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Open AccessJournal ArticleDOI

Fibroblast growth factors, their receptors and signaling.

Ciaran Powers, +2 more
- 01 Sep 2000 - 
- Vol. 7, Iss: 3, pp 165-197
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TLDR
FGF signaling also appears to play a role in tumor growth and angiogenesis, and autocrine FGF signaling may be particularly important in the progression of steroid hormone-dependent cancers to a hormone-independent state.
Abstract
Fibroblast growth factors (FGFs) are small polypeptide growth factors, all of whom share in common certain structural characteristics, and most of whom bind heparin avidly. Many FGFs contain signal peptides for secretion and are secreted into the extracellular environment, where theycan bind to the heparan-like glycosaminoglycans (HLGAGs) of the extracellular matrix (ECM). From this reservoir, FGFs mayact directlyon target cells, or theycan be released through digestion of the ECM or the activityof a carrier protein, a secreted FGF binding protein. FGFs bind specific receptor tyrosine kinases in the context of HLGAGs and this binding induces receptor dimerization and activation, ultimatelyresulting in the activation of various signal transduction cascades. Some FGFs are potent angiogenic factors and most playimportant roles in embry onic development and wound healing. FGF signaling also appears to playa role in tumor growth and angiogenesis, and autocrine FGF signaling maybe particularlyimportant in the progression of steroid hormone-dependent cancers to a hormone-independent state.

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Suppressors of cytokine signaling (SOCS) 1 and SOCS3 interact with and modulate fibroblast growth factor receptor signaling

TL;DR: It is shown that activation of FGFR in chondrocytes induces the expression of SOCS1 and SOCS3 mRNA, and that these proteins are constitutively associated with FGFR3, as demonstrated by co-immunoprecipitation studies.
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Tricyclic antidepressant amitriptyline activates fibroblast growth factor receptor signaling in glial cells: involvement in glial cell line-derived neurotrophic factor production.

TL;DR: The current data show that amitriptyline-induced FGFR activation might occur by the MMP-dependent shedding of FGFR ligands, such as FGF-2, thus resulting in GDNF production, and suggest thatAmitriptYline- induced FGFRactivation might occur through an extracellular pathway, in contrast to that of 5-HT.
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Synthetic peptide F2A4-K-NS mimics fibroblast growth factor-2 in vitro and is angiogenic in vivo.

TL;DR: The hypothesis that F2A4-K-NS is a mimetic of F GF-2 that can substitute for FGF-2 in vitro and in vivo is supported.
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Anti-Acne Agents Attenuate FGFR2 Signal Transduction in Acne

TL;DR: The hypothesis that known anti-acne agents may operate by downregulation of increased FGFR2 signaling is elucidated to help clarify the role of FG FR2 signaling in the pathogenesis of acne.
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Activation of FGFR1beta signaling pathway promotes survival, migration and resistance to chemotherapy in acute myeloid leukemia cells.

TL;DR: It is shown that FGF-2, through activation of FGFR1β signaling, promotes survival, proliferation and migration of AML cells, andFGFR1 targeting may be of therapeutic benefit in subsets ofAML.
References
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Journal ArticleDOI

Cell surface, heparin-like molecules are required for binding of basic fibroblast growth factor to its high affinity receptor.

TL;DR: It is demonstrated that free heparin and heparan sulfate can reconstitute a low affinity receptor that is, in turn, required for the high affinity binding of bFGF.
Journal ArticleDOI

Protein modules and signalling networks

TL;DR: This work highlights conserved protein domains that act as key regulatory participants in many of these different signalling pathways in multicellular organisms.
Journal ArticleDOI

Thalidomide is an inhibitor of angiogenesis.

TL;DR: Electron microscopic examination of the corneal neovascularization of thalidomide-treated rabbits revealed specific ultrastructural changes similar to those seen in the deformed limb bud vasculature of Thalidomid-treated embryos.
Journal ArticleDOI

Receptor specificity of the fibroblast growth factor family.

TL;DR: It is demonstrated that FGF 1 is the only FGF that can activate all FGF receptor splice variants and the relative activity of all the other members of the FGF family is determined.
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