Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse. - Wikidata - awgldk - TriplyDB

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

http://www.wikidata.org/entity/Q34185739

about

Inhibitor of ppGalNAc-T3-mediated O-glycosylation blocks cancer cell invasiveness and lowers FGF23 levels.Systemic Control of Bone Homeostasis by FGF23 Signaling.Heritable and acquired disorders of phosphate metabolism: Etiologies involving FGF23 and current therapeutics.Genetic Knockout and Rescue Studies in Mice Unravel Abnormal Phosphorus Threshold in Hypophosphatemic Rickets.

P2860

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P2860

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

http://www.wikidata.org/entity/Q34185739

description

2014 nî lūn-bûn

@nan

2014 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հուլիսին հրատարակված գիտական հոդված

@hy

2014年の論文

@ja

2014年論文

@yue

2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@ast

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@en

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@nl

type

label

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@ast

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@en

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@nl

prefLabel

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@ast

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@en

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@nl

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P1476

Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.

@en

P2093

Amie K Gray

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

Kenneth E White

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

Leah R Padgett

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

Matthew R Allen

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

Nicole M Sarpa

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

Shoji Ichikawa

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

P2860

Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23

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

Polypeptide GalNAc-transferase T3 and familial tumoral calcinosis. Secretion of fibroblast growth factor 23 requires O-glycosylation

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

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

Mutations in GALNT3, encoding a protein involved in O-linked glycosylation, cause familial tumoral calcinosis

Tumoral calcinosis presenting with eyelid calcifications due to novel missense mutations in the glycosyl transferase domain of the GALNT3 gene

Hyperostosis-hyperphosphatemia syndrome: a congenital disorder of O-glycosylation associated with augmented processing of fibroblast growth factor 23.

Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans.

Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice.

P304

3891-3898

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P31

scholarly article

P356

10.1210/EN.2014-1199

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P407

P433

10

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P478

155

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P50

Michael J Econs

Erica L. Clinkenbeard

P577

2014-07-22T00:00:00Z

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25051439

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P932

4164931

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