Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Osteochondroma formation is independent of heparanase expression as revealed in a mouse model of hereditary multiple exostoses.

Journal of orthopaedic research : official publication of the Orthopaedic Research Society - 1 Oct 2022

Mundy Christina, Chung Juliet, Koyama Eiki, Bunting Stuart, Mahimkar Rajeev, Pacifici Maurizio

Abstract excerpt

Hereditary multiple exostoses (HME) is a rare, pediatric disorder characterized by osteochondromas that form along growth plates and provoke significant musculoskeletal problems. HME is caused by mutations in heparan sulfate (HS)-synthesizing enzymes EXT1 or EXT2. Seemingly paradoxically, osteochondromas were found to contain excessive extracellular heparanase (Hpse) that could further reduce HS levels and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Exostoses, Multiple Hereditary
Share to Exostosin 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Glucuronidase

Share to Heparitin Sulfate

Share to N-Acetylglucosaminyltransferases

Share to Retinoids

Share to Tamoxifen

Share to X-Ray Microtomography

Source

Open in PubMed Open full text

Identifiers

PMID: 34996123
DOI: 10.1002/jor.25260
PMCID: PMC9259764

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Osteochondroma formation is independent of heparanase expression as revealed in a mouse model of hereditary multiple exostoses.PMID 34996123Read ↗

The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses.Semantic proximity Read ↗

The molecular and cellular basis of exostosis formation in hereditary multiple exostosesSemantic proximity Read ↗

Mice deficient in Ext2 lack heparan sulfate and develop exostosesSemantic proximity Read ↗

Hereditary Multiple Exostoses: New Insights into Pathogenesis, Clinical Complications, and Potential Treatments.Semantic proximity Read ↗

Heparan sulfate in skeletal development, growth, and pathology: The case of hereditary multiple exostosesSemantic proximity Read ↗

A mouse model of chondrocyte-specific somatic mutation reveals a role for Ext1 loss of heterozygosity in multiple hereditary exostoses.Semantic proximity Read ↗

Unsuspected osteochondroma-like outgrowths in the cranial base of Hereditary Multiple Exostoses patients and modeling and treatment with a BMP antagonist in mice.Semantic proximity Read ↗

Heparan sulfate abnormalities in exostosis growth plates.Semantic proximity Read ↗

Hereditary multiple exostoses and heparan sulfate polymerization.Semantic proximity Read ↗

Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic StrategiesSemantic proximity Read ↗

Cell biology of osteochondromas: bone morphogenic protein signalling and heparan sulphates.Semantic proximity Read ↗

New perspectives on the molecular basis of hereditary bone tumours.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.