Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression.
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The FGF23-Klotho axis: endocrine regulation of phosphate homeostasisMiscellaneous non-inflammatory musculoskeletal conditions. Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)Fibroblast growth factor 23Mucin-type O-glycosylation during developmentControl of mucin-type O-glycosylation: a classification of the polypeptide GalNAc-transferase gene familyFibroblast Growth Factor-23-A Potential Uremic ToxinA mouse with an N-Ethyl-N-nitrosourea (ENU) Induced Trp589Arg Galnt3 mutation represents a model for hyperphosphataemic familial tumoural calcinosisOsteocyte-specific deletion of Fgfr1 suppresses FGF23N-ethyl-N-Nitrosourea (ENU) induced mutations within the klotho gene lead to ectopic calcification and reduced lifespan in mouse modelsA phenotype survey of 36 mutant mouse strains with gene-targeted defects in glycosyltransferases or glycan-binding proteins.O-glycosylation regulates polarized secretion by modulating Tango1 stability.Low density lipoprotein receptor class A repeats are O-glycosylated in linker regionsThe role of mucin-type O-glycans in eukaryotic developmentHypophosphatemic rickets: revealing novel control points for phosphate homeostasis.Nicotinamide treatment in a murine model of familial tumoral calcinosis reduces serum Fgf23 and raises heart calciumGenetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.Overexpression of Galnt3 in chondrocytes resulted in dwarfism due to the increase of mucin-type O-glycans and reduction of glycosaminoglycansDissecting the biological role of mucin-type O-glycosylation using RNA interference in Drosophila cell culture.Upregulation of calcitriol during pregnancy and skeletal recovery after lactation do not require parathyroid hormone.Recent advances in renal phosphate handling.Altered renal FGF23-mediated activity involving MAPK and Wnt: effects of the Hyp mutationPhosphate sensing.Polypeptide N-acetylgalactosaminyltransferase 6 disrupts mammary acinar morphogenesis through O-glycosylation of fibronectinCoupling fibroblast growth factor 23 production and cleavage: iron deficiency, rickets, and kidney disease.Familial tumoral calcinosis: from characterization of a rare phenotype to the pathogenesis of ectopic calcificationHyperphosphatemic familial tumoral calcinosis: odontostomatologic management and pathological features.Dietary phosphate restriction normalizes biochemical and skeletal abnormalities in a murine model of tumoral calcinosisPhosphatonins: new hormones involved in numerous inherited bone disordersA Phex mutation in a murine model of X-linked hypophosphatemia alters phosphate responsiveness of bone cells.Complex N-glycans are essential, but core 1 and 2 mucin O-glycans, O-fucose glycans, and NOTCH1 are dispensable, for mammalian spermatogenesisDeconstruction of O-glycosylation--GalNAc-T isoforms direct distinct subsets of the O-glycoproteome.In vivo impact of Dlx3 conditional inactivation in neural crest-derived craniofacial bonesHexa-D-arginine treatment increases 7B2•PC2 activity in hyp-mouse osteoblasts and rescues the HYP phenotype.Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23.1,25-Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression.The lectin domain of the polypeptide GalNAc transferase family of glycosyltransferases (ppGalNAc Ts) acts as a switch directing glycopeptide substrate glycosylation in an N- or C-terminal direction, further controlling mucin type O-glycosylationThe rachitic tooth.FGF23 and syndromes of abnormal renal phosphate handlingIron and fibroblast growth factor 23 in X-linked hypophosphatemia.Hormone-like (endocrine) Fgfs: their evolutionary history and roles in development, metabolism, and disease.
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Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 12 February 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Ablation of the Galnt3 gene le ...... te increased Fgf23 expression.
@en
Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23
@nl
type
label
Ablation of the Galnt3 gene le ...... te increased Fgf23 expression.
@en
Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23
@nl
prefLabel
Ablation of the Galnt3 gene le ...... te increased Fgf23 expression.
@en
Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23
@nl
P2093
P2860
P356
P1433
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Ablation of the Galnt3 gene le ...... te increased Fgf23 expression.
@en
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Andrea H Sorenson
Anthony M Austin
Donald S Mackenzie
Shoji Ichikawa
Timothy A Fritz
P2860
P304
P356
10.1210/EN.2008-0877
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P577
2009-02-12T00:00:00Z