2023
KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic
Zhang S, Cao J, Yan Q. KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic. Advances In Experimental Medicine And Biology 2023, 1433: 113-137. PMID: 37751138, DOI: 10.1007/978-3-031-38176-8_6.ChaptersConceptsPlant homeodomainFamily proteinsKey epigenetic markCell fate determinationHistone methylation marksCancer type-dependent mannerKetoglutarate-dependent dioxygenasesSelective KDM5 inhibitorsTumor suppressive functionType-dependent mannerEpigenetic marksTumor suppressive roleFate determinationJumonji CLysine 4Active chromatinMethylation marksHistone H3Lysine demethylasesCatalytic coreKDM5 inhibitorsDrug targetsKDM5Cancer metastasisSuppressive role
2022
Acly Deficiency Enhances Myelopoiesis through Acetyl Coenzyme A and Metabolic–Epigenetic Cross-Talk
Greenwood D, Ramsey H, Nguyen P, Patterson A, Voss K, Bader J, Sugiura A, Bacigalupa Z, Schaefer S, Ye X, Dahunsi D, Madden M, Wellen K, Savona M, Ferrell P, Rathmell J. Acly Deficiency Enhances Myelopoiesis through Acetyl Coenzyme A and Metabolic–Epigenetic Cross-Talk. ImmunoHorizons 2022, 6: 837-850. PMID: 36547387, PMCID: PMC9935084, DOI: 10.4049/immunohorizons.2200086.Peer-Reviewed Original ResearchConceptsChromatin accessibilityMyeloid differentiationTransposase-accessible chromatin sequencingEpigenetic cross talkHematopoietic stemSingle-cell RNA sequencingFamily transcription factorsProgenitor cellsSmall molecule inhibitionSingle-cell assaysATP-citrate lyaseEpigenetic marksAcetyl coenzyme AGene expression signaturesEpigenetic modificationsTranscription factorsRNA sequencingACLY inhibitionMitochondrial metabolismReactive oxygen speciesMitochondrial polarizationMurine hematopoiesisCell metabolismMus musculusEssential substrateThe genetic basis of Gilles de la Tourette syndrome
Abdallah S, Realbuto E, Kaka M, Yang K, Topaloudi A, Paschou P, Scharf J, Fernandez T. The genetic basis of Gilles de la Tourette syndrome. International Review Of Movement Disorders 2022, 4: 3-38. DOI: 10.1016/bs.irmvd.2022.07.001.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsGenome-wide association studiesGenetic architectureCell type-specific gene expressionAssociation studiesComplex genetic architectureSingle causative geneFull genetic architectureSpecific gene expressionCandidate gene association studiesComprehensive genomic studiesCommon variant effectsPleiotropic gene effectsCommon genetic variantsGene association studiesEpigenetic marksGene regulationIndividual genesGenomic studiesLarge-scale approachGenetic basisGene expressionWhole-exome sequencing analysisBiological processesBiological pathwaysMendelian inheritanceChapter 11 Oncometabolites, epigenetic marks, and DNA repair
Dow J, Glazer P. Chapter 11 Oncometabolites, epigenetic marks, and DNA repair. 2022, 191-202. DOI: 10.1016/b978-0-323-91081-1.00008-x.Peer-Reviewed Original ResearchDNA damage repairJmjC domain-containing histone demethylasesDamage repairDouble-strand break sitesHallmarks of cancerEpigenetic marksHistone demethylasesEpigenetic signalingDNA demethylaseDependent dioxygenasesEpigenetic mechanismsDNA repairMajor translational impactGenomic instabilityMethylation signalsRepair pathwaysBreak siteDNA hypermethylationDNA damageΑ-ketoglutarateGlobal histoneOncometaboliteCancer cellsCompetitive inhibitorProfound sensitivity
2021
Deficiency of histone lysine methyltransferase SETDB2 in hematopoietic cells promotes vascular inflammation and accelerates atherosclerosis
