2021
Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer
Sadras T, Martin M, Kume K, Robinson ME, Saravanakumar S, Lenz G, Chen Z, Song JY, Siddiqi T, Oksa L, Knapp AM, Cutler J, Cosgun KN, Klemm L, Ecker V, Winchester J, Ghergus D, Soulas-Sprauel P, Kiefer F, Heisterkamp N, Pandey A, Ngo V, Wang L, Jumaa H, Buchner M, Ruland J, Chan WC, Meffre E, Martin T, Müschen M. Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer. Molecular Cell 2021, 81: 2094-2111.e9. PMID: 33878293, PMCID: PMC8239336, DOI: 10.1016/j.molcel.2021.03.043.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CD19AutoimmunityB-LymphocytesCalciumCell DifferentiationCell Transformation, NeoplasticEnzyme ActivationHumansImmune ToleranceLymphoma, B-CellMiceModels, GeneticNeoplasm ProteinsNeoplasmsNFATC Transcription FactorsPhosphatidylinositol 3-KinasesProtein BindingReceptors, Antigen, B-CellSignal TransductionSyk KinaseZAP-70 Protein-Tyrosine KinasePON2 subverts metabolic gatekeeper functions in B cells to promote leukemogenesis
Pan L, Hong C, Chan LN, Xiao G, Malvi P, Robinson ME, Geng H, Reddy ST, Lee J, Khairnar V, Cosgun KN, Xu L, Kume K, Sadras T, Wang S, Wajapeyee N, Müschen M. PON2 subverts metabolic gatekeeper functions in B cells to promote leukemogenesis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2016553118. PMID: 33531346, PMCID: PMC7896313, DOI: 10.1073/pnas.2016553118.Peer-Reviewed Original ResearchConceptsTransplant recipient miceDNA double-strand breaksNormal B cell developmentDouble-strand breaksB cell developmentGenetic deletionB cellsLymphoid transcription factorsGlucose transporter GLUT1Gatekeeper functionGlucose uptakeRecipient miceTranscription factorsSomatic recombinationSynthetic lethalityB-cell acute lymphoblastic leukemiaCell developmentMetabolic gatekeeperRefractory B-ALLDeficient murineCell acute lymphoblastic leukemiaPoor clinical outcomeCell typesAcute lymphoblastic leukemiaGlucose transport
2014
A Compensatory Role of NF-κB to p53 in Response to 5-FU–Based Chemotherapy for Gastric Cancer Cell Lines
Endo F, Nishizuka SS, Kume K, Ishida K, Katagiri H, Ishida K, Sato K, Iwaya T, Koeda K, Wakabayashi G. A Compensatory Role of NF-κB to p53 in Response to 5-FU–Based Chemotherapy for Gastric Cancer Cell Lines. PLOS ONE 2014, 9: e90155. PMID: 24587255, PMCID: PMC3937424, DOI: 10.1371/journal.pone.0090155.Peer-Reviewed Original ResearchMeSH KeywordsAntimetabolites, AntineoplasticCell Line, TumorCodonDrug Resistance, NeoplasmFluorouracilGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansNF-kappa BProtein BindingProtein TransportStomach NeoplasmsTranscription Factor RelATumor Suppressor Protein p53ConceptsGastric cancer cell linesCancer cell linesNF-κBAdjuvant chemotherapyPrediction markersCell linesNF-κB-dependent mannerGastric cancer patientsKnockdown of RelANF-κB bindingArg homozygosityCurative resectionRelapse rateCancer patientsGastric cancerPrediction biomarkersChemotherapyP65 subunitTP53 knockdownChemotherapeutic efficacyProtein levelsCompensatory roleP53Target protein levelsTreatment