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

JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation-dependent and -independent mechanisms.

Journal of cell science - 15 Nov 2002

David Jean-Pierre, Sabapathy Kanaga, Hoffmann Oskar, Idarraga Maria H, Wagner Erwin F

Abstract excerpt

Phosphorylation of the N-terminal domain of Jun by the Jun kinases (JNKs) modulates the transcriptional activity of AP-1, a dimeric transcription factor typically composed of c-Jun and c-Fos, the latter being essential for osteoclast differentiation. Using mice lacking JNK1 or JNK2, we demonstrate that JNK1, but not JNK2, is specifically activated by the osteoclast-differentiating factor RANKL. Activation of...

Topics

Join the communities discussing this publication.

Mitogen-Activated Protein Kinase 8
Myeloid Progenitor Cells
Osteoclasts
Osteoprotegerin
Proto-Oncogene Proteins c-jun

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Receptors, Cytoplasmic and Nuclear

Receptors, Tumor Necrosis Factor

Transcription Factor AP-1

Source

Identifiers

PMID: 12376563
DOI: 10.1242/jcs.00082

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation-dependent and -independent mechanisms.PMID 12376563Read ↗

c-Jun N-Terminal Kinases (JNKs) Are Critical Mediators of Osteoblast Activity In VivoSemantic proximity Read ↗

Critical roles of c-Jun signaling in regulation of NFAT family and RANKL-regulated osteoclast differentiationSemantic proximity Read ↗

From JNK to Pay Dirt: Jun Kinases, their Biochemistry, Physiology and Clinical ImportanceSemantic proximity Read ↗

The isoform‐specific functions of the c‐Jun N‐terminal Kinases (JNKs): differences revealed by gene targetingSemantic proximity Read ↗

RANKing c-Jun in osteoclast developmentSemantic proximity Read ↗

The platelet-derived growth factor controls c-myc expression through a JNK- and AP-1-dependent signaling pathway.Semantic proximity Read ↗

Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects.Semantic proximity Read ↗

Activator protein 1 (Fos/Jun) functions in inflammatory bone and skin diseaseSemantic proximity Read ↗

Bone development and inflammatory disease is regulated by AP-1 (Fos/Jun)Semantic proximity Read ↗

Signalling in inflammatory skin disease by AP-1 (Fos/Jun).Semantic proximity Read ↗

Defective endochondral ossification in mice with strongly compromised expression of JunB.Semantic proximity Read ↗

Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation.Semantic proximity Read ↗

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