Zhang X, Sun J, Canfrán-Duque A, Aryal B, Tellides G, Chang YJ, Suárez Y, Osborne TF, Fernández-Hernando C. Deficiency of histone lysine methyltransferase SETDB2 in hematopoietic cells promotes vascular inflammation and accelerates atherosclerosis. JCI Insight 2021, 6: e147984. PMID: 34003795, PMCID: PMC8262461, DOI: 10.1172/jci.insight.147984.Peer-Reviewed Original ResearchConceptsHematopoietic cellsHistone methylation/acetylationSingle-cell RNA-seq analysisMethylation/acetylationHistone H3 Lys9RNA-seq analysisProgression of atherosclerosisEpigenetic marksLysine methyltransferasesH3 Lys9Epigenetic modificationsDNA methylationNoncoding RNAsCell regulatorsSETDB2Vascular inflammationAtherosclerotic lesionsAtherosclerotic plaquesMyeloid cell recruitmentGenetic deletionLDLR knockout miceEnhanced expressionHepatic lipid metabolismMurine atherosclerotic lesionsGenesSingle cell epigenetic visualization assay
Kint S, Van Criekinge W, Vandekerckhove L, De Vos WH, Bomsztyk K, Krause DS, Denisenko O. Single cell epigenetic visualization assay. Nucleic Acids Research 2021, 49: e43-e43. PMID: 33511400, PMCID: PMC8096246, DOI: 10.1093/nar/gkab009.Peer-Reviewed Original ResearchMeSH Keywords5-MethylcytosineAcetylationCell LineDNA MethylationEarly Growth Response Protein 1Epigenesis, GeneticEpigenomicsFemaleGene Expression RegulationGene SilencingHistonesHIV-1HumansImage Processing, Computer-AssistedIn Situ Hybridization, FluorescenceProvirusesReal-Time Polymerase Chain ReactionRNA, Long NoncodingSingle-Cell AnalysisConceptsEpigenetic marksEpigenetic statusGene allelesFemale somatic cellsCurrent sequencing approachesGene of interestGene-specific oligonucleotidesQuantitative fluorescent readoutTranscription stateRNA FISHHuman cell linesSomatic cellsTranscription statusTarget genesSequencing approachH3K9ac levelsDifferent genesGenesIndividual cellsAntibody-conjugated alkaline phosphataseDNA oligosSingle cellsCell linesSame cellsFluorescent readout
2020
H3K4me1 Distribution Predicts Transcription State and Poising at Promoters
Bae S, Lesch BJ. H3K4me1 Distribution Predicts Transcription State and Poising at Promoters. Frontiers In Cell And Developmental Biology 2020, 8: 289. PMID: 32432110, PMCID: PMC7214686, DOI: 10.3389/fcell.2020.00289.Peer-Reviewed Original ResearchGerm cellsGene regulatory statesDifferent epigenetic marksTranscription start siteEmbryonic stem cellsMouse germ cellsGene expression levelsTranscription stateChromatin stateEpigenetic memoryEpigenetic stateEpigenetic marksLysine 4Histone H3Somatic cellsDistal enhancerStart siteActive promotersH3K4me1Transcriptional activityPromoter regionH3K4me3Possible rolePromoterCell typesMammalian ALKBH1 serves as an N6-mA demethylase of unpairing DNA
Zhang M, Yang S, Nelakanti R, Zhao W, Liu G, Li Z, Liu X, Wu T, Xiao A, Li H. Mammalian ALKBH1 serves as an N6-mA demethylase of unpairing DNA. Cell Research 2020, 30: 197-210. PMID: 32051560, PMCID: PMC7054317, DOI: 10.1038/s41422-019-0237-5.Peer-Reviewed Original ResearchConceptsN6-mAMammalian genomesStructure-based mutagenesis studiesBase unpairing regionsChromosome regulationDNA demethylasesStructural studiesEpigenetic marksDNA demethylaseMouse genomeEarly embryogenesisGenomic studiesBase flippingN6-methyladenineALKBH1Mutagenesis studiesFlipped baseGenomeProfiling studiesDNACatalytic centerDemethylaseActive regulationRegulationDemethylases
2019
Genomic sites hypersensitive to ultraviolet radiation
