Genetic evidence of serum phosphate-independent functions of FGF-23 on bone - Wikidata - wikimedia - TriplyDB

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

http://www.wikidata.org/entity/Q28473286

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Effects of PTH on osteocyte function FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player?Nuclear receptors in bone physiology and diseases Regulation and function of the FGF23/klotho endocrine pathways Fibroblast Growth Factor 23: A New Dimension to Diseases of Calcium-Phosphorus Metabolism Deletion of PTH rescues skeletal abnormalities and high osteopontin levels in Klotho-/- mice Functional diversity of fibroblast growth factors in bone formation MEPE is a novel regulator of growth plate cartilage mineralization In vivo genetic evidence for suppressing vascular and soft-tissue calcification through the reduction of serum phosphate levels, even in the presence of high serum calcium and 1,25-dihydroxyvitamin d levels Constitutive nuclear expression of dentin matrix protein 1 fails to rescue the Dmp1-null phenotype.Dietary and genetic evidence for phosphate toxicity accelerating mammalian aging.Altered bone development and an increase in FGF-23 expression in Enpp1(-/-) mice.Fibroblast growth factor-23 and parathyroid hormone are associated with post-transplant bone mineral density loss.A Phe377del mutation in ANK leads to impaired osteoblastogenesis and osteoclastogenesis in a mouse model for craniometaphyseal dysplasia (CMD)Molecular regulation of phosphate metabolism by fibroblast growth factor-23-klotho system Reversal of mineral ion homeostasis and soft-tissue calcification of klotho knockout mice by deletion of vitamin D 1alpha-hydroxylase FGF-23/Klotho signaling is not essential for the phosphaturic and anabolic functions of PTH.Parathyroid hormone receptor signaling in osteocytes increases the expression of fibroblast growth factor-23 in vitro and in vivo Familial tumoral calcinosis: from characterization of a rare phenotype to the pathogenesis of ectopic calcification PTH ablation ameliorates the anomalies of Fgf23-deficient mice by suppressing the elevated vitamin D and calcium levels.FGF23 in skeletal modeling and remodeling.Phosphate Binding with Sevelamer Preserves Mechanical Competence of Bone Despite Acidosis in Advanced Experimental Renal Insufficiency.Targeted deletion of Klotho in kidney distal tubule disrupts mineral metabolism.Fibroblast-growth factor 23 promotes terminal differentiation of ATDC5 cells.Entpd5 is essential for skeletal mineralization and regulates phosphate homeostasis in zebrafish.Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23.Fibroblast growth factor 23 and bone mineralisation.1,25-Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression.Endocrine functions of bone in mineral metabolism regulation.Glucocorticoids and osteocyte autophagy.Regression of vascular calcification in chronic kidney disease - feasible or fantasy? a review of the clinical evidence.Effect of chronic kidney disease on the healing of titanium implants Novel regulators of Fgf23 expression and mineralization in Hyp bone Influence of estrogen therapy on calcium, phosphorus, and other regulatory hormones in postmenopausal women: the MESA study.Inactivation of klotho function induces hyperphosphatemia even in presence of high serum fibroblast growth factor 23 levels in a genetically engineered hypophosphatemic (Hyp) mouse model.Seven novel and six de novo PHEX gene mutations in patients with hypophosphatemic rickets.Do osteocytes contribute to phosphate homeostasis?Disorders of phosphate homeostasis and tissue mineralisation.FGF23 and syndromes of abnormal renal phosphate handling Increased osteopontin contributes to inhibition of bone mineralization in FGF23-deficient mice.

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P2860

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

http://www.wikidata.org/entity/Q28473286

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2008 nî lūn-bûn

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2008 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2008 թվականի օգոստոսին հրատարակված գիտական հոդված

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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name

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

@ast

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

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Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

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type

label

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

@ast

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

@en

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

@nl

prefLabel

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

@ast

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

@en

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

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JOURNAL.PGEN.1000154

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Genetic evidence of serum phosphate-independent functions of FGF-23 on bone

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Beate Lanske

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Christiane Schüler

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Clemens Bergwitz

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Mohammed S Razzaque

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Reinhold G Erben

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Somi Kim

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Takashi Taguchi

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P2860

The parathyroid hormone (PTH)/PTH-related peptide receptor mediates actions of both ligands in murine bone

Growth-related renal type II Na/Pi cotransporter

Overexpression of fibroblast growth factor 23 suppresses osteoblast differentiation and matrix mineralization in vitro

FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis

Molecular insights into the klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members

FGF23, PHEX, and MEPE regulation of phosphate homeostasis and skeletal mineralization

Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice

Characterization of a murine type II sodium-phosphate cotransporter expressed in mammalian small intestine

Type II Na+-Pi cotransporters in osteoblast mineral formation: regulation by inorganic phosphate

Targeted inactivation of Npt2 in mice leads to severe renal phosphate wasting, hypercalciuria, and skeletal abnormalities

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