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Article

Chronic inhibition of ERK1/2 signaling improves disordered bone and mineral metabolism in hypophosphatemic (Hyp) mice.

Endocrinology - 1 Apr 2012

Zhang Martin Y H, Ranch Daniel, Pereira Renata C, Armbrecht Harvey J, Portale Anthony A, Perwad Farzana

Abstract excerpt

The X-linked hypophosphatemic (Hyp) mouse carries a loss-of-function mutation in the phex gene and is characterized by hypophosphatemia due to renal phosphate (Pi) wasting, inappropriately suppressed 1,25-dihydroxyvitamin D [1,25(OH)₂D] production, and rachitic bone disease. Increased serum fibroblast growth factor-23 concentration is responsible for the disordered metabolism of Pi and 1,25(OH)₂D. In the present...

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Identifiers

PMID: 22334725
DOI: 10.1210/en.2011-1831
PMCID: PMC3320256

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Chronic inhibition of ERK1/2 signaling improves disordered bone and mineral metabolism in hypophosphatemic (Hyp) mice.PMID 22334725Read ↗

Transgenic mice expressing fibroblast growth factor 23 under the control of the alpha1(I) collagen promoter exhibit growth retardation, osteomalacia, and disturbed phosphate homeostasis.Semantic proximity Read ↗

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

Nuclear isoforms of fibroblast growth factor 2 are novel inducers of hypophosphatemia via modulation of FGF23 and KLOTHO.Semantic proximity Read ↗

Increased bone volume and correction of HYP mouse hypophosphatemia in the Klotho/HYP mouse.Semantic proximity Read ↗

Effect of phosphate supplementation on the expression of the mutant phenotype in murine X-linked hypophosphatemic rickets.Semantic proximity Read ↗

Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signalingSemantic proximity Read ↗

Altered renal FGF23-mediated activity involving MAPK and Wnt: effects of the Hyp mutation.Semantic proximity Read ↗

Overexpression of the DMP1 C-terminal fragment stimulates FGF23 and exacerbates the hypophosphatemic rickets phenotype in Hyp mice.Semantic proximity Read ↗

Increased renal 25-hydroxyvitamin D3-24-hydroxylase messenger ribonucleic acid and immunoreactive protein in phosphate-deprived Hyp mice: a mechanism for accelerated 1,25-dihydroxyvitamin D3 catabolism in X-linked hypophosphatemic rickets.Semantic proximity Read ↗

Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype.Semantic proximity Read ↗

A Mutation in the Dmp1 Gene Alters Phosphate Responsiveness in Mice.Semantic proximity Read ↗

Genetic evidence of serum phosphate-independent functions of FGF-23 on bone.Semantic proximity Read ↗

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