Premi S, Han L, Mehta S, Knight J, Zhao D, Palmatier MA, Kornacker K, Brash DE. Genomic sites hypersensitive to ultraviolet radiation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 24196-24205. PMID: 31723047, PMCID: PMC6883822, DOI: 10.1073/pnas.1907860116.Peer-Reviewed Original ResearchMeSH Keywords5' Untranslated RegionsCells, CulturedDNA DamageFibroblastsGene Expression RegulationGenome, HumanHigh-Throughput Nucleotide SequencingHumansMelanocytesMelanomaMutationPromoter Regions, GeneticProtein BiosynthesisPyrimidine DimersPyrimidine NucleotidesSkin NeoplasmsTOR Serine-Threonine KinasesUltraviolet RaysConceptsCyclobutane pyrimidine dimersETS family transcription factorsIndividual gene promotersFamily transcription factorsRNA-binding proteinPrimary human melanocytesSingle-base resolutionEpigenetic marksGenomic averageTranslation regulationGenomic sitesMotif locationsTranscription factorsCell physiologyGene promoterCancer driversGenomeHuman melanocytesCell typesTumor evolutionCell pathwaysRare mutationsUV targetPyrimidine dimersApurinic sitesTET enzymes augment AID expression via 5hmC modifications at the Aicda superenhancer
Lio C, Shukla V, Samaniego-Castruita D, Avalos E, Chakraborty A, Yue X, Schatz D, Rao A. TET enzymes augment AID expression via 5hmC modifications at the Aicda superenhancer. The Journal Of Immunology 2019, 202: 123.15-123.15. DOI: 10.4049/jimmunol.202.supp.123.15.Peer-Reviewed Original ResearchClass switch recombinationChromatin accessibilityTranscription factorsBasic region-leucine zipper (bZIP) transcription factorsBZIP transcription factorsZipper transcription factorAID expressionCytidine deaminase AIDExpression of AicdaTet-responsive elementEpigenetic marksTET enzymesEnhancer dynamicsAicda locusDNA demethylationGenomic regionsAicda expressionMurine B cellsEnhancer activitySwitch recombinationB cellsSuperenhancersTetExpressionCell activationTET enzymes augment activation-induced deaminase (AID) expression via 5-hydroxymethylcytosine modifications at the Aicda superenhancer
Lio CJ, Shukla V, Samaniego-Castruita D, González-Avalos E, Chakraborty A, Yue X, Schatz DG, Ay F, Rao A. TET enzymes augment activation-induced deaminase (AID) expression via 5-hydroxymethylcytosine modifications at the Aicda superenhancer. Science Immunology 2019, 4 PMID: 31028100, PMCID: PMC6599614, DOI: 10.1126/sciimmunol.aau7523.Peer-Reviewed Original ResearchMeSH Keywords5-MethylcytosineAnimalsB-LymphocytesBasic-Leucine Zipper Transcription FactorsCell DifferentiationCells, CulturedCytidine DeaminaseDioxygenasesDNA DemethylationDNA-Binding ProteinsGene Expression RegulationGenetic LociImmunoglobulin Class SwitchingLymphocyte ActivationMiceMice, TransgenicPrimary Cell CultureProto-Oncogene ProteinsResponse ElementsConceptsClass switch recombinationTranscription factorsChromatin accessibilityDNA demethylationBasic region-leucine zipper (bZIP) transcription factorsBZIP transcription factorsZipper transcription factorKey transcription factorEpigenetic marksTET enzymesEnhancer dynamicsGenomic regionsDeficient B cellsMurine B cellsEnhancer activityEnzyme essentialEnhancer elementsSwitch recombinationActivation-induced deaminase (AID) expressionAID expressionB cellsSuperenhancersTetDemethylationExpressionIntegrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma
Hlady RA, Sathyanarayan A, Thompson JJ, Zhou D, Wu Q, Pham K, Lee J, Liu C, Robertson KD. Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma. Hepatology 2019, 69: 639-652. PMID: 30136421, PMCID: PMC6351162, DOI: 10.1002/hep.30211.Peer-Reviewed Original ResearchConceptsHistone modification profilesPromoter/enhancer functionGenome-wide assessmentTranscription of genesEpigenetic marksHistone modificationsEpigenome deregulationEpigenetic regulatorsBioinformatics strategyEpigenetic mechanismsModification profilesEpigenetic underpinningsLiver epigenomeEpigenetic profilesEnhancer functionEpigenetic parametersEpigenomeDecrease cell viabilityDriver lociSignificant deregulationCancer initiationTranscriptionHuman cancersCancer cell linesCell lines
