◀ Back to FGF2
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