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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

Clinical findings in a patient with FGFR1 P252R mutation and comparison with the literature.

TL;DR: Molecular analysis of the fibroblast growth factor receptor 1 gene identified a heterozygous P252R missense mutation, previously only reported with FGFR1-Pfeiffer syndrome like manifestations, which is a further example of the phenomenon of an activated FGFR molecule resulting in overlapping manifestations in FGFR syndromes.
Book

FGF Signalling in Vertebrate Development

TL;DR: The focus of the present review is to look at the fundamental components of the FGF pathway and illustrate how this highly conserved regulatory cassette has been deployed to regulate multiple, diverse processes during vertebrate development.
Journal ArticleDOI

Fgf15 is required for proper morphogenesis of the mouse cardiac outflow tract

TL;DR: The phenotype of mice lacking fibroblast growth factor 15 (Fgf 15), which encodes a secreted signaling molecule expressed within the developing pharyngeal arches, is described and a novel role of Fgf15 during development of the cardiac outflow tract is revealed.
Journal ArticleDOI

Expression of keratinocyte growth factor/fibroblast growth factor-7 and its receptor in human lung cancer: correlation with tumour proliferative activity and patient prognosis.

TL;DR: It is indicated that co‐expression of KGF KGFR correlates significantly with poor prognosis in adenocarcinoma, but not in squamous cell carcinoma, of the lung, particularly in relation to cancer cell kinetics and prognosis.
Journal ArticleDOI

A novel homozygous mutation in FGFR3 causes tall stature, severe lateral tibial deviation, scoliosis, hearing impairment, camptodactyly, and arachnodactyly.

TL;DR: This is the first report of a homozygous loss‐of‐function mutation in FGFR3 in human that results in a skeletal overgrowth syndrome.
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