2020
ASCL1- and DLX2-induced GABAergic neurons from hiPSC-derived NPCs
Barretto N, Zhang H, Powell SK, Fernando MB, Zhang S, Flaherty EK, Ho SM, Slesinger PA, Duan J, Brennand KJ. ASCL1- and DLX2-induced GABAergic neurons from hiPSC-derived NPCs. Journal Of Neuroscience Methods 2020, 334: 108548. PMID: 32065989, PMCID: PMC7426253, DOI: 10.1016/j.jneumeth.2019.108548.Peer-Reviewed Original ResearchNeural progenitor cellsHiPSC-NPCsSomatic cell reprogrammingGABAergic neuronsHiPSC-derived neural progenitor cellsDifferentiation of hiPSCsDistinct transcriptional profilesPluripotent stem cellsCell reprogrammingPatient-derived cellsElectrophysiological maturityFunctional GABAergic neuronsTranscriptional profilesNeuronal inductionStem cellsProgenitor cellsLentiviral overexpressionPure populationsDlx2Study of diseasesAscl1HiPSCsNeuronal populationsInduction protocolCell source
2019
Differential regulation of OCT4 targets facilitates reacquisition of pluripotency
Thakurela S, Sindhu C, Yurkovsky E, Riemenschneider C, Smith ZD, Nachman I, Meissner A. Differential regulation of OCT4 targets facilitates reacquisition of pluripotency. Nature Communications 2019, 10: 4444. PMID: 31570708, PMCID: PMC6768871, DOI: 10.1038/s41467-019-11741-5.Peer-Reviewed Original ResearchConceptsEctopic transcription factorsReacquisition of pluripotencySomatic cell reprogrammingCis-regulatory elementsTranscription factor expressionExact molecular mechanismsOCT4 targetsPluripotent stem cellsPluripotency inductionCell reprogrammingTranscription factorsSomatic cellsMolecular mechanismsDifferential regulationPluripotencyStem cellsVivo differentiationPrimary targetCellsFactor expressionFinal stepExperimental systemReprogrammingTargetDifferentiationMKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation
Hu X, Liu ZZ, Chen X, Schulz VP, Kumar A, Hartman AA, Weinstein J, Johnston JF, Rodriguez EC, Eastman AE, Cheng J, Min L, Zhong M, Carroll C, Gallagher PG, Lu J, Schwartz M, King MC, Krause DS, Guo S. MKL1-actin pathway restricts chromatin accessibility and prevents mature pluripotency activation. Nature Communications 2019, 10: 1695. PMID: 30979898, PMCID: PMC6461646, DOI: 10.1038/s41467-019-09636-6.Peer-Reviewed Original ResearchConceptsCell fate reprogrammingChromatin accessibilityActin cytoskeletonSomatic cell reprogrammingPluripotency transcription factorsGlobal chromatin accessibilityGenomic accessibilityCytoskeleton (LINC) complexCell reprogrammingCytoskeletal genesTranscription factorsReprogrammingPluripotencyChromatinCytoskeletonMKL1Unappreciated aspectPathwayNuclear volumeNucleoskeletonSUN2CellsActivationGenesExpression
2016
Regulation of the DNA Methylation Landscape in Human Somatic Cell Reprogramming by the miR-29 Family
Hysolli E, Tanaka Y, Su J, Kim KY, Zhong T, Janknecht R, Zhou XL, Geng L, Qiu C, Pan X, Jung YW, Cheng J, Lu J, Zhong M, Weissman SM, Park IH. Regulation of the DNA Methylation Landscape in Human Somatic Cell Reprogramming by the miR-29 Family. Stem Cell Reports 2016, 7: 43-54. PMID: 27373925, PMCID: PMC4945581, DOI: 10.1016/j.stemcr.2016.05.014.Peer-Reviewed Original ResearchConceptsDNA methylation stateEmbryonic stem cellsInduced pluripotent stem cellsHuman somatic cell reprogrammingSomatic cell reprogrammingMethylation stateCell reprogrammingMiR-29 familyDNA methylation landscapeImportant epigenetic regulatorsStem cellsOverexpression of Oct4Global DNA methylationMiRNA-based approachesPluripotent stem cellsMethylation landscapeHistone modificationsDNA demethylationEpigenomic changesEarly reprogrammingEpigenetic regulatorsEpigenetic differencesDNA methylationHydroxymethylation analysisReprogramming
2015
