Overexpression of human PHEX under the human beta-actin promoter does not fully rescue the Hyp mouse phenotype.
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Degradation of MEPE, DMP1, and release of SIBLING ASARM-peptides (minhibins): ASARM-peptide(s) are directly responsible for defective mineralization in HYPSkeletal secretion of FGF-23 regulates phosphate and vitamin D metabolismExcessive Osteocytic Fgf23 Secretion Contributes to Pyrophosphate Accumulation and Mineralization Defect in Hyp MiceGenetic evidence of serum phosphate-independent functions of FGF-23 on boneFGF23 neutralization improves bone quality and osseointegration of titanium implants in chronic kidney disease mice.Kbus/Idr, a mutant mouse strain with skeletal abnormalities and hypophosphatemia: identification as an allele of 'Hyp'.Biomineralization of bone: a fresh view of the roles of non-collagenous proteins.Chronic inhibition of ERK1/2 signaling improves disordered bone and mineral metabolism in hypophosphatemic (Hyp) mice.Phosphate: known and potential roles during development and regeneration of teeth and supporting structures.Correction of the mineralization defect in hyp mice treated with protease inhibitors CA074 and pepstatinAberrant Phex function in osteoblasts and osteocytes alone underlies murine X-linked hypophosphatemia.Overexpression of the DMP1 C-terminal fragment stimulates FGF23 and exacerbates the hypophosphatemic rickets phenotype in Hyp mice.Hexa-D-arginine treatment increases 7B2•PC2 activity in hyp-mouse osteoblasts and rescues the HYP phenotype.CYP24 inhibition as a therapeutic target in FGF23-mediated renal phosphate wasting disordersRegulation of phosphate homeostasis by PTH, vitamin D, and FGF23.Endocrine functions of bone in mineral metabolism regulation.The PHEX transgene corrects mineralization defects in 9-month-old hypophosphatemic mice.Aberrant cementum phenotype associated with the hypophosphatemic hyp mouse.The metabolic bone disease associated with the Hyp mutation is independent of osteoblastic HIF1α expression.Hypophosphatemic rickets due to perturbations in renal tubular function.The biological function of DMP-1 in osteocyte maturation is mediated by its 57-kDa C-terminal fragmentMutation in Phex gene predisposes BALB/c-Phex(Hyp-Duk)/Y mice to otitis media.1alpha,25-dihydroxyvitamin D3 acts predominately in mature osteoblasts under conditions of high extracellular phosphate to increase fibroblast growth factor 23 production in vitro.CRISPR/Cas9-mediated mutation of PHEX in rabbit recapitulates human X-linked hypophosphatemia (XLH).Defective Mineralization in X-Linked Hypophosphatemia Dental Pulp Cell Cultures.Phex mutation causes the reduction of npt2b mRNA in teeth.
P2860
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P2860
Overexpression of human PHEX under the human beta-actin promoter does not fully rescue the Hyp mouse phenotype.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh
2005年學術文章
@zh-hant
name
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@en
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@nl
type
label
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@en
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@nl
prefLabel
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@en
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@nl
P2093
P2860
P356
P1476
Overexpression of human PHEX u ...... escue the Hyp mouse phenotype.
@en
P2093
Beate Lanske
Dagmar Mayer
Harald Jüppner
Kenneth Jonsson
Reinhold G Erben
P2860
P304
P356
10.1359/JBMR.050212
P50
P577
2005-02-21T00:00:00Z