1) Biber J, Hernando N, Foster I, et al. Regulation of phosphate transport in proximal tubules. Pflugers Arch. 2009; 458: 39-52
|
|
|
2) Custer M, Lötscher M, Biber J, et al. Expression of Na-P(i) cotransport in rat kidney: Localization by RT-PCR and immunohistochemistry. Am J Physiol. 1994; 265(5 Pt2): F767-74
|
|
|
3) Segawa H, Kaneko I, Takahashi A, et al. Growth-related renal type II Na/Pi cotransporter. J Biol Chem. 2002; 277: 19665-72
|
|
|
4) Tenenhouse HS, Martel J, Gauthier C, et al. Differential effects of Npt2a gene ablation and X-linked Hyp mutation on renal expression of Npt2c. Am J Physiol Renal Physiol. 2003; 285: F1271-8
|
|
|
5) Bergwitz C, Roslin NM, Tieder M, et al. SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis. Am J Hum Genet. 2006; 78: 179-92
|
|
|
6) Lorenz-Depiereux B, Benet-Pages A, Eckstein G, et al. Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. Am J Hum Genet. 2006; 78: 193-201
|
|
|
7) Villa-Bellosta R, Ravera S, Sorribas V, et al. The Na+-Pi cotransporter PiT-2 (SLC20A2) is expressed in the apical membrane of rat renal proximal tubules and regulated by dietary Pi. Am J Physiol Renal Physiol. 2009; 296: F691-9
|
|
|
8) The ADHR Consortium. Autosomal dominant hypophosphatemic rickets is associated with mutations in FGF23. Nat Genet. 2000; 26: 345-8
|
|
|
9) 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 U S A. 2001; 98: 6500-5
|
|
|
10) Endo I, Fukumoto S, Ozono K, et al. Clinical usefulness of measurement of fibroblast growth factor 23 (FGF23) in hypophosphatemic patients: proposal of diagnostic criteria using FGF23 measurement. Bone. 2008; 42: 1235-9
|
|
|
11) Feng JQ, Ward LM, Liu S, et al. Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. Nat Genet. 2006; 38: 1310-5
|
|
|
12) The HYP Consortium: A gene (PEX) with homologies to endopeptidases in mutated in patients with X-linked hypophosphatemic rickets. Nat Genet. 1995; 11: 130-6
|
|
|
13) Aono Y, Yamazaki Y, Yasutake J, et al. Therapeutic effects of anti-FGF23 antibodies in hypophosphatemic rickets/osteomalacia. J Bone Miner Res. 2009; May 6 [E-pub ahead of print]
|
|
|
14) Riminucci M, Collins MT, Fedarko NS, et al. FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting. J Clin Invest. 2003; 112: 689-92
|
|
|
15) Shimizu Y, Tada Y, Yamauchi M, et al. Hypophosphatemia induced by intravenous administration of saccharide ferric oxide. Another form of FGF23-related hypophosphatemia. Bone. 2009; Jun 23 [E-pub ahead of print]
|
|
|
16) Yamamoto T, Michigami T, Aranami F, et al. Hereditary hypophosphatemic rickets with hypercalciuria: a study for the phosphate transporter gene type IIc and osteoblast function. J Bone Miner Metab. 2007; 25: 407-13
|
|
|
17) 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
|
|
|
18) Larsson T, Yu X, Davis SI, et al. A novel recessive mutation in fibroblast growth factor-23 causes familial tumoral calcinosis. J Clin Endocrinol Metab. 2005; 90: 2424-7
|
|
|
19) Ichikawa S, Imel EA, Kreiter ML, et al. A homozygous mutation in human KLOTHO causes severe tumoral calcinosis. J Clin Invest. 2007; 117: 2684-91
|
|
|
20) Frishberg Y, Ito N, Rinat C, et al. Hyperostosis-hyperphosphatemia syndrome: a congenital disorder of O-glycosylation associated with augmented processing of fibroblast growth factor 23. J Bone Miner Res. 2007; 22: 235-42
|
|
|
