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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

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Citations
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Journal ArticleDOI

Tumor angiogenesis: causes, consequences, challenges and opportunities.

TL;DR: The current understanding of cellular and molecular mechanisms involved in tumor angiogenesis is summarized and challenges and opportunities associated with vascular targeting are discussed.
Journal ArticleDOI

Fibroblast growth factor signaling in skeletal development and disease

TL;DR: Progress made on understanding the functions of the FGF signaling pathway during critical stages of skeletogenesis is examined, and the mechanisms by which mutations in FGF signalling molecules cause skeletal malformations in humans are explored.
Journal ArticleDOI

The molecular basis of endothelial cell plasticity

TL;DR: The endothelium is capable of remarkable plasticity in the embryo and in the adult, maintenance of differentiated endothelial state is an active process requiring constant signalling input that leads to the development of endothelial-to-mesenchymal transition that plays an important role in pathogenesis of a number of diseases.
References
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Journal Article

Analysis of phenotypic features and FGFR2 mutations in Apert syndrome

TL;DR: In all but one patient, an FGFR2 mutation, either S252W or P253R, was found in exon IIIa (exon U or 7), which is likely to have similar biological, and therefore phenotypic, consequences in Apert syndrome.
Journal ArticleDOI

A secreted FGF-binding protein can serve as the angiogenic switch in human cancer.

TL;DR: Investigating whether the expression in tumors of a secreted fibroblast growth factor-binding protein (FGF-BP) that mobilizes and activates locally stored FGFs can serve as an angiogenic switch molecule found that the reduction of FGF- BP reduced the release of biologically active basic FGF (bFGF) from cells in culture.

Required, tissue-specific roles for Fgf8 in outflow tract formation and remodeling

TL;DR: Conditional mutagenesis provides a novel insight into how the formation and remodeling of primary and anterior heart field-derived structures rely on Fgf8 signals from discrete temporospatial domains.
Journal ArticleDOI

MicroRNA-140-5p suppresses tumor growth and metastasis by targeting transforming growth factor β receptor 1 and fibroblast growth factor 9 in hepatocellular carcinoma†‡

TL;DR: A tumor suppressor role for miR‐140‐5p in HCC development and progression with therapeutic potential is elucidated and correlation studies in clinical HCC samples further suggest that miR-140-5p could be a valuable biomarker for HCC prognosis.
Journal ArticleDOI

FGF4 is required for lineage restriction and salt-and-pepper distribution of primitive endoderm factors but not their initial expression in the mouse

TL;DR: The phenotype resulting from zygotic and maternal/zygotic inactivation of Fgf4 heterozygous blastocysts is investigated and it is proposed that heterogeneities in the availability of FGF produce the salt-and-pepper distribution of lineage-biased cells.
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