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
2019
TDAG51 is a crucial regulator of maternal care and depressive-like behavior after parturition
Yun H, Park E, Choi S, Shin B, Yu J, Yu J, Amarasekara D, Kim S, Lee N, Choi J, Choi Y, Rho J. TDAG51 is a crucial regulator of maternal care and depressive-like behavior after parturition. PLOS Genetics 2019, 15: e1008214. PMID: 31251738, PMCID: PMC6599150, DOI: 10.1371/journal.pgen.1008214.Peer-Reviewed Original ResearchConceptsDepressive-like behaviorPostpartum depressionDevelopment of postpartum depressionImpaired maternal behaviorRegulation of maternal careMonoamine neurotransmitter levelsCombination of physical changesNest-building testInfluence of genetic risk factorsTDAG51 deficiencyMaternity careGenetic risk factorsPup retrievalMental disordersPsychiatric illnessNeurotransmitter levelsMaternal behaviorPostpartumRisk factorsDepressionBuilding testsT-cell death-associated geneDeath-associated genesNursesCare
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
2007
Early embryonic lethality caused by targeted disruption of the TRAF-interacting protein (TRIP) gene
Park E, Choi S, Kim J, Jeong Y, Choe J, Park C, Choi Y, Rho J. Early embryonic lethality caused by targeted disruption of the TRAF-interacting protein (TRIP) gene. Biochemical And Biophysical Research Communications 2007, 363: 971-977. PMID: 17927961, DOI: 10.1016/j.bbrc.2007.09.103.Peer-Reviewed Original ResearchConceptsTumor necrosis factor receptor (TNFR)-associated factorsTRAF-interacting proteinCylindromatosis tumor suppressor geneFamilial cylindromatosis tumour suppressor geneHomozygous mouse embryosComplex in vitroEarly embryonic lethalityTumor suppressor geneExcessive cell deathNF-kappaB signalingAdaptor moleculeEmbryonic lethalityProliferation defectEmbryonic development in vivoSignaling in vitroSuppressor geneSignaling cascadesCell deathActivity in vitroDevelopment in vivoTargeted disruptionNF-kappaB activation in vitroFunctional roleCell proliferationMouse embryos