Transcriptome Signature and Regulation in Human Somatic Cell Reprogramming
Tanaka Y, Hysolli E, Su J, Xiang Y, Kim KY, Zhong M, Li Y, Heydari K, Euskirchen G, Snyder MP, Pan X, Weissman SM, Park IH. Transcriptome Signature and Regulation in Human Somatic Cell Reprogramming. Stem Cell Reports 2015, 4: 1125-1139. PMID: 26004630, PMCID: PMC4471828, DOI: 10.1016/j.stemcr.2015.04.009.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsBase SequenceCellular ReprogrammingCyclin EEmbryonic Stem CellsGene Expression RegulationHumansInduced Pluripotent Stem CellsKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceMolecular Sequence DataOctamer Transcription Factor-3Oncogene ProteinsPolymorphism, Single NucleotidePrincipal Component AnalysisProto-Oncogene Proteins c-mycRNASequence Analysis, RNASOXB1 Transcription FactorsTranscriptomeConceptsHuman somatic cell reprogrammingMonoallelic gene expressionSomatic cell reprogrammingPrevious transcriptome studiesHuman iPSC reprogrammingPluripotent stem cellsCell reprogrammingIPSC reprogrammingTranscriptome dataEarly reprogrammingTranscriptome studiesTranscriptome changesBiallelic expressionRNA-seqSomatic cellsExpression analysisGene expressionSpliced formsReprogrammingTranscriptome signaturesStem cellsInvaluable resourceCellular surface markersBiomedical researchCellsConcise Review: Modeling Multiple Sclerosis With Stem Cell Biological Platforms: Toward Functional Validation of Cellular and Molecular Phenotypes in Inflammation-Induced Neurodegeneration
Orack JC, Deleidi M, Pitt D, Mahajan K, Nicholas JA, Boster AL, Racke MK, Comabella M, Watanabe F, Imitola J. Concise Review: Modeling Multiple Sclerosis With Stem Cell Biological Platforms: Toward Functional Validation of Cellular and Molecular Phenotypes in Inflammation-Induced Neurodegeneration. Stem Cells Translational Medicine 2015, 4: 252-260. PMID: 25593207, PMCID: PMC4339849, DOI: 10.5966/sctm.2014-0133.Peer-Reviewed Original ResearchConceptsSomatic cell reprogrammingStem cellsInduced pluripotent stem cell (iPSC) technologyPluripotent stem cell (iPSC) technologyOligodendrocyte progenitor cellsMultiple sclerosisGeneration of neuronsNew mechanistic insightsCell reprogrammingNovel stem cellFunctional validationStem cell technologyMolecular mechanismsBiological toolsMesenchymal stem cellsMolecular phenotypesNovel mechanismProgenitor cellsImmune cell functionPhase I clinical trialMechanistic insightsBiological platformCell functionSignificant unmet needBrain atrophyFrom “Directed Differentiation” to “Neuronal Induction”: Modeling Neuropsychiatric Disease
Ho S, Topol A, Brennand K. From “Directed Differentiation” to “Neuronal Induction”: Modeling Neuropsychiatric Disease. Biomarker Insights 2015, 10s1: bmi.s20066. PMID: 26045654, PMCID: PMC4444490, DOI: 10.4137/bmi.s20066.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsNeuronal inductionSomatic cell reprogrammingNeuropsychiatric diseasesPsychiatric disordersPluripotent stem cell (iPSC) technologyCell reprogrammingDirected DifferentiationMost neurological diseasesStem cell technologyHuman postmortem samplesFunction of neuronsPolygenic originHuman neuronsDisease onsetAnimal modelsNeurological diseasesDisease initiationPostmortem samplesDiseaseNeuronsDifferentiationPrimary causeLimitless numberDisordersAberrant behavior
2014
X Chromosome of Female Cells Shows Dynamic Changes in Status during Human Somatic Cell Reprogramming
