◀ Back to FGF23

FGF19 — FGF23

Pathways - manually collected, often from reviews:

• Reactome Reaction: FGF19 → FGF23 (reaction) Carpenter et al., Exp Cell Res 1999, Hart et al., Mol Biol Cell 2001, Wong et al., Proc Natl Acad Sci U S A 2002, Lax et al., Mol Cell 2002, Fong et al., J Biol Chem 2003, Mohammadi et al., Nature 1992, Agazie et al., Oncogene 2003, Mohammadi et al., Mol Cell Biol 1991, Ahmed et al., Biochem J 2008, Schüller et al., Biochem J 2008, Klint et al., J Biol Chem 1995, Wang et al., Mol Cell Biol 1994, Mohammadi et al., Mol Cell Biol 1996, 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

Text-mined interactions from Literome

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
Kurosu et al., J Biol Chem 2007 : Accordingly, FGF19 , but not FGF21, activates FGF signaling in hepatocytes that primarily express FGFR4 and reduces transcription of CYP7A1 that encodes the rate limiting enzyme for bile acid synthesis
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
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