
IndraLab
Statements
sparser
"Syndecan-4 connects 2 important signaling pathways (proteoglycans in cancer and ECM–receptors interactions) and it has been reported that blocking interactions between syndecan-4 and fibronectin decreases focal adhesions in cells, leading to increased cell proliferation in tumors."
sparser
"Since tenascin-C competed with syndecan-4 binding to fibronectin, it is possible that syndecan-4 is exclusively available as a coreceptor for growth factor receptors in the presence of tenascin-C. In summary, in addition to its role in regulating the inflammatory response, there is strong evidence that tenascin-C may also play a direct role in the control of growth factor signaling that promotes ECM synthesis."
sparser
"Once again, cells were able to spread without PKCα engagement; however, for focal complexes to form, interaction of syndecan-4 with fibronectin to recruit PKCα-mediated Rac1 activation was required, as knock down or drug-mediated inhibition of this kinase failed to activate Rac1 and induce the maturation of focal complexes ( xref )."
reach
"Following Sdc4 binding to FN in the extracellular matrix, the Sdc4 cytoplasmic domain binds phosphatidylinositol 4,5-bisphosphate, which stimulates PKCalpha activation, leading to the activation of small GTPases and assembly of focal adhesions (Oh et al., 1997; Saoncella et al., 1999; Couchman, 2003; Lim et al., 2003; Dovas et al., 2006)."
sparser
"In tetrapods (amphibians, reptiles, birds and mammals) there are 4 tenascin genes:
tenascin-C, tenascin-R, tenascin-W and tenascin-X ( xref ). xref Tenascin-C is the original “tenascin” that was first described independently in
the myotendinous junctions and brains of the chicken Gallus gallus xref as well as in
human glioblastoma-derived cells. xref The
best studied of the tenascins, tenascin-C is expressed by motile cells such as the neural
crest, at sites of connective tissue differentiation and in the adult in numerous stem cell
niches; it also reappears during inflammation, at the margins of healing wounds and in the
stroma of solid tumors. xref Tenascin-C from G. gallus binds to
α9β1 integrins via the isoleucine-aspartic acid-glycine (IDG) motif found in the
B-C loop of its third FNIII domain xref and to αVβ3 integrins via an RGD motif in the F-G loop of the same FNIII
domain. xref Tenascin-C can also bind
to fibronectin and prevent syndecan-4-fibronectin interactions, which in turn influences
fibronectin signaling through integrins. xref Tenascin-C knockout mice have profound behavioral
abnormalities and other phenotypes that are primarily associated with aberrant stem cell
migration, proliferation and differentiation. xref Tenascin-R, the second tenascin to be discovered, is restricted
in its expression to the nervous system xref and tenascin-R knockout mice also display abnormal behavior. xref Tenascin-W is often co-expressed with
tenascin-C both in development and in stem cell niches. xref Murine tenascin-W has an RGD motif in the F-G loop of the second
FNIII domain that appears to act as an α8β1 integrin-binding site. xref It and the tenascin-W of other species
have the related lysine-glycine-aspartic acid (KGD) motif in the F-G loop of one or more
FNIII domains, and synthetic peptides that contain this motif and neighboring conserved
sequences promote cell proliferation. xref Tenascin-W knockout mice have not been analyzed."
sparser
"Following Sdc4 binding to FN in the extracellular matrix, the Sdc4 cytoplasmic domain binds phosphatidylinositol 4,5-bisphosphate, which stimulates PKCα activation, leading to the activation of small GTPases and assembly of focal adhesions (Oh et al., 1997; Saoncella et al., 1999; Couchman, 2003; Lim et al., 2003; Dovas et al., 2006)."
sparser
"The SDC4-α5β1 integrin mediated cell adhesion to fibronectin reduces tumor cell proliferation, whilst the tenascin-C-mediated inhibition of SDC4-fibronectin interaction and consequently the impaired fibronectin-induced signaling enhances the proliferation of glioblastoma cells [ xref ]."
sparser
"TN-C has been reported to compete with the binding site of fibronectin with syndecan-4, and this interaction with syndecan-4 partially abrogates the effects of this co-receptor, as well as attenuates the interaction of syndecan-4 with fibronectin, enhancing tumor cell malignancy."
reach
"Moreover, blocking of FN binding to Sdc4 with Tenascin-C (TEN) selectively impaired the ability of Wnt7a to stimulate the expansion of the Pax7 + / YFP - satellite stem cell pool on myofibers cultured for 42h (XREF_FIG) without any effect on Pax7 + / YFP + satellite myogenic cells (XREF_SUPPLEMENTARY)."
sparser
"Ruiz and colleagues [ xref ] and Lange and colleagues [ xref ] have associated triggering of glioma cell migration with a simultaneous mechanism of competitive inhibition of syndecan-4 binding of fibronectin and signalling by lysophosphatidic acid and platelet-derived growth factor (reviewed in [ xref ])."