Gene interactions and pathways from curated databases and text-mining

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FGF2 — SDC2

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: FGF2 → Complex of FGF2-SDC2 (directlyDecreases)
    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].
  • OpenBEL Selventa BEL large corpus: FGF2 → Complex of FGF2-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].
  • Reactome Reaction: FGF2 → SDC2 (direct_complex) Steinfeld et al., J Cell Biol 1996*
  • Reactome Reaction: FGF2 → SDC2 (reaction) Steinfeld et al., J Cell Biol 1996*

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

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
Forsten et al., J Theor Biol 2000 : Fibroblast growth factor-2 (FGF-2) is one of the best characterized of the heparin binding growth factors and it has been shown experimentally that heparin regulation of FGF-2 activity is dependent on the level of cell HSPG and the concentration of heparin
Chabut et al., Mol Pharmacol 2003 : Basic fibroblast growth factor ( FGF-2 ) activates its high-affinity receptors ( FGFRs ) but also acts through interaction with heparan sulfate proteoglycans (HSPG)
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
Song et al., Dev Dyn 2004 : The spatiotemporal expression of syndecan-3 during feather development suggests that this cell-surface HSPG may be involved in the response of competent embryonic skin dermis to FGF-2
Velleman et al., Poult Sci 2007 : This result indicates that FGF2 responsiveness was not affected by the overexpression of syndecan-1, syndecan-4 , and glypican-1 during differentiation
Levenstein et al., Stem Cells 2008 : These HSPG and other heparinoids can stabilize basic fibroblast growth factor ( FGF2 ) in unconditioned medium at levels comparable to those observed in CM
Lee et al., J Biol Chem 2009 (Melanoma) : Syndecan-2 expression was enhanced by fibroblast growth factor-2 , which is known to stimulate melanoma cell migration ; however, alpha-melanocyte stimulating hormone decreased syndecan-2 expression and melanoma cell migration and invasion in a melanin synthesis independent manner
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
Aviezer et al., J Biol Chem 1994 : Moreover, most of these species of HS inhibited in a dose dependent manner the restoration of bFGF-receptor binding induced by heparin or by total HSPG
Fannon et al., J Biol Chem 1996 : Although the presence of HSPG on the cell surface increases the affinity of bFGF for its receptors, our observations suggest that HSPG are not `` absolutely '' required for binding, internalization, or stimulation of mitogenic activity
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
Bansal et al., Mol Cell Neurosci 1996 : The levels of mRNA expression were regulated by FGF-2 : in late progenitors, FGF-2 induced a doubling of the mRNA levels of syndecan-2, -3, and -4, while those for syndecan-1 and glypican remained unaffected ; in mature OLs, the levels of syndecan-1 mRNA were up-regulated, the levels of syndecan-2 and -4 and glypican were down-regulated
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
Lambrecht et al., Exp Cell Res 1998 (Breast Neoplasms) : Modification of HSPG induced by TGFbeta-1 or NaB treatments in normal and breast cancer epithelial cells resulted in an increase in 125I-fibroblast growth factor-2 (FGF-2) binding on HSPG