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Article

Serum levels of sclerostin, Dickkopf-1, and secreted frizzled-related protein-4 are not changed in individuals with high bone mass causing mutations in LRP5.

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA - 1 Oct 2014

Simpson C A, Foer D, Lee G S, Bihuniak J, Sun B, Sullivan R, Belsky J, Insogna K L

Abstract excerpt

SUMMARY: We compared circulating levels of Wnt inhibitors among patients with high bone mass mutations in LRP5, unaffected kindred, and unrelated normal controls. Inhibitors were unchanged in affected and unaffected kindred. We saw no meaningful differences between controls and affected individua...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Open in PubMed Open full text

Identifiers

PMID: 24927689
DOI: 10.1007/s00198-014-2767-5
PMCID: PMC4659359

Genes

LRP5
SOST

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-24927689-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Serum levels of sclerostin, Dickkopf-1, and secreted frizzled-related protein-4 are not changed in individuals with high bone mass causing mutations in LRP5.PMID 24927689Read ↗

Elevated circulating Sclerostin concentrations in individuals with high bone mass, with and without LRP5 mutations.Semantic proximity Read ↗

LRP5 mutations linked to high bone mass diseases cause reduced LRP5 binding and inhibition by SOST.Semantic proximity Read ↗

Pathogenic mutations and polymorphisms in the lipoprotein receptor-related protein 5 reveal a new biological pathway for the control of bone mass.Semantic proximity Read ↗

LRP receptor family member associated bone disease.Semantic proximity Read ↗

Targeting the LRP5 pathway improves bone properties in a mouse model of osteogenesis imperfecta.Semantic proximity Read ↗

Novel LRP5 missense mutation in a patient with a high bone mass phenotype results in decreased DKK1-mediated inhibition of Wnt signaling.Semantic proximity Read ↗

Identification of the first deletion in the LRP5 gene in a patient with autosomal dominant osteopetrosis type I.Semantic proximity Read ↗

Reduced affinity to and inhibition by DKK1 form a common mechanism by which high bone mass-associated missense mutations in LRP5 affect canonical Wnt signaling.Semantic proximity Read ↗

Lrp4 Mediates Bone Homeostasis and Mechanotransduction through Interaction with Sclerostin In VivoSemantic proximity Read ↗

The Anti-Osteoanabolic Function of Sclerostin Is Blunted in Mice Carrying a High Bone Mass Mutation of Lrp5.Semantic proximity Read ↗

Lrp4, a novel receptor for Dickkopf 1 and sclerostin, is expressed by osteoblasts and regulates bone growth and turnover in vivo.Semantic proximity Read ↗

Association between polymorphisms in sclerostin, dickkopfs and secreted frizzled-related protein genes and bone mineral density in postmenopausal Korean women.Semantic proximity Read ↗

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