2018
N 6 -methyladenine DNA Modification in Glioblastoma
Xie Q, Wu TP, Gimple RC, Li Z, Prager BC, Wu Q, Yu Y, Wang P, Wang Y, Gorkin DU, Zhang C, Dowiak AV, Lin K, Zeng C, Sui Y, Kim LJY, Miller TE, Jiang L, Lee-Poturalski C, Huang Z, Fang X, Zhai K, Mack SC, Sander M, Bao S, Kerstetter-Fogle AE, Sloan AE, Xiao AZ, Rich JN. N 6 -methyladenine DNA Modification in Glioblastoma. Cell 2018, 175: 1228-1243.e20. PMID: 30392959, PMCID: PMC6433469, DOI: 10.1016/j.cell.2018.10.006.Peer-Reviewed Original ResearchMeSH KeywordsAdenineAdultAgedAlkB Homolog 1, Histone H2a DioxygenaseAnimalsAstrocytesBrain NeoplasmsCell HypoxiaChildDNA MethylationEpigenomicsFemaleGlioblastomaHeterochromatinHistonesHumansKaplan-Meier EstimateMaleMiceMiddle AgedNeoplastic Stem CellsRNA InterferenceRNA, Small InterferingTumor Suppressor Protein p53ConceptsDNA modificationsHeterochromatic histone modificationsRegulation of transcriptionNovel DNA modificationChromatin accessibilityEpigenetic marksHistone modificationsTranscriptional silencingEpigenetic modificationsGenetic driversHuman diseasesOncogenic pathwaysTumor cell proliferationPotential therapeutic targetALKBH1Cell proliferationTumor-bearing miceCritical roleTherapeutic targetDNAHuman tissuesHuman glioblastoma modelGlioblastoma modelGlioblastomaSilencingMIWI2 targets RNAs transcribed from piRNA‐dependent regions to drive DNA methylation in mouse prospermatogonia
Watanabe T, Cui X, Yuan Z, Qi H, Lin H. MIWI2 targets RNAs transcribed from piRNA‐dependent regions to drive DNA methylation in mouse prospermatogonia. The EMBO Journal 2018, 37: embj201695329. PMID: 30108053, PMCID: PMC6138435, DOI: 10.15252/embj.201695329.Peer-Reviewed Original ResearchConceptsDNA methylationRetrotransposon sequencesSmall RNAsArgonaute/Piwi proteinsPiwi protein MIWI2Suppressive epigenetic marksMouse prospermatogoniaChromatin statePIWI proteinsUnderlying molecular mechanismsDiverse organismsEpigenetic marksPiRNA clustersNascent RNAEpigenetic regulationTranslational regulationMIWI2RNA degradationRepeat sequencesGene expressionMolecular mechanismsTarget RNAMethylationRNAPiRNAs5-Hydroxymethylcytosine alterations in the human postmortem brains of autism spectrum disorder
Cheng Y, Li Z, Manupipatpong S, Lin L, Li X, Xu T, Jiang YH, Shu Q, Wu H, Jin P. 5-Hydroxymethylcytosine alterations in the human postmortem brains of autism spectrum disorder. Human Molecular Genetics 2018, 27: 2955-2964. PMID: 29790956, PMCID: PMC6097011, DOI: 10.1093/hmg/ddy193.Peer-Reviewed Original ResearchConceptsEssential epigenetic markGenome-wide distributionCell-cell communicationEpigenetic marksDisease association analysisPsychiatric genesGenomic DNAAssociation analysisDhMRsPathogenesis of ASDHuman postmortem brainGenesHeterogeneous phenotypesPostmortem cerebellumEarly development stagesCI functionDevelopment stagesUnderlying mechanismPostmortem brainsClear underlying mechanismDNAPhenotypeSignificant fractionGroup of syndromesLarge group
2017
Hoxa1 targets signaling pathways during neural differentiation of ES cells and mouse embryogenesis
De Kumar B, Parker H, Paulson A, Parrish M, Zeitlinger J, Krumlauf R. Hoxa1 targets signaling pathways during neural differentiation of ES cells and mouse embryogenesis. Developmental Biology 2017, 432: 151-164. PMID: 28982536, DOI: 10.1016/j.ydbio.2017.09.033.Peer-Reviewed Original ResearchConceptsTarget genesEar developmentES cellsDifferential gene expression analysisGenome-wide analysisNeural crest specificationFunctional rolePutative target genesTransgenic mouse embryosMajor signaling pathwaysNeural crest migrationRelevant target genesDown-stream componentsMouse ES cellsGene expression analysisImportant functional roleRetinoic acidEvolutionary conservationEpigenetic marksHox cofactorsMutant phenotypeMouse embryogenesisNearby genesNeural fateMouse development
