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http://purl.uniprot.org/citations/15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15579309http://www.w3.org/2000/01/rdf-schema#comment"Fibroblast growth factor-23 (FGF-23), a recently identified molecule that is mutated in patients with autosomal dominant hypophosphatemic rickets (ADHR), appears to be involved in the regulation of phosphate homeostasis. Although increased levels of circulating FGF-23 were detected in patients with different phosphate-wasting disorders such as oncogenic osteomalacia (OOM) and X-linked hypophosphatemia (XLH), it is not yet clear whether FGF-23 is directly responsible for the abnormal regulation of mineral ion homeostasis and consequently bone development. To address some of these unresolved questions, we generated a mouse model, in which the entire Fgf-23 gene was replaced with the lacZ gene. Fgf-23 null (Fgf-23-/-) mice showed signs of growth retardation by day 17, developed severe hyperphosphatemia with elevated serum 1,25(OH)2D3 levels, and died by 13 weeks of age. Hyperphosphatemia in Fgf-23-/-mice was accompanied by skeletal abnormalities, as demonstrated by histological, molecular, and various other morphometric analyses. Fgf-23-/-) mice had increased total-body bone mineral content (BMC) but decreased bone mineral density (BMD) of the limbs. Overall, Fgf-23-/-mice exhibited increased mineralization, but also accumulation of unmineralized osteoid leading to marked limb deformities. Moreover, Fgf-23-/-mice showed excessive mineralization in soft tissues, including heart and kidney. To further expand our understanding regarding the role of Fgf-23 in phosphate homeostasis and skeletal mineralization, we crossed Fgf-23-/-animals with Hyp mice, the murine equivalent of XLH. Interestingly, Hyp males lacking both Fgf-23 alleles were indistinguishable from Fgf-23/-/ mice, both in terms of serum phosphate levels and skeletal changes, suggesting that Fgf-23 is upstream of the phosphate regulating gene with homologies to endopeptidases on the X chromosome (Phex) and that the increased plasma Fgf-23 levels in Hyp mice (and in XLH patients) may be at least partially responsible for the phosphate imbalance in this disorder."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.org/dc/terms/identifier"doi:10.1016/j.matbio.2004.09.007"xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Taguchi T."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Lanske B."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Razzaque M.S."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Juppner H."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Hesse M."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Yoganathan S."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Sitara D."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/author"Erben R.G."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/name"Matrix Biol"xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/pages"421-432"xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/title"Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice."xsd:string
http://purl.uniprot.org/citations/15579309http://purl.uniprot.org/core/volume"23"xsd:string
http://purl.uniprot.org/citations/15579309http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15579309
http://purl.uniprot.org/citations/15579309http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15579309
http://purl.uniprot.org/uniprot/Q9EPC2#attribution-5248EB4606E9B93C372CEE6A51122154http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/15579309
http://purl.uniprot.org/uniprot/#_D3Z116-mappedCitation-15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15579309
http://purl.uniprot.org/uniprot/#_P70669-mappedCitation-15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15579309
http://purl.uniprot.org/uniprot/#_Q0VBJ8-mappedCitation-15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15579309
http://purl.uniprot.org/uniprot/#_A2ICR0-mappedCitation-15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15579309
http://purl.uniprot.org/uniprot/#_A2AC80-mappedCitation-15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15579309
http://purl.uniprot.org/uniprot/#_D3Z4N2-mappedCitation-15579309http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15579309