Post-translational modification of fibroblast growth factor 23

Therapeutic Apheresis and Dialysis

Volumn 9, Issue 4, 2005, Pages 319-322

  Fukumoto, Seiji ^a  

^a UNIVERSITY OF TOKYO HOSPITAL   (Japan)

Author keywords

Fibroblast growth factor 23; Hypophosphatemia; Inhibitor; Modification; O glycosylation; Osteomalacia; Rickets

Indexed keywords

AMINO ACID; ARGININE; COMPLEMENTARY DNA; FIBROBLAST GROWTH FACTOR 23; FURIN; PHOSPHATE; SERINE; SUBTILISIN;

ARTICLE; NONHUMAN; OSTEOMALACIA; PHOSPHATE BLOOD LEVEL; PRIORITY JOURNAL; PROTEIN GLYCOSYLATION; PROTEIN PROCESSING; SIGNAL TRANSDUCTION; VITAMIN D RESISTANT RICKETS;

EID: 29144434668     PISSN: 17449979     EISSN: 17449987     Source Type: Journal    
DOI: 10.1111/j.1744-9987.2005.00289.x     Document Type: Article

References (21)

1. Brown EM, Gamba G, Riccardi D et al. Cloning and characterization of an extracellular Ca(2+)-sensing receptor from bovine parathyroid. Nature 1993;366:575-80.
2. The ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet 2000;26:345-8.
3. Shimada T, Mizutani S, Muto T et al. Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proc Natl Acad Sci USA 2001;98:6500-5.
4. Yamazaki Y, Okazaki R, Shibata M et al. Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia. J Clin Endocrinol Metab 2002;87:4957-60.
5. Jonsson KB, Zahradnik R, Larsson T et al. Fibroblast growth factor 23 in oncogenic osteomalacia and X-linked hypophosphatemia. N Engl J Med 2003;348:1656-63.
6. Shimada T, Kakitani M, Yamazaki Y et al. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF-23 in phosphate and vitamin D metabolism. J Clin Invest 2004;113:561-8.
7. The HYP Consortium. A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. Nat Genet 1995;11:130-6.
8. Morgan JM, Hawley WL, Chenoweth AI, Retan WJ, Diethelm AG. Renal transplantation in hypophosphatemia with vitamin D-resistant rickets. Arch Intern Med 1974; 134:549-52.
9. Beck L, Soumounou Y, Martel J et al. Pex/PEX tissue distribution and evidence for a deletion in the 3′ region of the Pex gene in X-linked hypophosphatemic mice. J Clin Invest 1997;99:1200-9.
10. Nesbitt T, Coffman TM, Griffiths R, Drezner MK. Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect. J Clin Invest 1992;89:1453-9.
11. Kumar R. Phosphatonin - a new phosphaturetic hormone? (lessons from tumour-induced osteomalacia and X-linked hypophosphataemia). Nephrol Dial Transplant 1997;12:11-13.
12. Bowe AE, Finnegan R, Jan de Beur SM et al. FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate. Biochem Biophys Res Commun 2001;284:977-81.
13. Guo R, Liu S, Spurney RF, Quarles LD. Analysis of recombinant Phex: an endopeptidase in search of a substrate. Am J Physiol Endocrinol Metab 2001;281:E837-47.
14. Liu S, Guo R, Simpson LG, Xian ZS, Burnham CE, Quarles LD. Regulation of FGF23 expression but not degradation by phex. J Biol Chem 2003;278:37419-26.
15. Benet-Pages A, Lorenz-Depiereux B, Zischka H, White KE, Econs MJ, Strom TM. FGF23 is processed by proprotein convertases but not by PHEX. Bone 2004;35:455-62.
16. Shimada T, Muto T, Urakawa I et al. Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Endocrinology 2001;143:3179-82.
17. White KE, Carn G, Lorenz-Depiereux B, Benet-Pages A, Strom TM, Econs MG. Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23. Kidney Int 2001;60:2079-86.
18. Lyles KW, Halsey DL, Friedman NE, Lobaugh B. Correlations of serum concentrations of 1,25-dihydroxyvitmain D, phosphorus, and parathyroid hormone in tumoral calcinosis. J Cin Endocrinol Metab 1988;67:88-92.
19. Topaz O, Shurman DL, Bergman R et al. Mutations in GALNT3, encoding a protein involved in O-linked glycosylation, cause familial tumoral calcinosis. Nat Genet 2004;36:579-81.
20. Jaeken J, Carchon H. Congenital disorders of glycosylation: a booming chapter of pediatrics. Curr Opin Pediatr 2004;16:434-9.
21. Benet-Pages A, Orlik P, Strom TM, Lorenz-Depiereux B. An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia. Hum Mol Genet 2005;14:385-90.