21) Ichikawa S, Sorenson AH, Austin AM, et al. Ablartion of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression. Endocrinology. 2009; 150: 2543-50
|
|
|
22) Liu S, Zhou J, Tang W, et al. Pathogenic role of Ffg23 in Hyp mice. Am J Physiol Endocrinol Metab. 2006; 291: E38-49
|
|
|
23) Goetz R, Beenken A, Ibrahimi OA, et al. Molecular insights into the klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members. Mol Cell Biol. 2007; 27: 3417-28
|
|
|
24) Quarles LD. Endocrine functions of bone in mineral metabolism regulation. J Clin Invest. 2008; 118: 3820-8
|
|
|
25) Urakawa I, Yamazaki Y, Shimada T, et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature. 2006; 444: 770-4
|
|
|
26) Kurosu H, Ogawa Y, Miyoshi M, et al. Regulation of fibroblast growth factor-23 signaling by klotho. J Biol Chem. 2006; 281: 6120-3
|
|
|
27) Liu S, Vierthaler L, Tang W, et al. FGFR3 and FGFR4 do not mediate renal effects of FGF23. J Am Soc Nephrol. 2008; 19: 2342-50
|
|
|
28) Gattineni J, Bates C, Twombley K, et al. FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Renal Physiol. 2009; 297: F282-91
|
|
|
29) Kuro-o M, Matsumura Y, Aizawa H, et al. Mutation of the mouse klotho gene leads to a syndrome resembling aging. Nature. 1997; 390: 45-51
|
|
|
30) Imura A, Iwano A, Tohyama O, et al. Secreted Klotho protein in sera and CSF: implication for post-translational cleavage in release of Klotho protein from cell membrane. FEBS Lett. 2004; 565: 143-7
|
|
|
31) Farrow EG, Davis SI, Summers LJ, et al. Initial FGF23-mediated signaling occurs in the distal convoluted tubule. J Am Soc Nephrol. 2009; 20: 955-60
|
|
|
32) Brownstein CA, Adler F, Nelson-Williams C, et al. A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism. Proc Natl Acad Sci U S A. 2008; 105: 3455-60
|
|
|
33) Ben-Dov IZ, Galitzer H, Lavi-Moshavoff V, et al. The parathyroid is a target organ for FGF23 in rats. J Clin Invest. 2007: 117: 403-6
|
|
|
34) Imura A, Tsuji Y, Murata M, et al. Alpha-Klotho as a regulator of calcium homeostasis. Science. 2007; 316: 1615-8
|
|
|
35) Medici D, Razzaque MS, Deluca S, et al. FGF-23-Klotho signaling stimulates proliferation and prevents vitamin D-induced apoptosis. J Cell Biol. 2008; 182: 459-65
|
|
|
36) Sitara D, Kim S, Razzaque MS, et al. Genetic evidence of serum phosphate-independent functions of FGF-23 on bone. PLos Genet. 2008; 4: e1000154
|
|
|
37) Liu S, Tang W, Zhou J, et al. Fibroblast growth factor 23 is a counter-regulattory phosphaturic hormone for vitamin D. J Am Soc Nephrol. 2006; 17: 1305-15
|
|
|
38) Saji F, Shiizaki K, Shimada S, et al. Regulation of fibroblast growth factor 23 production in bone in uremic rats. Nephron Physiol. 2009; 111: 59-66
|
|
|
39) Weber TJ, Liu S, Indridason OS, et al. Serum FGF23 levels in normal and disordered phosphorus homeostasis. J Bone Miner Res. 2003; 18: 1227-34
|
|
|
40) Perwad F, Azam N, Zhang MY, et al. Dietary and serum phosphorus regulate fibroblast growth factor 23 expression and 1, 25-dihydroxyvitamin D metabolism in mice. Endocrinology. 2005; 146: 5358-64
|
|
|
41) Ferrari SL, Bonjour JP, Rizzoli R. Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. J Clin Endocrinol Metab. 2005; 90: 1519-24
|
|
|
42) Nishida Y, Taketani Y, Yamanaka-Okumura H, et al. Acute effect of oral phosphate loading on serum fibroblast growth factor 23 levels in healthy men. Kidney Int. 2006; 70: 2141-7
|
|
|