2016
Dnmt1 regulates the myogenic lineage specification of muscle stem cells
Liu R, Kim KY, Jung YW, Park IH. Dnmt1 regulates the myogenic lineage specification of muscle stem cells. Scientific Reports 2016, 6: 35355. PMID: 27752090, PMCID: PMC5082760, DOI: 10.1038/srep35355.Peer-Reviewed Original ResearchConceptsImportant epigenetic markKnockout mouse approachesDNA methylation patternsMuscle stem cellsDaughter DNA strandsDNMT1 regulationEpigenetic marksLineage specificationCellular identityDNA methylationMethylation patternsDNMT1 depletionMyogenic genesMyogenic differentiationLineage fidelityNegative regulatorGene expressionDNMT1Osteogenic lineageFunctional roleFunctional consequencesMouse approachDNA strandsId-1Stem cells
2015
Roles for Histone Acetylation in Regulation of Telomere Elongation and Two‐cell State in Mouse ES Cells
Dan J, Yang J, Liu Y, Xiao A, Liu L. Roles for Histone Acetylation in Regulation of Telomere Elongation and Two‐cell State in Mouse ES Cells. Journal Of Cellular Physiology 2015, 230: 2337-2344. PMID: 25752831, PMCID: PMC4711819, DOI: 10.1002/jcp.24980.Peer-Reviewed Original ResearchConceptsHistone acetylation levelsES cellsHistone acetylationHistone hypoacetylationHistone hyperacetylationTelomere elongationAcetylation levelsWild-type ES cellsRepressive DNA methylationRepressive epigenetic marksTelomere length maintenanceTwo-cell stateMouse ES cellsMammalian telomeresHeterochromatic stateEpigenetic marksHistone methylationLength maintenanceEpigenetic modificationsDNA methylationTelomere recombinationHistone deacetylase inhibitorsSpecific genesGene expressionTelomeresEpigenetic Mechanisms of Serotonin Signaling
Holloway T, González-Maeso J. Epigenetic Mechanisms of Serotonin Signaling. ACS Chemical Neuroscience 2015, 6: 1099-1109. PMID: 25734378, PMCID: PMC4838281, DOI: 10.1021/acschemneuro.5b00033.Peer-Reviewed Original ResearchConceptsEpigenetic mechanismsHeritable epigenetic modificationsNumerous physiological responsesSignal transduction mechanismsReceptor-dependent signalingEpigenetic marksHistone modificationsGene functionEpigenetic modificationsDNA methylationCellular phenotypesGene expressionTransduction mechanismsPhysiological responsesFundamental roleDiverse setComplex interactionsCentral nervous systemRecent advancesFundamental questionsIntense researchMethylationNervous systemSignalingMechanism
2014
Histone Variant H2A.X Deposition Pattern Serves as a Functional Epigenetic Mark for Distinguishing the Developmental Potentials of iPSCs
Wu T, Liu Y, Wen D, Tseng Z, Tahmasian M, Zhong M, Rafii S, Stadtfeld M, Hochedlinger K, Xiao A. Histone Variant H2A.X Deposition Pattern Serves as a Functional Epigenetic Mark for Distinguishing the Developmental Potentials of iPSCs. Cell Stem Cell 2014, 15: 281-294. PMID: 25192463, DOI: 10.1016/j.stem.2014.06.004.Peer-Reviewed Original ResearchConceptsEmbryonic stem cellsLineage gene expressionHistone variant H2A.XCell lineage commitmentDevelopmental potentialMouse iPSC linesIPSC linesPluripotent stem cell (iPSC) technologyEpigenetic marksLineage genesEpigenetic mechanismsLineage commitmentLineage differentiationExtraembryonic differentiationStem cell technologyGene expressionTetraploid complementationIPSC clonesIPSC qualityStem cellsFunctional markersH2A.XDifferentiationIPSCsComplementation
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