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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 ArticleDOI

Control of neuronal ion channel function by glycogen synthase kinase-3: new prospective for an old kinase

TL;DR: This new emerging role of GSK-3 in controling the activity of voltage-gated Na+, K+, Ca2+ channels and ligand-gator glutamate receptors is revised with the goal of highlighting new relevant endpoints of the neuronal G SK-3 cascade that could provide a platform for a better understanding of the mechanisms underlying the dysfunction of this kinase in the CNS and serve as a guidance for medication development against the broad range of Gsk-3-linked human diseases.
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Redundant and dosage sensitive requirements for Fgf3 and Fgf10 in cardiovascular development.

TL;DR: It is reported that Fgf3 and FgF10, which are expressed dynamically in and near these cardiovascular progenitors, have redundant and dosage sensitive requirements in multiple aspects of early murine cardiovascular development.
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FGFR2-Cbl interaction in lipid rafts triggers attenuation of PI3K/Akt signaling and osteoblast survival.

TL;DR: A role for phosphatidylinositol 3-kinase (PI3K) signaling in cell apoptosis induced by FGFR2 activation in osteoblasts is identified and a novel role for PI3K/Akt attenuation in the control of osteoblast survival byFGFR2 signaling is revealed.
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Overexpression of FGF9 in colon cancer cells is mediated by hypoxia-induced translational activation

TL;DR: FGF9 IRES functions as a cellular switch to turn FGF9 protein synthesis ‘on’ during hypoxia, a likely mechanism underlying F GF9 overexpression in cancer cells, and evidence is provided to show that Hypoxia-induced translational activation promotes FGF 9 protein expression in colon cancer cells.
Journal ArticleDOI

ERK-Mediated Phosphorylation of Fibroblast Growth Factor Receptor 1 on Ser777 Inhibits Signaling

TL;DR: The data suggest that an ERK-dependent mechanism initiated by activation ofFGFR1 or other growth factor receptors prevents excessive FGFR1 signaling, and a negative feedback mechanism that controls FGF signaling and thereby protects the cell from excessive activation of FGFR is revealed.
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