2025
Predicting adenine base editing efficiencies in different cellular contexts by deep learning
Kissling L, Mollaysa A, Janjuha S, Mathis N, Marquart K, Weber Y, Moon W, Lin P, Fan S, Muramatsu H, Vadovics M, Allam A, Pardi N, Tam Y, Krauthammer M, Schwank G. Predicting adenine base editing efficiencies in different cellular contexts by deep learning. Genome Biology 2025, 26: 115. PMID: 40340964, PMCID: PMC12060317, DOI: 10.1186/s13059-025-03586-7.Peer-Reviewed Original ResearchConceptsBase editing efficiencyEditing efficiencyCell linesPathogenic mutationsBase editingPrimary cells in vivoBase editing screensBase editing outcomesCells in vivoHEK293T cellsAdenine base editingIn vivo settingTarget lociT cellsLipid nanoparticlesCellular contextTarget sequenceMRNA deliveryBase pairsOn-target editingBystander effectEditing outcomesBase editorsIn vitro datasetsMurine liver
2024
Mechanistic Investigation of Human DPP9 Deficiency
Xiao T, Brewer J, Zhou L, Han A, Takabe Y, Carlino M, Blackburn H, Flavell R. Mechanistic Investigation of Human DPP9 Deficiency. Blood 2024, 144: 5699-5699. DOI: 10.1182/blood-2024-211123.Peer-Reviewed Original ResearchHuman HSPCsDevelopment of human immune systemHuman NLRP1Loss of hematopoietic cellsHumanized mouse modelHuman hematopoietic stemStem cells in vivoSensors of infectionLaboratory mouse strainsCells in vivoHuman immune systemMouse genomeHematopoietic stemHuman hematopoiesisHematopoietic cellsCellular stressNegative regulatorPancytopeniaProgenitor cellsMouse strainsRegulatory pathwaysMouse modelHSPCsImmune systemDeletionTumor-Specific Antigen Delivery for T-cell Therapy via a pH-Sensitive Peptide Conjugate.
Yurkevicz A, Liu Y, Katz S, Glazer P. Tumor-Specific Antigen Delivery for T-cell Therapy via a pH-Sensitive Peptide Conjugate. Molecular Cancer Therapeutics 2024, 24: 105-117. PMID: 39382073, PMCID: PMC11695185, DOI: 10.1158/1535-7163.mct-23-0809.Peer-Reviewed Original ResearchMajor histocompatibility complexT cellsTumor cellsTreatment of tumor-bearing miceMajor histocompatibility complex class I pathwaySuppression of tumor growthTumor cells in vivoT-cell therapySyngeneic tumor modelsTumor-specific antigensTumor-bearing miceMelanoma tumor cellsT cell activationHealthy tissueTarget tumor cellsIn vivoIn vitroMicroenvironment of tumorsUnique delivery platformsClass I pathwayCell-based therapiesTargeted cancer therapyCells in vivoAntigen processing pathwayAcidic microenvironment of tumorsPRMT6 facilitates EZH2 protein stability by inhibiting TRAF6-mediated ubiquitination degradation to promote glioblastoma cell invasion and migration
Wang J, Shen S, You J, Wang Z, Li Y, Chen Y, Tuo Y, Chen D, Yu H, Zhang J, Wang F, Pang X, Xiao Z, Lan Q, Wang Y. PRMT6 facilitates EZH2 protein stability by inhibiting TRAF6-mediated ubiquitination degradation to promote glioblastoma cell invasion and migration. Cell Death & Disease 2024, 15: 524. PMID: 39043634, PMCID: PMC11266590, DOI: 10.1038/s41419-024-06920-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrain NeoplasmsCell Line, TumorCell MovementEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticGlioblastomaHumansMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessNuclear ProteinsProtein StabilityProtein-Arginine N-MethyltransferasesProteolysisTNF Receptor-Associated Factor 6UbiquitinationConceptsProtein arginine methyltransferase 6Glioblastoma cell invasionStability of EZH2Protein stabilityCell invasionOverexpression of PRMT6Inhibited glioblastoma cell invasionGlioblastoma cellsEZH2 protein stabilityHistone methylation marksMigration of glioblastoma cellsHallmarks of cancerProliferation of glioblastoma cellsMethylation marksTumor cell invasionEpigenetic regulationGlioblastoma cells in vivoBioinformatics analysisMigration in vitroRegulatory relationshipsEZH2 proteinUbiquitination degradationProteinCells in vivoTRAF6ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.
