2015
Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia
Swaminathan S, Klemm L, Park E, Papaemmanuil E, Ford A, Kweon SM, Trageser D, Hasselfeld B, Henke N, Mooster J, Geng H, Schwarz K, Kogan SC, Casellas R, Schatz DG, Lieber MR, Greaves MF, Müschen M. Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia. Nature Immunology 2015, 16: 766-774. PMID: 25985233, PMCID: PMC4475638, DOI: 10.1038/ni.3160.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAnimalsAntibody DiversityB-LymphocytesChildChild, PreschoolClonal EvolutionCytidine DeaminaseDNA-Binding ProteinsFemaleFlow CytometryHomeodomain ProteinsHumansImmunoblottingInfantMaleMice, Inbred NODMice, KnockoutMice, SCIDMice, TransgenicMicroscopy, FluorescencePrecursor Cell Lymphoblastic Leukemia-LymphomaPrecursor Cells, B-LymphoidReverse Transcriptase Polymerase Chain ReactionTumor Cells, Cultured
2012
Dendritic cell–mediated activation-induced cytidine deaminase (AID)–dependent induction of genomic instability in human myeloma
Koduru S, Wong E, Strowig T, Sundaram R, Zhang L, Strout MP, Flavell RA, Schatz DG, Dhodapkar KM, Dhodapkar MV. Dendritic cell–mediated activation-induced cytidine deaminase (AID)–dependent induction of genomic instability in human myeloma. Blood 2012, 119: 2302-2309. PMID: 22234692, PMCID: PMC3311257, DOI: 10.1182/blood-2011-08-376236.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell Line, TumorCell SurvivalCells, CulturedCoculture TechniquesCytidine DeaminaseDendritic CellsDNA Breaks, Double-StrandedFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGenomic InstabilityHumansInterleukin Receptor Common gamma SubunitMiceMice, Inbred NODMice, KnockoutMice, SCIDMultiple MyelomaNF-kappa BRANK LigandReverse Transcriptase Polymerase Chain ReactionTransplantation, HeterologousTumor Cells, CulturedConceptsInduction of AIDMultiple myelomaTumor microenvironmentTumor cellsReceptor activatorActivation-induced cytidine deaminaseDendritic cell infiltrationCapacity of DCPrimary MM cellsNF-κB/receptor activatorGenetics of tumorsGrowth of tumorsGenomic damageMyeloma cell linesRANKL inhibitionPlasmacytoid DCsIndolent behaviorCell infiltrationMM cellsHuman myelomaCytidine deaminaseMyelomaDNA double-strand breaksGenomic instabilityCell lines
2008
Ebf1-dependent control of the osteoblast and adipocyte lineages
Hesslein DG, Fretz JA, Xi Y, Nelson T, Zhou S, Lorenzo JA, Schatz DG, Horowitz MC. Ebf1-dependent control of the osteoblast and adipocyte lineages. Bone 2008, 44: 537-546. PMID: 19130908, PMCID: PMC2657874, DOI: 10.1016/j.bone.2008.11.021.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAnimalsBlotting, WesternCell DifferentiationCell LineageImmunohistochemistryMiceMice, KnockoutOsteoblastsOsteogenesisReverse Transcriptase Polymerase Chain ReactionTrans-ActivatorsConceptsNumber of osteoclastsBone formation parametersBone formation rateAdipocyte lineageBone marrow cellsOlfactory sensory neuronsSerum osteocalcinOsteoid volumeSensory neuronsAdipocyte numberBone marrowOsteoclast developmentMutant miceMarrow cellsMiceSubcutaneous sitesBone formationAdipocyte developmentStriking increaseDecreased depositionTranscription factorsOsteoblastsB cell fate specificationEBF1Adiposity
2004
B cell–specific loss of histone 3 lysine 9 methylation in the VH locus depends on Pax5
Johnson K, Pflugh DL, Yu D, Hesslein DG, Lin KI, Bothwell AL, Thomas-Tikhonenko A, Schatz DG, Calame K. B cell–specific loss of histone 3 lysine 9 methylation in the VH locus depends on Pax5. Nature Immunology 2004, 5: 853-861. PMID: 15258579, PMCID: PMC1635547, DOI: 10.1038/ni1099.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceB-LymphocytesCell LineageCells, CulturedDNA-Binding ProteinsFlow CytometryGene Rearrangement, B-LymphocyteHematopoietic Stem CellsHistonesImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionLysineMethylationMiceModels, ImmunologicalMolecular Sequence DataPAX5 Transcription FactorPrecipitin TestsReverse Transcriptase Polymerase Chain ReactionTranscription FactorsConceptsH3-K9 methylationDJH recombinationVH locusHistone 3 lysine 9 methylationLysine 9 methylationFunction of Pax5Non-B lineage cellsB cell-specific lossB cell commitmentHistone exchangeInactive chromatinLysine 9Histone H3Transcription factorsCell commitmentCell-specific lossInhibitory modificationMethylationLineage cellsLociPAX5B cellsHeavy chain rearrangementRecombinationChain rearrangement
2002
The Activation-induced Deaminase Functions in a Postcleavage Step of the Somatic Hypermutation Process
Papavasiliou FN, Schatz DG. The Activation-induced Deaminase Functions in a Postcleavage Step of the Somatic Hypermutation Process. Journal Of Experimental Medicine 2002, 195: 1193-1198. PMID: 11994424, PMCID: PMC2193708, DOI: 10.1084/jem.20011858.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsB-LymphocytesCytidine DeaminaseImmunoglobulin Constant RegionsImmunoglobulin mu-ChainsMiceMice, KnockoutMolecular Sequence DataMutagenesisPoint MutationRecombination, GeneticReverse Transcriptase Polymerase Chain ReactionConceptsActivation-induced cytidine deaminaseClass switch recombinationSomatic hypermutationDNA lesionsDownstream constant region genesCytidine deaminase motifDominant-negative formConstant region genesInitial DNA lesionsSomatic hypermutation processHeavy chain constant regionIg genesNegative formImmunoglobulin genesChain constant regionTarget sequencePoint mutationsCytidine deaminaseHypermutation processGenesAID functionRegion genesMechanistic overlapVariable regionsConstant region