The Fibroblast Growth Factor signaling pathway
David M. Ornitz,Nobuyuki Itoh +1 more
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, Incread more
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Anti-Cancer Effect of Cordycepin on FGF9-Induced Testicular Tumorigenesis
Ming Min Chang,Siou Ying Hong,Shang Hsun Yang,Chia Ching Wu,Chia Yih Wang,Bu Miin Huang,Bu Miin Huang +6 more
TL;DR: Cordycepin inhibited FGF9-induced testicular tumor growth by suppressing the ERK1/2, Rb/E2F1, cell cycle pathways, and the expressions of FGFR1-4 proteins, suggesting that cordyce pin can be used as a novel anticancer drug for testicular cancers.
Journal ArticleDOI
FGFR2-activating mutations disrupt cell polarity to potentiate migration and invasion in endometrial cancer cell models
Samantha J. Stehbens,Samantha J. Stehbens,Robert J. Ju,Robert J. Ju,Mark N. Adams,Samuel R. Perry,Nikolas K. Haass,David M. Bryant,Pamela M. Pollock +8 more
TL;DR: These findings uncover collective cell polarity and invasion as common targets of disease-associated FGFR2 mutations that lead to poor outcome in endometrial cancer patients.
Journal ArticleDOI
FGF23 signalling and physiology.
Bryan B. Ho,Clemens Bergwitz +1 more
TL;DR: Non-canonical FGF23 signalling through binding and activation of FGFR3/FGFR4/calcineurin/NFAT in an alpha-KLOTHO-independent fashion mainly occurs at extremely elevated circulating F GF23 levels and may contribute to mortality due to cardiovascular disease and left ventricular hypertrophy in chronic kidney disease.
Journal ArticleDOI
Distinct mechanisms for PDGF and FGF signaling in primitive endoderm development.
Andrei Molotkov,Philippe Soriano +1 more
TL;DR: Results suggest a model where FGFR1-engaged ERK1/2 signaling governs PrE specification while PDGFRα- and by analogy possibly FGFR2- engaged PI3K signaling regulates PrE survival and positioning in the embryo and indicate how multiple growth factors and signaling pathways can cooperate in preimplantation development.
Journal ArticleDOI
Fgf9 Negatively Regulates Bone Mass by Inhibiting Osteogenesis and Promoting Osteoclastogenesis Via MAPK and PI3K/AKT Signaling.
Lingyun Tang,Min Wu,Shunyuan Lu,Hong-Xin Zhang,Yan Shen,Chunling Shen,Hui Liang,Haoyang Ge,Xiaoyi Ding,Zhugang Wang +9 more
TL;DR: It is demonstrated that Fgf9 is a negative regulator of bone homeostasis by regulating osteogenesis and osteoclastogenesis and provides a potential therapeutic target for bone degenerative diseases.
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