Pages that link to "Q61849366"
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The following pages link to NovelGALNT3Mutations Causing Hyperostosis-Hyperphosphatemia Syndrome Result in Low Intact Fibroblast Growth Factor 23 Concentrations (Q61849366):
Displaying 32 items.
- Fibroblast growth factor 23 (Q26829294) (← links)
- A mouse with an N-Ethyl-N-nitrosourea (ENU) Induced Trp589Arg Galnt3 mutation represents a model for hyperphosphataemic familial tumoural calcinosis (Q28482201) (← links)
- Multiple members of the UDP-GalNAc: polypeptide N-acetylgalactosaminyltransferase family are essential for viability in Drosophila (Q30422393) (← links)
- Newly discovered mutations in the GALNT3 gene causing autosomal recessive hyperostosis-hyperphosphatemia syndrome (Q33660188) (← links)
- An O-glycosyltransferase promotes cell adhesion during development by influencing secretion of an extracellular matrix integrin ligand (Q33911414) (← links)
- Nicotinamide treatment in a murine model of familial tumoral calcinosis reduces serum Fgf23 and raises heart calcium (Q34147642) (← links)
- Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse (Q34185739) (← links)
- Overexpression of Galnt3 in chondrocytes resulted in dwarfism due to the increase of mucin-type O-glycans and reduction of glycosaminoglycans (Q34249099) (← links)
- Long-term clinical outcome and phenotypic variability in hyperphosphatemic familial tumoral calcinosis and hyperphosphatemic hyperostosis syndrome caused by a novel GALNT3 mutation; case report and review of the literature (Q34273172) (← links)
- Computational Prediction of O-linked Glycosylation Sites that Preferentially Map on Intrinsically Disordered Regions of Extracellular Proteins (Q35002236) (← links)
- Familial tumoral calcinosis: from characterization of a rare phenotype to the pathogenesis of ectopic calcification (Q35203191) (← links)
- Normophosphatemic familial tumoral calcinosis is caused by deleterious mutations in SAMD9, encoding a TNF-alpha responsive protein (Q35203230) (← links)
- Dietary phosphate restriction normalizes biochemical and skeletal abnormalities in a murine model of tumoral calcinosis (Q35590824) (← links)
- The N's and O's of Drosophila glycoprotein glycobiology (Q36542361) (← links)
- Molecular genetic and biochemical analyses of FGF23 mutations in familial tumoral calcinosis (Q36956055) (← links)
- Recent insights into the biological roles of mucin-type O-glycosylation (Q37130137) (← links)
- Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression (Q37210780) (← links)
- A case of familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome due to a compound heterozygous mutation in GALNT3 demonstrating new phenotypic features (Q37216979) (← links)
- Familial tumoral calcinosis and the role of O-glycosylation in the maintenance of phosphate homeostasis (Q37327002) (← links)
- The skeleton: endocrine regulator of phosphate homeostasis (Q37334547) (← links)
- Disorders of phosphate homeostasis and tissue mineralisation (Q37507342) (← links)
- FGF23 and syndromes of abnormal renal phosphate handling (Q37584801) (← links)
- N-acetylgalactosaminyltransferases in cancer (Q37619873) (← links)
- Hyperphosphatemic familial tumoral calcinosis: genetic models of deficient FGF23 action (Q38345898) (← links)
- GALNT3, a gene associated with hyperphosphatemic familial tumoral calcinosis, is transcriptionally regulated by extracellular phosphate and modulates matrix metalloproteinase activity (Q38353574) (← links)
- Ablation of systemic phosphate-regulating gene fibroblast growth factor 23 (Fgf23) compromises the dentoalveolar complex (Q41959145) (← links)
- Giantin-knockout models reveal a feedback loop between Golgi function and glycosyltransferase expression. (Q47674167) (← links)
- Familial tumoral calcinosis and hyperostosis-hyperphosphataemia syndrome are different manifestations of the same disease: novel missense mutations in GALNT3. (Q54458912) (← links)
- Clinical variability of familial tumoral calcinosis caused by novel GALNT3 mutations (Q61831294) (← links)
- Novel mutations in GALNT3 causing hyperphosphatemic familial tumoral calcinosis (Q83469034) (← links)
- Hyperphosphatemic familial tumoral calcinosis secondary to fibroblast growth factor 23 (FGF23) mutation: a report of two affected families and review of the literature (Q89161363) (← links)
- Mechanisms and Regulation of Intestinal Phosphate Absorption (Q89442831) (← links)