Hu B, Wiesehöfer M, de Miguel F, Liu Z, Chan L, Choi J, Melnick M, Arnal Estape A, Walther Z, Zhao D, Lopez-Giraldez F, Wurtz A, Cai G, Fan R, Gettinger S, Xiao A, Yan Q, Homer R, Nguyen D, Politi K. ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer Research 2024, 84: 1303-1319. PMID: 38359163, DOI: 10.1158/0008-5472.can-23-0438.Peer-Reviewed Original ResearchTyrosine kinase inhibitorsPatient-derived xenograftsEGFR mutant lung cancerMutant lung cancerPre-treatment tumorsResidual diseaseDrug toleranceLung cancerResidual tumor cells in vivoEGFR mutant lung adenocarcinomaTyrosine kinase inhibitor osimertinibEGFR tyrosine kinase inhibitorsTyrosine kinase inhibitor treatmentTumor cells in vivoMutant lung adenocarcinomaMaximal tumor regressionTranscription factor Ascl1Drug-tolerant cellsTime of maximal responseEvidence of cellsCells in vivoOsimertinib treatmentTumor regressionSingle cell transcriptional profilingTumor cells
2015
Enhanced MAF Oncogene Expression and Breast Cancer Bone Metastasis
Pavlovic M, Arnal-Estapé A, Rojo F, Bellmunt A, Tarragona M, Guiu M, Planet E, Garcia-Albéniz X, Morales M, Urosevic J, Gawrzak S, Rovira A, Prat A, Nonell L, Lluch A, Jean-Mairet J, Coleman R, Albanell J, Gomis R. Enhanced MAF Oncogene Expression and Breast Cancer Bone Metastasis. Journal Of The National Cancer Institute 2015, 107: djv256. PMID: 26376684, PMCID: PMC4681582, DOI: 10.1093/jnci/djv256.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkers, TumorBone NeoplasmsBreast NeoplasmsCell Line, TumorDNA Copy Number VariationsFemaleGene Expression Regulation, NeoplasticHeterograftsHumansImmunohistochemistryIn Situ Hybridization, FluorescenceIncidenceMiceMice, Inbred BALB COdds RatioPredictive Value of TestsPrognosisProportional Hazards ModelsProto-Oncogene Proteins c-mafUp-RegulationConceptsBreast cancer bone metastasisCopy number aberrationsCancer bone metastasisBone metastasesRisk of bone metastasisAssociated with bone metastasisBreast cancer cells in vivoPrimary breast tumorsBreast cancer patient populationCancer cells in vivoMetastasis to boneClinical follow-upBreast cancer cellsAssociated with riskCells in vivoCancer patient populationBone relapseCause-specific hazard modelBreast tumorsFollow-upMAF overexpressionMetastasisPatient populationProtein overexpressionCancer cells
2014
Characterization of Cre Recombinase Activity for In Vivo Targeting of Adipocyte Precursor Cells
Krueger K, Costa M, Du H, Feldman B. Characterization of Cre Recombinase Activity for In Vivo Targeting of Adipocyte Precursor Cells. Stem Cell Reports 2014, 3: 1147-1158. PMID: 25458893, PMCID: PMC4264060, DOI: 10.1016/j.stemcr.2014.10.009.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipogenesisAnimalsEnzyme ActivationFatty Acid-Binding ProteinsFemaleGene ExpressionGene TargetingHomeodomain ProteinsHomologous RecombinationImmunophenotypingIntegrasesMaleMiceOrgan SpecificityPhenotypePromoter Regions, GeneticReceptor, Platelet-Derived Growth Factor alphaStem CellsConceptsAdipose precursor cellsFabp4-CreModulate gene expressionPrx1-CreDiscovery of cell-surface markersAdipose tissue developmentAdipocyte precursor cellsCre-mediated recombinationGene expressionPrecursor cellsRecombinase activityTissue developmentCells in vivoCre recombinase activityMature tissuesAdipose expressionAdipose depotsMetabolic diseasesMouse linesIn vivoCellsCell surface markersRecombinationTransgenic mouse linesAdipose tissue
2008
Stabilization of β-Catenin Induces Pancreas Tumor Formation
Heiser P, Cano D, Landsman L, Kim G, Kench J, Klimstra D, Taketo M, Biankin A, Hebrok M. Stabilization of β-Catenin Induces Pancreas Tumor Formation. Gastroenterology 2008, 135: 1288-1300. PMID: 18725219, PMCID: PMC2613004, DOI: 10.1053/j.gastro.2008.06.089.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsbeta CateninBiomarkers, TumorCarcinoma, PapillaryFemaleGene Expression Regulation, NeoplasticHumansIntegrasesMaleMiceMice, TransgenicPancreatic DuctsPancreatic NeoplasmsPhenotypePregnancyProto-Oncogene Proteins p21(ras)Signal TransductionStem CellsTranscription FactorsWnt ProteinsConceptsPancreatic ductal adenocarcinomaSolid pseudopapillary neoplasmBeta-catenin signalingPancreas tumorigenesisBeta-cateninPancreatic tumorsActivating mutationsPancreatic cells in vivoNuclear localization of beta-cateninHuman pancreatic ductal adenocarcinomaPancreatic intraepithelial neoplasiaLocalization of beta-cateninWnt pathwayActivation of beta-cateninFormation of pancreatic intraepithelial neoplasiaActive beta-cateninCells in vivoIntraepithelial neoplasiaRare tumorMalignant potentialPseudopapillary neoplasmPanIN lesionsStabilization of beta-cateninDuctal neoplasmsAdult mice
1999
Multipotential Marrow Stromal Cells Transduced to Produce L-DOPA: Engraftment in a Rat Model of Parkinson Disease
Schwarz E, Alexander G, Prockop D, Azizi S. Multipotential Marrow Stromal Cells Transduced to Produce L-DOPA: Engraftment in a Rat Model of Parkinson Disease. Human Gene Therapy 1999, 10: 2539-2549. PMID: 10543618, DOI: 10.1089/10430349950016870.Peer-Reviewed Original ResearchConceptsRat model of Parkinson's diseaseMarrow stromal cellsModel of Parkinson's diseaseRat marrow stromal cellsStromal cellsTyrosine hydroxylaseRat modelStriatum of 6-hydroxydopamine-lesioned ratsDenervated striatum of ratsL-DOPAHuman marrow stromal cellsApomorphine-induced rotationsAlternative source of cellsStriatum of ratsCells in vivoSource of cellsBone marrow stromal cellsDenervated striatumRetroviral transductionParkinson's diseaseNeural transplantationRatsConsistent with reportsIn vitroGTP cyclohydrolase I
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