Human Preosteoblastic Cell Culture from a Patient with Severe Tumoral Calcinosis-Hyperphosphatemia Due to a New GALNT3 Gene Mutation: Study of In Vitro Mineralization. (Q41032238)

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scientific article published on 23 April 2015

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English	Human Preosteoblastic Cell Culture from a Patient with Severe Tumoral Calcinosis-Hyperphosphatemia Due to a New GALNT3 Gene Mutation: Study of In Vitro Mineralization.	scientific article published on 23 April 2015

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6 March 2020

Human Preosteoblastic Cell Culture from a Patient with Severe Tumoral Calcinosis-Hyperphosphatemia Due to a New GALNT3 Gene Mutation: Study of In Vitro Mineralization (English)

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Alessandro Franchi

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Maria Luisa Brandi

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G Beltrami

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S Ottanelli

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F Franceschelli

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A Gozzini

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G Galli

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C Mavilia

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F Giusti

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R Capanna

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Calcified Tissue International

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6 March 2020

Tumoral calcinosis: pearls, polemics, and alternative possibilities

1 reference

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A novel mutation in fibroblast growth factor 23 gene as a cause of tumoral calcinosis

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An FGF23 missense mutation causes familial tumoral calcinosis with hyperphosphatemia.

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A novel homozygous missense mutation in FGF23 causes Familial Tumoral Calcinosis associated with disseminated visceral calcification

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A novel recessive mutation of fibroblast growth factor-23 in tumoral calcinosis.

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Familial tumoral calcinosis and testicular microlithiasis associated with a new mutation of GALNT3 in a white family.

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A novel GALNT3 mutation in a pseudoautosomal dominant form of tumoral calcinosis: evidence that the disorder is autosomal recessive

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Hyperphosphatemic familial tumoral calcinosis caused by a mutation in GALNT3 in a European kindred

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

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Identification of a recurrent mutation in GALNT3 demonstrates that hyperostosis-hyperphosphatemia syndrome and familial tumoral calcinosis are allelic disorders

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

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Mutation of the mouse klotho gene leads to a syndrome resembling ageing

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A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis

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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

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Calculation of renal tubular reabsorption of phosphate: the algorithm performs better than the nomogram

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Nomogram for derivation of renal threshold phosphate concentration

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Laboratory aspects of circulating α-Klotho

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A novel missense mutation in GALNT3 causing hyperostosis-hyperphosphataemia syndrome.

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Two novel nonsense mutations in GALNT3 gene are responsible for familial tumoral calcinosis

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

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A case of familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome due to a compound heterozygous mutation in GALNT3 demonstrating new phenotypic features

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GALNT3, a gene associated with hyperphosphatemic familial tumoral calcinosis, is transcriptionally regulated by extracellular phosphate and modulates matrix metalloproteinase activity

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Defective O-glycosylation due to a novel homozygous S129P mutation is associated with lack of fibroblast growth factor 23 secretion and tumoral calcinosis

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

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Establishment of sandwich ELISA for soluble alpha-Klotho measurement: Age-dependent change of soluble alpha-Klotho levels in healthy subjects

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A potential link between phosphate and aging--lessons from Klotho-deficient mice

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Discovery of alpha-Klotho unveiled new insights into calcium and phosphate homeostasis

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Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D.

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Klotho, a gene related to a syndrome resembling human premature aging, functions in a negative regulatory circuit of vitamin D endocrine system

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Genetic dissection of phosphate- and vitamin D-mediated regulation of circulating Fgf23 concentrations

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Klotho converts canonical FGF receptor into a specific receptor for FGF23

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Mineral metabolism and aging: the fibroblast growth factor 23 enigma

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Does Fgf23-klotho activity influence vascular and soft tissue calcification through regulating mineral ion metabolism?

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Fibroblast Growth Factor 23 (FGF23) and Alpha-Klotho Stimulate Osteoblastic MC3T3.E1 Cell Proliferation and Inhibit Mineralization

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