The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency - Wikidata - awgldk - TriplyDB

The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency

The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency

http://www.wikidata.org/entity/Q28202356

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Secreted frizzled-related protein 4 is a potent tumor-derived phosphaturic agent Viral infection and human disease--insights from minimotifs FGF23 and Phosphate Wasting Disorders Regulation and function of the FGF23/klotho endocrine pathways Calcium regulation and bone mineral metabolism in elderly patients with chronic kidney disease Fibroblast Growth Factor 23: A New Dimension to Diseases of Calcium-Phosphorus Metabolism Genetic disorders of phosphate regulation Protective roles of DMP1 in high phosphate homeostasis Fibroblast growth factor 23 impairs phosphorus and vitamin D metabolism in vivo and suppresses 25-hydroxyvitamin D-1alpha-hydroxylase expression in vitro Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice The parathyroid is a target organ for FGF23 in rats Amelogenesis imperfecta and other biomineralization defects in Fam20a and Fam20c null mice Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism Increased bone volume and correction of HYP mouse hypophosphatemia in the Klotho/HYP mouse.Analysis of Thisbe and Pyramus functional domains reveals evidence for cleavage of Drosophila FGFs Specific ablation of mouse Fam20C in cells expressing type I collagen leads to skeletal defects and hypophosphatemia.Fibroblast growth factor-23 increases mouse PGE2 production in vivo and in vitro.FGF23 induces left ventricular hypertrophy Analysis of the biochemical mechanisms for the endocrine actions of fibroblast growth factor-23 Decreased conversion of 25-hydroxyvitamin D3 to 24,25-dihydroxyvitamin D3 following cholecalciferol therapy in patients with CKD Relationship between Fibroblast Growth Factor-23 and Mineral Metabolism in Chronic Kidney Disease Mutational analysis of PHEX, FGF23 and DMP1 in a cohort of patients with hypophosphatemic rickets.Phosphate sensing.Vitamin D deficiency in chronic liver disease.FGF-23 regulates CYP27B1 transcription in the kidney and in extra-renal tissues.Regulation of phosphate transport by fibroblast growth factor 23 (FGF23): implications for disorders of phosphate metabolism.Fibroblast growth factor 23 regulates renal 1,25-dihydroxyvitamin D and phosphate metabolism via the MAP kinase signaling pathway in Hyp mice Approach to the hypophosphatemic patient The wrickkened pathways of FGF23, MEPE and PHEX.FGF-23 serum levels and bone histomorphometric results in adult patients with chronic kidney disease on dialysis 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 Correction of the mineralization defect in hyp mice treated with protease inhibitors CA074 and pepstatin Mineral (Mal)Adaptation to Kidney Disease--Young Investigator Award Address: American Society of Nephrology Kidney Week 2014 A clinical and molecular genetic study of hypophosphatemic rickets in children.Fibroblast growth factor 23 and its receptors.Structural and biochemical properties of fibroblast growth factor 23.Targeted deletion of Klotho in kidney distal tubule disrupts mineral metabolism."Phosphatonins" and the regulation of phosphorus homeostasis.Hexa-D-arginine treatment increases 7B2•PC2 activity in hyp-mouse osteoblasts and rescues the HYP phenotype.

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P2860

The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency

http://www.wikidata.org/entity/Q28202356

description

2003 nî lūn-bûn

@nan

2003 թուականի Մարտին հրատարակուած գիտական յօդուած

@hyw

2003 թվականի մարտին հրատարակված գիտական հոդված

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2003年の論文

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2003年論文

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2003年論文

@zh-hant

2003年論文

@zh-hk

2003年論文

@zh-mo

2003年論文

@zh-tw

2003年论文

@wuu

name

The autosomal dominant hypopho ...... ces in vivo biological potency

@ast

The autosomal dominant hypopho ...... ces in vivo biological potency

@en

The autosomal dominant hypopho ...... ces in vivo biological potency

@nl

type

label

The autosomal dominant hypopho ...... ces in vivo biological potency

@ast

The autosomal dominant hypopho ...... ces in vivo biological potency

@en

The autosomal dominant hypopho ...... ces in vivo biological potency

@nl

prefLabel

The autosomal dominant hypopho ...... ces in vivo biological potency

@ast

The autosomal dominant hypopho ...... ces in vivo biological potency

@en

The autosomal dominant hypopho ...... ces in vivo biological potency

@nl

P1433

Q28202356-028BAB65-7282-41BE-8942-215FC6946B21

P1476

Q28202356-A34339BA-EBCE-430D-9E30-93C899ECC950

P2093

Q28202356-3300ACEC-3AA2-4D1B-BAF0-409FEC9FC635

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P2860

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P304

Q28202356-9B535CC3-88AA-4425-97BF-19CC319CE6A4

P31

Q28202356-9EB1B492-3B56-4C7F-80BE-106DD4BCDDA8

P3181

Q28202356-28085201-0F1C-4A7E-8CF9-0A4FAFE12E98

P356

Q28202356-B9D421C6-5DF4-4B09-BC3B-592DCF3EFD72

P407

Q28202356-34FC2719-C046-4821-B1F9-2626BCE798BC

P433

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P921

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P3181

P356

P1433

Journal of Biological Chemistry

P1476

The autosomal dominant hypopho ...... ces in vivo biological potency

@en

P2093

Andrew C Karaplis

http://www.w3.org/2001/XMLSchema#string

David Goltzman

http://www.w3.org/2001/XMLSchema#string

Dengshun Miao

http://www.w3.org/2001/XMLSchema#string

Xiu-Ying Bai

http://www.w3.org/2001/XMLSchema#string

P2860

Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23

FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate

A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. The HYP Consortium

Cloning of human PEX cDNA. Expression, subcellular localization, and endopeptidase activity

Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia

Proprotein and prohormone convertases: a family of subtilases generating diverse bioactive polypeptides

Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23

Loss of renal phosphate wasting in a child with autosomal dominant hypophosphatemic rickets caused by a FGF23 mutation

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

Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP).

P304

9843-9

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P31

scholarly article

P3181

4958937

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P356

10.1074/JBC.M210490200

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P407

P433

11

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P478

278

http://www.w3.org/2001/XMLSchema#string

P577

2003-03-14T00:00:00Z

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P698

12519781

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P921

autosomal dominant hypophosphatemic rickets