2021
Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts
Kim H, Lee K, Kim J, Kim M, Kim J, Lee H, Chung Y, Shin H, Kim T, Park E, Rho J, Lee S, Kim N, Lee S, Choi Y, Jeong D. Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts. Nature Communications 2021, 12: 2258. PMID: 33859201, PMCID: PMC8050258, DOI: 10.1038/s41467-021-22565-7.Peer-Reviewed Original ResearchConceptsSelenoprotein WCell-cell fusionRNA sequencing analysisProfile of receptor activationOsteoclast differentiationNuclear factor of activated T cells cytoplasmic 1Bone remodelingBone mass phenotypeOsteoclastogenesis in vitroNuclear translocation of NF-kBTranslocation of NF-kBPhysiological bone remodelingBlocks osteoporosisNuclear translocationNuclear factorOsteoclastogenic genesMechanism of actionMass phenotypeBone metabolismBone resorptionReceptor activationOsteoclast maturationCytoplasmic 1Osteoclast formationNF-kB
2014
Secretion of a Truncated Osteopetrosis-associated Transmembrane Protein 1 (OSTM1) Mutant Inhibits Osteoclastogenesis through Down-regulation of the B Lymphocyte-induced Maturation Protein 1 (BLIMP1)-Nuclear Factor of Activated T Cells c1 (NFATc1) Axis*
Shin B, Yu J, Park E, Choi S, Yu J, Hwang J, Yun H, Chung Y, Hong K, Choi J, Takami M, Rho J. Secretion of a Truncated Osteopetrosis-associated Transmembrane Protein 1 (OSTM1) Mutant Inhibits Osteoclastogenesis through Down-regulation of the B Lymphocyte-induced Maturation Protein 1 (BLIMP1)-Nuclear Factor of Activated T Cells c1 (NFATc1) Axis*. Journal Of Biological Chemistry 2014, 289: 35868-35881. PMID: 25359771, PMCID: PMC4276856, DOI: 10.1074/jbc.m114.589614.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone ResorptionCell DifferentiationCell FusionCell SurvivalCells, CulturedDown-RegulationGene ExpressionLipopolysaccharidesMaleMembrane ProteinsMice, Inbred C57BLNFATC Transcription FactorsOsteoclastsOsteoporosisPositive Regulatory Domain I-Binding Factor 1Signal TransductionTranscription FactorsConceptsSecreted formTransmembrane domainOsteopetrosis-associated transmembrane protein 1Down-regulationAutosomal recessive osteopetrosis patientsTransmembrane protein 1Marker genesCell surfaceActivated T cells c1Genetic defectsExpression of OC marker genesCell fusionFunctional roleGenetic mutationsAutosomal recessive osteopetrosisMutationsProtein 1Bone destruction in vivoGene mutationsGenesDestruction in vivoRecessive osteopetrosisOsteoclast (OCOsteopetrosis patientsOsteoclastogenic genes
2010
ATP6v0d2 deficiency increases bone mass, but does not influence ovariectomy-induced bone loss
Kim T, Ha H, Kim N, Park E, Rho J, Kim E, Lorenzo J, Choi Y, Lee S. ATP6v0d2 deficiency increases bone mass, but does not influence ovariectomy-induced bone loss. Biochemical And Biophysical Research Communications 2010, 403: 73-78. PMID: 21040703, PMCID: PMC3026595, DOI: 10.1016/j.bbrc.2010.10.117.Peer-Reviewed Original ResearchConceptsColony forming unit-granulocyte/macrophageBone lossActions of bone-forming osteoblastsOsteoclast maturationOvariectomy (OVX)-induced bone lossOVX-induced bone lossBone homeostasisOVX-induced increaseIncreased bone resorptionBone marrow cellsOsteoclast formation in vitroExcessive bone lossPathological conditionsNormal developmentBone-forming osteoblastsBone-resorbing osteoclastsControl of bone homeostasisMarrow cellsBone massProtect miceBone resorptionFormation in vitroOsteoclast differentiationOsteoclast precursorsAtp6v0d2