scispace - formally typeset
Open AccessJournal ArticleDOI

The Fibroblast Growth Factor signaling pathway

TLDR
Members of the FGF family function in the earliest stages of embryonic development and during organogenesis to maintain progenitor cells and mediate their growth, differentiation, survival, and patterning.
Abstract
The signaling component of the mammalian Fibroblast Growth Factor (FGF) family is comprised of eighteen secreted proteins that interact with four signaling tyrosine kinase FGF receptors (FGFRs) Interaction of FGF ligands with their signaling receptors is regulated by protein or proteoglycan cofactors and by extracellular binding proteins Activated FGFRs phosphorylate specific tyrosine residues that mediate interaction with cytosolic adaptor proteins and the RAS-MAPK, PI3K-AKT, PLCγ, and STAT intracellular signaling pathways Four structurally related intracellular non-signaling FGFs interact with and regulate the family of voltage gated sodium channels Members of the FGF family function in the earliest stages of embryonic development and during organogenesis to maintain progenitor cells and mediate their growth, differentiation, survival, and patterning FGFs also have roles in adult tissues where they mediate metabolic functions, tissue repair, and regeneration, often by reactivating developmental signaling pathways Consistent with the presence of FGFs in almost all tissues and organs, aberrant activity of the pathway is associated with developmental defects that disrupt organogenesis, impair the response to injury, and result in metabolic disorders, and cancer © 2015 Wiley Periodicals, Inc

read more

Citations
More filters
Journal ArticleDOI

Effect of FGF/FGFR pathway blocking on lung adenocarcinoma and its cancer-associated fibroblasts

TL;DR: Evidence is provided that fibroblasts associated with the Fgf9‐induced lung adenocarcinoma provide multiple means of support to the tumour and the need for a combinatorial strategy to treat lung cancer is supported.
Journal ArticleDOI

FGF23, Biomarker or Target?

TL;DR: The hypothesis that FGF23 could be considered a therapeutic target is gaining relevance and may become a promising field of investigation in the future because of its role in the complex network between the bones and other organs.
Journal ArticleDOI

Genome-wide copy number variation pattern analysis and a classification signature for non-small cell lung cancer.

TL;DR: The genome‐wide pattern differences in copy number variations (CNVs) are analyzed and a CNV signature is developed as an adjunct test for the routine histopathologic classification of NSCLCs to offer the possibility of identifying the origin of tumors whose origin is unknown.
Journal ArticleDOI

FGF23 beyond Phosphotropic Hormone.

TL;DR: The recent reports concerning the actions of FGF23 on various tissues are reviewed and the remaining questions about FGF 23 are discussed.
References
More filters
Journal ArticleDOI

AKT/PKB signaling: navigating downstream.

TL;DR: Those Akt substrates that are most likely to contribute to the diverse cellular roles of Akt, which include cell survival, growth, proliferation, angiogenesis, metabolism, and migration are discussed.
Journal ArticleDOI

The Wnt signaling pathway in development and disease.

TL;DR: The data reveal that multiple extracellular, cytoplasmic, and nuclear regulators intricately modulate Wnt signaling levels, and that receptor-ligand specificity and feedback loops help to determine WNT signaling outputs.
Journal ArticleDOI

Mutation of the mouse klotho gene leads to a syndrome resembling ageing

TL;DR: A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes in the mouse, and may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.

Mutation of the mouse klotho gene leads to a syndrome resembling ageing

TL;DR: A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes in the mouse, including short lifespan, infertility, arteriosclerosis, skin atrophy, osteoporosis and emphysema as mentioned in this paper.
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.
Related Papers (5)