proteoglycans ( HSPGs ), the role of this interaction is unclear except for fibroblast growth factor which requires HSPG binding for signalling