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

Knockout and Double Knockout of Cathepsin K and Mmp9 reveals a novel function of Cathepsin K as a regulator of osteoclast gene expression and bone homeostasis

1 Jan 2022

Abstract excerpt

Cathepsins play a role in regulation of cell function through their presence in the cell nucleus. However, the role of Cathepsin K (Ctsk) as an epigenetic regulator in osteoclasts remains unknown. Our data demonstrated that Ctsk -/-Mmp9 -/-mice have a striking phenotype with a 5-fold increase in bone volume compared with WT. RNA-seq analysis of Ctsk -/-, Mmp9 -/-and Ctsk -/-/Mmp9 -/-osteoclasts revealed their...

Read the complete abstract on PubMed

Topics

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

Share to Bone and Dental Protein Studies
Share to Bone health and treatments
Share to Bone Metabolism and Diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36147479
DOI: 10.7150/ijbs.72211

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Knockout and Double Knockout of Cathepsin K and Mmp9 reveals a novel function of Cathepsin K as a regulator of osteoclast gene expression and bone homeostasisPMID 36147479Read ↗

Cathepsin K+ Non-Osteoclast Cells in the Skeletal System: Function, Models, Identity, and Therapeutic ImplicationsSemantic proximity Read ↗

Characterization of Mouse Cathepsin K Gene, the Gene Promoter, and the Gene ExpressionSemantic proximity Read ↗

Cathepsin K Controls Cortical Bone Formation by Degrading Periostin.Semantic proximity Read ↗

Mice lacking cathepsin K maintain bone remodeling but develop bone fragility despite high bone mass.Semantic proximity Read ↗

Linking osteopetrosis and pycnodysostosis: regulation of cathepsin K expression by the microphthalmia transcription factor family.Semantic proximity Read ↗

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model.Semantic proximity Read ↗

Osteoarthritic change is delayed in a Ctsk-knockout mouse model of osteoarthritis.Semantic proximity Read ↗

Hairy and enhancer of split 1 is a primary effector of NOTCH2 signaling and induces osteoclast differentiation and function.Semantic proximity Read ↗

Novel pycnodysostosis mouse model uncovers cathepsin K function as a potential regulator of osteoclast apoptosis and senescenceSemantic proximity Read ↗

Pycnodysostosis: role and regulation of cathepsin K in osteoclast function and human disease.Semantic proximity Read ↗

Cathepsin K deficiency partially inhibits, but does not prevent, bone destruction in human tumor necrosis factor-transgenic mice.Semantic proximity Read ↗

Visualizing Cathepsin K‐Cre Expression at the Single‐Cell Level with GFP ReportersSemantic proximity Read ↗

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