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1
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0029999082
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Characteristics and regulation of Pi transport in osteogenic cells for bone metabolism
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Caverzasio J, Bonjour JP. Characteristics and regulation of Pi transport in osteogenic cells for bone metabolism. Kidney Int 1996; 49:975-980.
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(1996)
Kidney Int
, vol.49
, pp. 975-980
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Caverzasio, J.1
Bonjour, J.P.2
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2
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0029656129
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Insulin-like growth factor I in the kidney
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Hirschberg R. Insulin-like growth factor I in the kidney. Miner Electrolyte Metab 1996; 22:128-132.
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(1996)
Miner Electrolyte Metab
, vol.22
, pp. 128-132
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Hirschberg, R.1
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3
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33646529865
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White KE, Larsson TM, Econs MJ. The roles of specific genes implicated as circulating factors involved in normal and disordered phosphate homeostasis: frizzled related protein-4, matrix extracellular phosphoglycoprotein, and fibroblast growth factor 23. Endocr Rev 2006; 27:221-241. An excellent and extensive review on phosphatonins and their effect on phosphate homeostasis.
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White KE, Larsson TM, Econs MJ. The roles of specific genes implicated as circulating factors involved in normal and disordered phosphate homeostasis: frizzled related protein-4, matrix extracellular phosphoglycoprotein, and fibroblast growth factor 23. Endocr Rev 2006; 27:221-241. An excellent and extensive review on phosphatonins and their effect on phosphate homeostasis.
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4
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33947111420
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Phosphate transport: Molecular basis, regulation and pathophysiology
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An interesting review focusing on renal phosphate transport and phosphate wasting disorders
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Tenenhouse HS. Phosphate transport: molecular basis, regulation and pathophysiology. J Steroid Biochem Mol Biol 2007; 103:572-577. An interesting review focusing on renal phosphate transport and phosphate wasting disorders.
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(2007)
J Steroid Biochem Mol Biol
, vol.103
, pp. 572-577
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Tenenhouse, H.S.1
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5
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33947192418
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1,25-Dihydroxyvitamin D(3)/VDR-mediated induction of FGF23 as well as transcriptional control of other bone anabolic and catabolic genes that orchestrate the regulation of phosphate and calcium mineral metabolism
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Barthel TK, Mathern DR, Whitfield GK, et al. 1,25-Dihydroxyvitamin D(3)/VDR-mediated induction of FGF23 as well as transcriptional control of other bone anabolic and catabolic genes that orchestrate the regulation of phosphate and calcium mineral metabolism. J Steroid Biochem Mol Biol 2007; 103:381-388.
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(2007)
J Steroid Biochem Mol Biol
, vol.103
, pp. 381-388
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Barthel, T.K.1
Mathern, D.R.2
Whitfield, G.K.3
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6
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33947132702
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The phosphatonins and the regulation of phosphate transport and vitamin D metabolism
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Sommer S, Berndt T, Craig T, Kumar R. The phosphatonins and the regulation of phosphate transport and vitamin D metabolism. J Steroid Biochem Mol Biol 2007; 103:497-503.
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(2007)
J Steroid Biochem Mol Biol
, vol.103
, pp. 497-503
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Sommer, S.1
Berndt, T.2
Craig, T.3
Kumar, R.4
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7
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33947385485
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Phosphorylated acidic serine-aspartate-rich MEPE-associated motif peptide from matrix extracellular phosphoglycoprotein inhibits phosphate regulating gene with homologies to endopeptidases on the X-chromosome enzyme activity
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Liu S, Rowe PS, Vierthaler L, et al. Phosphorylated acidic serine-aspartate-rich MEPE-associated motif peptide from matrix extracellular phosphoglycoprotein inhibits phosphate regulating gene with homologies to endopeptidases on the X-chromosome enzyme activity. J Endocrinol 2007; 192:261-267.
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(2007)
J Endocrinol
, vol.192
, pp. 261-267
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Liu, S.1
Rowe, P.S.2
Vierthaler, L.3
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8
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34247545717
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Sitara D, Razzaque MS, St-Arnaud R, et al. Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23-null animals. Am J Pathol 2006; 169:2161-2170. This interesting study provides strong evidence that the 1-hydroxyvitamin D metabolite mediates the hyperphosphatemia, the increased bone mineralization and the ectopic calcifications found in the absence of Fgf23 production.