Kim KY, Hysolli E, Tanaka Y, Wang B, Jung YW, Pan X, Weissman SM, Park IH. X Chromosome of Female Cells Shows Dynamic Changes in Status during Human Somatic Cell Reprogramming. Stem Cell Reports 2014, 2: 896-909. PMID: 24936474, PMCID: PMC4050354, DOI: 10.1016/j.stemcr.2014.04.003.Peer-Reviewed Original ResearchConceptsX chromosome stateInactive X chromosomeActive X chromosomeX chromosomeChromosome stateHuman somatic cell reprogrammingIPSC clonesSomatic cell reprogrammingX chromosome reactivationStem cellsEmbryonic stem cellsPluripotent stem cellsHuman iPSC clonesEpigenetic stateCell reprogrammingFemale iPSCsFemale cellsChromosomesHuman iPSCsParental cellsDisease modelingDynamic changesRobust reactivationIPSCsClones
2010
Highly Efficient Reprogramming to Pluripotency and Directed Differentiation of Human Cells with Synthetic Modified mRNA
Warren L, Manos PD, Ahfeldt T, Loh YH, Li H, Lau F, Ebina W, Mandal PK, Smith ZD, Meissner A, Daley GQ, Brack AS, Collins JJ, Cowan C, Schlaeger TM, Rossi DJ. Highly Efficient Reprogramming to Pluripotency and Directed Differentiation of Human Cells with Synthetic Modified mRNA. Cell Stem Cell 2010, 7: 618-630. PMID: 20888316, PMCID: PMC3656821, DOI: 10.1016/j.stem.2010.08.012.Peer-Reviewed Original ResearchConceptsInduced pluripotent stem cellsPluripotent stem cellsCell fateMultiple human cell typesSomatic cell reprogrammingCell typesUseful cell typesStem cellsHuman cell typesPatient-specific induced pluripotent stem cellsCell reprogrammingCellular reprogrammingInnate antiviral responseDirected DifferentiationIPSC derivationHuman cellsMyogenic cellsSynthetic mRNAAntiviral responseDisease modelingReprogrammingModified mRNARegenerative medicineFateMRNAFive classic articles in somatic cell reprogramming.
Park IH. Five classic articles in somatic cell reprogramming. The Yale Journal Of Biology And Medicine 2010, 83: 135-7. PMID: 20885901, PMCID: PMC2946127.Peer-Reviewed Original ResearchKruppel-like Factor 4 (Klf4) Prevents Embryonic Stem (ES) Cell Differentiation by Regulating Nanog Gene Expression*
Zhang P, Andrianakos R, Yang Y, Liu C, Lu W. Kruppel-like Factor 4 (Klf4) Prevents Embryonic Stem (ES) Cell Differentiation by Regulating Nanog Gene Expression*. Journal Of Biological Chemistry 2010, 285: 9180-9189. PMID: 20071344, PMCID: PMC2838337, DOI: 10.1074/jbc.m109.077958.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Morphogenetic Protein 4Cell DifferentiationEmbryonic Stem CellsGene Expression RegulationHomeodomain ProteinsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLeukemia Inhibitory FactorMiceModels, BiologicalNanog Homeobox ProteinSignal TransductionSTAT3 Transcription FactorConceptsES cell self-renewalES cell differentiationCell Self-RenewalSomatic cell reprogrammingCell differentiationKruppel-like factor 4Embryonic stemLeukemia inhibitory factorBone morphogenetic protein 4Cell reprogrammingPromoter region of NanogSelf-RenewalTranscription factor Kruppel-like factor 4KLF4 gene expressionMaintenance of pluripotencyFamily proteinsFactor 4Differentiation of ES cellsPromoter regionGene expressionES cellsExpression of NanogOverexpressing KLF4Protein 4Nanog expression
2009
Klf4 Interacts Directly with Oct4 and Sox2 to Promote Reprogramming
Wei Z, Yang Y, Zhang P, Andrianakos R, Hasegawa K, Lyu J, Chen X, Bai G, Liu C, Pera M, Lu W. Klf4 Interacts Directly with Oct4 and Sox2 to Promote Reprogramming. Stem Cells 2009, 27: 2969-2978. PMID: 19816951, DOI: 10.1002/stem.231.Peer-Reviewed Original ResearchConceptsInduced pluripotent stemEndogenous KLF4Sets of transcription factorsInduced pluripotent stem cellsTandem zinc fingerEmbryonic stemDominant negative mutantInduced iPS cellsMouse ES cellsSomatic cell reprogrammingWild-type Klf4Zinc fingerPluripotent stemTranscription factorsC-terminusIPS cellsInhibit reprogrammingEctopic expressionTarget genesNanog promoterSomatic cellsSOX2Cell reprogrammingES cellsKLF4
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