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

Over-expression of Adamts1 in mice alters bone mineral density.

Journal of bone and mineral metabolism - 1 May 2012

Hu Lijuan, Jonsson Kenneth B, Andersén Harriet, Edenro Anne, Bohlooly-Y Mohammad, Melhus Håkan, Lind Thomas

Abstract excerpt

ADAMTS1, a secreted multifunctional metalloproteinase with disintegrin and thrombospondin motifs, is an early response gene of parathyroid hormone (PTH) in osteoblasts. Mice engineered to lack Adamts1 are smaller compared to wild-type (WT) mice and ADAMTS1 metalloproteinase activity has been shown to increase osteoblastic growth in collagen gels. However, there are no reports investigating the consequence of...

Read the complete abstract on PubMed

Topics

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

Share to ADAM Proteins
Share to Bone Density
Share to Femur

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Organ Specificity

Share to Osteocalcin

Share to Paraffin Embedding

Share to Parathyroid Hormone

Share to Tomography, X-Ray Computed

Source

Identifiers

PMID: 22002813
DOI: 10.1007/s00774-011-0322-4

Genes

ADAMTS1
PTH

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Over-expression of Adamts1 in mice alters bone mineral density.PMID 22002813Read ↗

ADAM12-S Stimulates Bone Growth in Transgenic Mice by Modulating Chondrocyte Proliferation and MaturationSemantic proximity Read ↗

ADAMTS-1: a metalloproteinase-disintegrin essential for normal growth, fertility, and organ morphology and function.Semantic proximity Read ↗

Genetic dissection of femoral and tibial microarchitectureSemantic proximity Read ↗

Physiological function of the angiotensin AT1a receptor in bone remodeling.Semantic proximity Read ↗

Differential effects between the loss of MMP-2 and MMP-9 on structural and tissue-level properties of bone.Semantic proximity Read ↗

Compound deletion of thrombospondin-1 and -2 results in a skeletal phenotype not predicted by the single gene knockouts.Semantic proximity Read ↗

Skeletal overexpression of gremlin impairs bone formation and causes osteopenia.Semantic proximity Read ↗

Skeletal phenotype of growing transgenic mice that express a function-perturbing form of beta1 integrin in osteoblasts.Semantic proximity Read ↗

Conditional deletion of gremlin causes a transient increase in bone formation and bone mass.Semantic proximity Read ↗

In vivo inhibition of osteoblastic metalloproteinases leads to increased trabecular bone mass.Semantic proximity Read ↗

Skeletal abnormalities in mice with Dnmt3a missense mutations.Semantic proximity Read ↗

F-spondin deficient mice have a high bone mass phenotype.Semantic proximity Read ↗

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