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Sitara D, Razzaque MS, St-Arnaud R, et al. Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23-null animals. Am J Pathol 2006; 169:2161-2170. This interesting study provides strong evidence that the 1-hydroxyvitamin D metabolite mediates the hyperphosphatemia, the increased bone mineralization and the ectopic calcifications found in the absence of Fgf23 production.
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9
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33846566785
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•] work, the invalidation of a vitamin D gene prevents ectopic calcification and abnormal phosphorus and calcium metabolism. In addition, invalidation of the fgf23 gene may increase the animal responses to subcutaneous glucose tolerance tests and insulin secretion, changes that also require an intact vitamin D signaling pathway.
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•] work, the invalidation of a vitamin D gene prevents ectopic calcification and abnormal phosphorus and calcium metabolism. In addition, invalidation of the fgf23 gene may increase the animal responses to subcutaneous glucose tolerance tests and insulin secretion, changes that also require an intact vitamin D signaling pathway.
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10
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33846528466
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Hyperostosis-hyperphosphatemia syndrome: A congenital disorder of O-glycosylation associated with augmented processing of fibroblast growth factor 23
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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; 22:235-242.
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(2007)
J Bone Miner Res
, vol.22
, pp. 235-242
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Frishberg, Y.1
Ito, N.2
Rinat, C.3
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11
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34249855902
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Novel GALNT3 mutations causing hyperostosis-hyperphosphatemia syndrome result in low intact FGF23 concentrations
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Ichikawa S, Guigonis V, Imel EA, et al. Novel GALNT3 mutations causing hyperostosis-hyperphosphatemia syndrome result in low intact FGF23 concentrations. J Clin Endocrinol Metab 2007; 92:1943-1947.
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(2007)
J Clin Endocrinol Metab
, vol.92
, pp. 1943-1947
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Ichikawa, S.1
Guigonis, V.2
Imel, E.A.3
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12
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33845296928
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Vitamin D receptor in chondrocytes promotes osteoclastogenesis and regulates FGF23 production in osteoblasts
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This work gives convincing evidence that local expression of the vitamin D receptor in the growth-plate cartilage mediates local events that enhance bone formation and regulate FGF23 production in osteoblasts, thus controlling phosphate homeostasis
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Masuyama R, Stockmans I, Torrekens S, et al. Vitamin D receptor in chondrocytes promotes osteoclastogenesis and regulates FGF23 production in osteoblasts. J Clin Invest 2006; 116:3150-3159. This work gives convincing evidence that local expression of the vitamin D receptor in the growth-plate cartilage mediates local events that enhance bone formation and regulate FGF23 production in osteoblasts, thus controlling phosphate homeostasis.
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(2006)
J Clin Invest
, vol.116
, pp. 3150-3159
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Masuyama, R.1
Stockmans, I.2
Torrekens, S.3
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14
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0037179681
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Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mutations in the type 2a sodium-phosphate cotransporter
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Prie D, Huart V, Bakouh N, et al. Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mutations in the type 2a sodium-phosphate cotransporter. N Engl J Med 2002; 347:983-991.
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(2002)
N Engl J Med
, vol.347
, pp. 983-991
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Prie, D.1
Huart, V.2
Bakouh, N.3
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15
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31544481921
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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; 78:179-192. The reports by Bergwitz et al. and Lorenz-Depiereux et al. provide the first implication of the sodium-phosphate cotransporter NaPiIIc as an essential regulator of renal phosphate reabsorption and as the cause of hypophosphatemic rickets with hypercalciuria.
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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; 78:179-192. The reports by Bergwitz et al. and Lorenz-Depiereux et al. provide the first implication of the sodium-phosphate cotransporter NaPiIIc as an essential regulator of renal phosphate reabsorption and as the cause of hypophosphatemic rickets with hypercalciuria.
