2019
Histone H3 trimethylation at lysine 36 guides m6A RNA modification co-transcriptionally
Huang H, Weng H, Zhou K, Wu T, Zhao BS, Sun M, Chen Z, Deng X, Xiao G, Auer F, Klemm L, Wu H, Zuo Z, Qin X, Dong Y, Zhou Y, Qin H, Tao S, Du J, Liu J, Lu Z, Yin H, Mesquita A, Yuan CL, Hu YC, Sun W, Su R, Dong L, Shen C, Li C, Qing Y, Jiang X, Wu X, Sun M, Guan JL, Qu L, Wei M, Müschen M, Huang G, He C, Yang J, Chen J. Histone H3 trimethylation at lysine 36 guides m6A RNA modification co-transcriptionally. Nature 2019, 567: 414-419. PMID: 30867593, PMCID: PMC6438714, DOI: 10.1038/s41586-019-1016-7.Peer-Reviewed Original ResearchConceptsM6A methyltransferase complexHistone H3 trimethylationH3 trimethylationHistone modificationsImportant post-transcriptional mechanismMouse embryonic stem cellsGene expression regulationRNA polymerase IIPrevalent internal modificationPost-transcriptional mechanismsEmbryonic stem cellsN6-methyladenosine (m<sup>6</sup>A) mRNA modificationM6A depositionTranscription elongationNascent RNAMethyltransferase complexPolymerase IIExpression regulationGene expression1RNA methylationMRNA modificationMETTL14 knockdownH3K36me3M6A modificationCell stemness
2018
B-Cell-Specific Diversion of Glucose Carbon Utilization Reveals a Unique Vulnerability in B Cell Malignancies
Xiao G, Chan LN, Klemm L, Braas D, Chen Z, Geng H, Zhang QC, Aghajanirefah A, Cosgun KN, Sadras T, Lee J, Mirzapoiazova T, Salgia R, Ernst T, Hochhaus A, Jumaa H, Jiang X, Weinstock DM, Graeber TG, Müschen M. B-Cell-Specific Diversion of Glucose Carbon Utilization Reveals a Unique Vulnerability in B Cell Malignancies. Cell 2018, 173: 470-484.e18. PMID: 29551267, PMCID: PMC6284818, DOI: 10.1016/j.cell.2018.02.048.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB-LymphocytesCarbonCell Line, TumorCell SurvivalGlucoseGlucosephosphate DehydrogenaseGlycolysisHumansIkaros Transcription FactorMiceMice, Inbred C57BLMice, Inbred NODOxidative StressPAX5 Transcription FactorPentose Phosphate PathwayPrecursor Cell Lymphoblastic Leukemia-LymphomaProtein Phosphatase 2Proto-Oncogene Proteins c-bcl-2Transcription, GeneticConceptsPentose phosphate pathwayCarbon utilizationSerine/threonine protein phosphatase 2AB-cell transcription factor PAX5Transcription factor Pax5Favor of glycolysisSmall molecule inhibitionPhosphatase 2ATranscriptional repressionRedox homeostasisOncogenic transformationTumor suppressorMolecule inhibitionPP2AGenetic studiesPhosphate pathwayB cell activationEssential roleB-cell malignanciesCell malignanciesB cellsAntioxidant protectionOxidative stressB-cell tumorsCell activation
2011
BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition
Duy C, Hurtz C, Shojaee S, Cerchietti L, Geng H, Swaminathan S, Klemm L, Kweon SM, Nahar R, Braig M, Park E, Kim YM, Hofmann WK, Herzog S, Jumaa H, Koeffler HP, Yu JJ, Heisterkamp N, Graeber TG, Wu H, Ye BH, Melnick A, Müschen M. BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition. Nature 2011, 473: 384-388. PMID: 21593872, PMCID: PMC3597744, DOI: 10.1038/nature09883.Peer-Reviewed Original ResearchMeSH KeywordsADP-Ribosylation Factor 1AnimalsCell SurvivalDNA-Binding ProteinsDrug Resistance, NeoplasmFusion Proteins, bcr-ablGene Expression Regulation, NeoplasticHumansMiceMice, Inbred NODMice, SCIDPrecursor Cell Lymphoblastic Leukemia-LymphomaProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-6Transcription, GeneticTumor Suppressor Protein p53ConceptsTyrosine kinase inhibitorsAcute lymphoblastic leukemia cellsBCR-ABL1 mutationsLymphoblastic leukemia cellsDrug resistanceLeukemia cellsLeukemia-initiating cellsXenograft modelBCR-ABL1Anticancer responseTargeted inhibitionDual inhibitionKinase inhibitorsOncogene withdrawalCancer therapyBCL6Kinase inhibitionLeukemiaInhibitionCellsTherapyMutationsUpregulation
2010
BCL6 is critical for the development of a diverse primary B cell repertoire
Duy C, Yu JJ, Nahar R, Swaminathan S, Kweon SM, Polo JM, Valls E, Klemm L, Shojaee S, Cerchietti L, Schuh W, Jäck HM, Hurtz C, Ramezani-Rad P, Herzog S, Jumaa H, Koeffler HP, de Alborán IM, Melnick AM, Ye BH, Müschen M. BCL6 is critical for the development of a diverse primary B cell repertoire. Journal Of Experimental Medicine 2010, 207: 1209-1221. PMID: 20498019, PMCID: PMC2882829, DOI: 10.1084/jem.20091299.Peer-Reviewed Original ResearchMeSH KeywordsADP-Ribosylation FactorsAnimalsApoptosisBase SequenceB-LymphocytesCell ProliferationCell SurvivalCells, CulturedCytoprotectionDNA DamageDNA-Binding ProteinsDown-RegulationGene Rearrangement, B-Lymphocyte, Light ChainHumansInterleukin-7LymphopoiesisMiceMolecular Sequence DataPre-B Cell ReceptorsPrecursor Cells, B-LymphoidProto-Oncogene Proteins c-bcl-6Proto-Oncogene Proteins c-mycRecombination, GeneticSignal TransductionTranscription, GeneticUp-RegulationConceptsDNA damage-induced apoptosisDamage-induced apoptosisImmunoglobulin light chain gene recombinationPre-B cell receptorBone marrow immature B cellsB cell developmentClass switch recombinationAbsence of Bcl6B cell repertoireExpression of BCL6Immature B cellsMu heavy chainDNA breaksNegative regulationPrimary B-cell repertoireGene recombinationCell developmentClonal diversityB cellsGerminal center B cellsSomatic hypermutationB cell precursorsExpression levelsBCL6 expressionCell precursors