2015
CA‐074Me compound inhibits osteoclastogenesis via suppression of the NFATc1 and c‐FOS signaling pathways
Patel N, Nizami S, Song L, Mikami M, Hsu A, Hickernell T, Chandhanayingyong C, Rho S, Compton JT, Caldwell J, Kaiser PB, Bai H, Lee HG, Fischer CR, Lee FY. CA‐074Me compound inhibits osteoclastogenesis via suppression of the NFATc1 and c‐FOS signaling pathways. Journal Of Orthopaedic Research® 2015, 33: 1474-1486. PMID: 25428830, DOI: 10.1002/jor.22795.Peer-Reviewed Original ResearchConceptsOsteolytic disordersOsteoclast biologyBone resorptionCA-074MeC-FOSMechanisms of cathepsinsCathepsin B knockout miceB knockout miceCathepsin B inhibitor CA-074Dose-dependent mannerOsteoclast resorption pitsCathepsin B inhibitionInhibits osteoclastogenesisNFATc1 pathwayNew therapiesOsteoclastogenic effectsCA-074Knockout miceLysosomal proteasesMature osteoclastsResorption pitsCathepsin KNew targetsOsteoclastsCompound inhibits
2011
Nuclear presence of nuclear factor of activated T cells (NFAT) c3 and c4 is required for Toll-like receptor-activated innate inflammatory response of monocytes/macrophages
Minematsu H, Shin MJ, Aydemir A, Kim KO, Nizami SA, Chung GJ, Lee FY. Nuclear presence of nuclear factor of activated T cells (NFAT) c3 and c4 is required for Toll-like receptor-activated innate inflammatory response of monocytes/macrophages. Cellular Signalling 2011, 23: 1785-1793. PMID: 21726630, PMCID: PMC3169434, DOI: 10.1016/j.cellsig.2011.06.013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone MarrowCell NucleusChromatin ImmunoprecipitationCytokinesHumansImmunity, InnateImmunohistochemistryLipopeptidesLipopolysaccharidesMacrophagesMiceMice, KnockoutMonocytesNFATC Transcription FactorsNF-kappa BOligopeptidesPrimary Cell CultureRNA Polymerase IIRNA, MessengerSignal TransductionToll-Like ReceptorsTumor Necrosis Factor-alphaConceptsBone marrow-derived macrophagesInnate immune responseImmune responseLPS stimulationNuclear factorNFAT-luciferase reporterProinflammatory cytokine expressionInnate inflammatory responseTLR ligand stimulationToll-like receptorsActivated T cells c3Monocytes/macrophagesActivated T cellsInnate immune regulationRole of NFATsTNF mRNA expressionMarrow-derived macrophagesImmune regulatory proteinsTLR4 ligandCytokine expressionLess TNFTLR1/2 ligandInflammatory responseImmune regulationT cells
2005
μ-Calpain Regulates Receptor Activator of NF-κB Ligand (RANKL)-supported Osteoclastogenesis via NF-κB Activation in RAW 264.7 Cells*
Lee FY, Kim DW, Karmin JA, Hong D, Chang SS, Fujisawa M, Takayanagi H, Bigliani LU, Blaine TA, Lee HJ. μ-Calpain Regulates Receptor Activator of NF-κB Ligand (RANKL)-supported Osteoclastogenesis via NF-κB Activation in RAW 264.7 Cells*. Journal Of Biological Chemistry 2005, 280: 29929-29936. PMID: 15955824, DOI: 10.1074/jbc.m414600200.Peer-Reviewed Original ResearchConceptsRAW 264.7 cellsNF-kappaB activationReceptor activatorCalpain inhibitorsCell-permeable calpain inhibitorMatrix metalloproteinase-9Regulation of RANKLNF-κB activationNF-κB ligandNF-kappaB ligandMonocyte/macrophage progenitorsRole of calpainMurine RAW 264.7 cellsCell typesMetalloproteinase-9Osteoclastogenic markersCalpain activationResistant acidDecreased expressionOsteoclastogenesisRANKLCalpain activityMu-calpainInhibitorsActivation