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16
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31544460435
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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. The reports by Bergwitz et al. and Lorenz-Depiereux et al. provide the first implication of the sodium-phosphate cotransporter NaPiIIc as an essential regulator of renal phosphate reabsorption and as the cause of hypophosphatemic rickets with hypercalciuria.
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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. The reports by Bergwitz et al. and Lorenz-Depiereux et al. provide the first implication of the sodium-phosphate cotransporter NaPiIIc as an essential regulator of renal phosphate reabsorption and as the cause of hypophosphatemic rickets with hypercalciuria.
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17
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33750427897
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Lorenz-Depiereux B, Bastepe M, Benet-Pages A, et al. DMP1 mutations in autosomal recessive hypophosphatemia implicate a bone matrix protein in the regulation of phosphate homeostasis. Nat Genet 2006; 38:1248-1250. This report shows the first homozygous mutation in the gene encoding Dmp1 in three multiplex families with hypophosphatemic rickets. Parents were heterozygous for the mutations and nonaffected. Of interest, affected patients had elevated intact parathyroid hormone, even in the absence of phosphate substitution.
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Lorenz-Depiereux B, Bastepe M, Benet-Pages A, et al. DMP1 mutations in autosomal recessive hypophosphatemia implicate a bone matrix protein in the regulation of phosphate homeostasis. Nat Genet 2006; 38:1248-1250. This report shows the first homozygous mutation in the gene encoding Dmp1 in three multiplex families with hypophosphatemic rickets. Parents were heterozygous for the mutations and nonaffected. Of interest, affected patients had elevated intact parathyroid hormone, even in the absence of phosphate substitution.
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18
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32544458785
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Somatic and germline mosaicism for a mutation of the PHEX gene can lead to genetic transmission of X-linked hypophosphatemic rickets that mimics an autosomal dominant trait
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Goji K, Ozaki K, Sadewa AH, et al. Somatic and germline mosaicism for a mutation of the PHEX gene can lead to genetic transmission of X-linked hypophosphatemic rickets that mimics an autosomal dominant trait. J Clin Endocrinol Metab 2006; 91:365-370.
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(2006)
J Clin Endocrinol Metab
, vol.91
, pp. 365-370
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Goji, K.1
Ozaki, K.2
Sadewa, A.H.3
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19
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1542511325
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Tumor-induced rickets: Usefulness of MR gradient echo recall imaging for tumor localization
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Shulman DI, Hahn G, Benator R, et al. Tumor-induced rickets: usefulness of MR gradient echo recall imaging for tumor localization. J Pediatr 2004; 144:381-385.
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(2004)
J Pediatr
, vol.144
, pp. 381-385
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Shulman, D.I.1
Hahn, G.2
Benator, R.3
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20
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33845964211
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Oncogenic osteomalacia: Exact tumor localization by co-registration of positron emission and computed tomography
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Hesse E, Moessinger E, Rosenthal H, et al. Oncogenic osteomalacia: exact tumor localization by co-registration of positron emission and computed tomography. J Bone Miner Res 2007; 22:158-162.
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(2007)
J Bone Miner Res
, vol.22
, pp. 158-162
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Hesse, E.1
Moessinger, E.2
Rosenthal, H.3
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21
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33746406756
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Burnett SA, Gunawardene SC, Bringhurst FR, et al. Regulation of C-terminal and intact FGF-23 by dietary phosphate in men and women. J Bone Miner Res 2006; 21:1187-1196. This study in healthy adults shows a 50% increase in circulating fgf23 within 1-3 days following an increase in phosphate intake from 900 mg to 2.5 g/day, as well as a 25% decrease after phosphate depletion. It also confirms that the choice of the fgf23 assay is critical, the assay detecting only the intact fgf23 peptide giving the best results.
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Burnett SA, Gunawardene SC, Bringhurst FR, et al. Regulation of C-terminal and intact FGF-23 by dietary phosphate in men and women. J Bone Miner Res 2006; 21:1187-1196. This study in healthy adults shows a 50% increase in circulating fgf23 within 1-3 days following an increase in phosphate intake from 900 mg to 2.5 g/day, as well as a 25% decrease after phosphate depletion. It also confirms that the choice of the fgf23 assay is critical, the assay detecting only the intact fgf23 peptide giving the best results.
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