◀ Back to FGF23

FGF23 — FGF3

Pathways - manually collected, often from reviews:

• Reactome Reaction: FGF3 → FGF23 (reaction) Carpenter et al., Exp Cell Res 1999, Wong et al., Proc Natl Acad Sci U S A 2002, Lax et al., Mol Cell 2002, Fong et al., J Biol Chem 2003, Agazie et al., Oncogene 2003, Takeda et al., Clin Cancer Res 2007, Ahmed et al., Biochem J 2008, Schüller et al., Biochem J 2008, Qing et al., J Clin Invest 2009, Turner et al., Nat Rev Cancer 2010, Bai et al., Cancer Res 2010, Dutt et al., PloS one 2011, Wesche et al., Biochem J 2011, Klint et al., J Biol Chem 1995, Wang et al., Mol Cell Biol 1994, Ong et al., Biochem Biophys Res Commun 1996, Kanai et al., J Biol Chem 1997, Kouhara et al., Cell 1997, Ong et al., Biochem Biophys Res Commun 1997, Hadari et al., Mol Cell Biol 1998, Raffioni et al., J Biol Chem 1998

Text-mined interactions from Literome

Wilson et al., Curr Biol 2000 : Fgf3 was also found to be expressed in the early epiblast, and ongoing FGF signalling in epiblast cells was required for acquisition of neural fate and for the suppression of Bmp4 and Bmp7 expression
Shimada et al., American journal of physiology. Renal physiology 2005 : Taken together, FGF23 works, at least in part, in a VDR independent manner, and FGF23 production is also regulated by multiple mechanisms involving VDR independent pathways
Torres et al., Kidney Int 2007 : Klotho can act as a circulating factor or hormone, which binds to a not yet identified high-affinity receptor and inhibits the intracellular insulin/insulin-like growth factor-1 (IGF-1) signaling cascade ; klotho can function as a novel beta-glucuronidase, which deglycosylates steroid beta-glucuronides and the calcium channel transient receptor potential vallinoid-5 ( TRPV5 ) ; as a cofactor essential for the stimulation of fibroblast growth factor ( FGF ) receptor by FGF23
Liu et al., Mol Endocrinol 2009 (Disease Models, Animal) : Moreover, activation of Fgf and Wnt signaling stimulated Fgf23 promoter activity in osteoblasts
Liu et al., Am J Physiol Heart Circ Physiol 2009 (Hypertrophy, Left Ventricular...) : To assess whether FGF-23 influences the function and structure of the CVS and whether the effect of FGF-23 on the CVS is mediated by FGF receptors directly or indirectly by hypophosphatemia, FGF-23 transgenic mice and their wild-type littermates were fed a normal diet or a high-phosphate diet comprising a normal diet plus 1.25 % phosphate in drinking water from weaning for 5 wk, and the phenotypes of the CVS were compared between FGF-23 transgenic mice and their wild-type littermates on the same diet
Yamamoto et al., J Endocrinol 2010 : Parathyroid hormone, stanniocalcin 1, prostaglandin E ( 2 ), FGF2 , and foscarnet did not increase FGF23 mRNA expression
Isakova et al., Nephrol Dial Transplant 2011 (Kidney Failure, Chronic) : Despite the significant reductions in 24-h urinary phosphate excretion, no group demonstrated a significant reduction in FGF23 levels ; FGF23 levels actually increased significantly in the 1500-mg diet plus placebo group, suggesting dietary phosphorus loading
Pearson et al., Development 2011 : We show that collar cells are composed of Fgf3 ( + ) SOX3 ( + ) proliferating progenitors, the induction of which is SHH dependent, but the maintenance of which requires FGF signalling
Bergwitz et al., Adv Exp Med Biol 2012 (Abnormalities, Multiple...) : FGF23 acts through FGF-receptors and the coreceptor Klotho to reduce 1,25 ( OH ) ( 2 ) D synthesis in the kidney and probably the synthesis of parathyroid hormone (PTH) by the parathyroid glands
Razzaque et al., Adv Exp Med Biol 2012 (Kidney Diseases) : Vitamin D can induce the expression of both FGF23 and klotho while, FGF23 can suppress renal expression of 1a ( OH ) ase to reduce 1,25 ( OH ) ( 2 ) D activity
Bhattacharyya et al., Trends Endocrinol Metab 2012 (Iron Metabolism Disorders...) : In physiologic states, FGF23 signaling is mediated by an FGF receptor and the coreceptor, Klotho
Vendrell et al., Mech Dev 2013 (Wnt Signaling Pathway) : Interestingly however, Wnt8a and Fgf3 are redundantly required for expression of Fgf15 in the hindbrain indicating additional reciprocal interactions between Fgf and Wnt signalling