2013
Deletion of the Transforming Growth Factor β Receptor Type II Gene in Articular Chondrocytes Leads to a Progressive Osteoarthritis‐like Phenotype in Mice
Shen J, Li J, Wang B, Jin H, Wang M, Zhang Y, Yang Y, Im H, O'Keefe R, Chen D. Deletion of the Transforming Growth Factor β Receptor Type II Gene in Articular Chondrocytes Leads to a Progressive Osteoarthritis‐like Phenotype in Mice. Arthritis & Rheumatism 2013, 65: 3107-3119. PMID: 23982761, PMCID: PMC3928444, DOI: 10.1002/art.38122.Peer-Reviewed Original ResearchMeSH KeywordsADAM ProteinsADAMTS5 ProteinAnimalsCartilage, ArticularChondrocytesCore Binding Factor Alpha 2 SubunitDisease ProgressionMatrix Metalloproteinase 13MiceMice, KnockoutOsteoarthritisPhenotypeProtein Serine-Threonine KinasesReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionUp-RegulationConceptsCritical downstream target genesDownstream target genesTarget genesGrowth factor β signalingRegulation of Runx2Mouse genetic approachesLoss of TGFβType II geneGene expression analysisInhibition of TGFβDevelopment of osteoarthritisRat chondrosarcoma cellsGenetic approachesExpression analysisConditional knockout miceTGFβ signalingOsteoarthritis-like phenotypeGenesΒ signalingADAMTS5 geneReceptor type IIChondrosarcoma cellsTGFβCartilage homeostasisOA-like phenotype
2010
Smad3 Prevents β-Catenin Degradation and Facilitates β-Catenin Nuclear Translocation in Chondrocytes*
Zhang M, Wang M, Tan X, Li TF, Zhang YE, Chen D. Smad3 Prevents β-Catenin Degradation and Facilitates β-Catenin Nuclear Translocation in Chondrocytes*. Journal Of Biological Chemistry 2010, 285: 8703-8710. PMID: 20097766, PMCID: PMC2838293, DOI: 10.1074/jbc.m109.093526.Peer-Reviewed Original ResearchConceptsBeta-catenin protein stabilityBeta-catenin nuclear translocationNuclear translocationDownstream target genesBeta-catenin proteinN-terminal regionDetailed molecular mechanismsΒ-catenin degradationTGF-beta/Smad3Β-catenin nuclear translocationProtein complexesProtein stabilityTarget genesRegulatory mechanismsSmad3 interactionMolecular mechanismsChondrocyte developmentDependent degradationNovel mechanismDependent mannerWntSmad3Growth factorTranslocationPathway