2024
Dexamethasone Targets E2F4 to Induce Erythroid Progenitor Renewal
Papoin J, Schulz V, Khan F, Barnes B, Lipton J, Steiner L, Narla M, Gallagher P, Blanc L. Dexamethasone Targets E2F4 to Induce Erythroid Progenitor Renewal. Blood 2024, 144: 1076. DOI: 10.1182/blood-2024-211687.Peer-Reviewed Original ResearchDiamond-Blackfan anemiaCD34+ cellsErythroid progenitorsSteroid responsivenessExpression of E2F4Peripheral bloodBone marrowE2F4 expressionDEX treatmentCultured CD34+ cellsInherited bone marrow failure syndromeMechanisms of steroid responseSide effectsBone marrow failure syndromesDiamond-Blackfan anemia patientsBone marrow erythroid progenitorsIncreased expressionMechanisms of corticosteroid actionAssociated with side effectsIncreased risk of infectionMarrow failure syndromesResponse to steroidsGene promoterSerum-free culture systemMarrow erythroid progenitorsLiver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency
Hong S, Yu X, Zhu Y, Chen Y. Liver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency. Chemico-Biological Interactions 2024, 398: 111093. PMID: 38830566, PMCID: PMC11223951, DOI: 10.1016/j.cbi.2024.111093.Peer-Reviewed Original ResearchS-adenosyl methionineGene promoterArray-based DNA methylation profilingPeripheral blood cellsFatty liver diseaseDNA methylation profilesDNA methylation statusMethyl donor S-adenosyl methionineGene promoter regionFunctional enrichment analysisMethylation enrichmentMouse modelOxidative stressLiver epigenomeEpigenomic changesIn vivo interplayMethylation profilesPromoter regionEpigenetic regulationEpigenomic signaturesEpigenetic mechanismsLipid homeostasisBlood cellsEnrichment analysisCellular survival
2022
Better late than never: A unique strategy for late gene transcription in the beta- and gammaherpesviruses
Dremel S, Didychuk A. Better late than never: A unique strategy for late gene transcription in the beta- and gammaherpesviruses. Seminars In Cell And Developmental Biology 2022, 146: 57-69. PMID: 36535877, PMCID: PMC10101908, DOI: 10.1016/j.semcdb.2022.12.001.Peer-Reviewed Original ResearchConceptsViral transcriptional activityViral preinitiation complexPol IITranscription of late genesGene transcriptionCellular RNA polymerase IITATA-binding proteinRNA polymerase IIModified TATA boxCis-acting elementsSubfamily of herpesvirusesPolymerase IITATA boxPreinitiation complexConsensus sequenceLate genesTranscriptional activityGene promoterLytic replicationGenesTemporal cascadeTranscriptionViral mimicPolPromoter
2021
BACH1, the master regulator of oxidative stress, has a dual effect on CFTR expression
NandyMazumdar M, Paranjapye A, Browne J, Yin S, Leir SH, Harris A. BACH1, the master regulator of oxidative stress, has a dual effect on CFTR expression. Biochemical Journal 2021, 478: 3741-3756. PMID: 34605540, PMCID: PMC8589331, DOI: 10.1042/bcj20210252.Peer-Reviewed Original ResearchMeSH KeywordsBasic-Leucine Zipper Transcription FactorsCell Line, TumorCell ProliferationCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsGene Expression ProfilingGene Expression RegulationGlutamate-Cysteine LigaseGlutathioneHeme Oxygenase-1HumansHydrogen PeroxideNF-E2-Related Factor 2Oxidative StressOxygenPromoter Regions, GeneticRNA, Small InterferingSignal TransductionConceptsCis-regulatory elementsTranscription factorsCFTR expressionMaster regulatorHigher-order chromatin structureOrder chromatin structureMultiple cis-regulatory elementsFine-tune expressionSpecific transcription factorsCystic fibrosis transmembrane conductance regulator (CFTR) geneCFTR gene expressionCell-specific expressionTransmembrane conductance regulator geneOxidative stressArchitectural proteinsChromatin structureLocus architectureTune expressionBTB domainCNC homolog 1SiRNA screenRegulator geneGene promoterEnvironmental cuesPhysiological oxygenTAZ inhibits glucocorticoid receptor and coordinates hepatic glucose homeostasis in normal physiological states
Xu S, Liu Y, Hu R, Wang M, Stöhr O, Xiong Y, Chen L, Kang H, Zheng L, Cai S, He L, Wang C, Copps K, White M, Miao J. TAZ inhibits glucocorticoid receptor and coordinates hepatic glucose homeostasis in normal physiological states. ELife 2021, 10: e57462. PMID: 34622775, PMCID: PMC8555985, DOI: 10.7554/elife.57462.Peer-Reviewed Original ResearchConceptsGluconeogenic gene promotersBinding of GRGene promoterGlucocorticoid receptorGlucose homeostasisLigand-binding domainGlucose productionOverexpression of TAZHepatic glucose homeostasisWW domainsBlood glucose concentrationPhysiological fastingGluconeogenic genesGR response elementResponse elementNovel roleTAZNormal physiological stateGR transactivationPhysiological statePromoterMouse liverPericentral hepatocytesPathological statesGlucose concentrationTNF stimulation primarily modulates transcriptional burst size of NF‐κB‐regulated genes
Bass VL, Wong VC, Bullock ME, Gaudet S, Miller‐Jensen K. TNF stimulation primarily modulates transcriptional burst size of NF‐κB‐regulated genes. Molecular Systems Biology 2021, 17: msb202010127. PMID: 34288498, PMCID: PMC8290835, DOI: 10.15252/msb.202010127.Peer-Reviewed Original ResearchConceptsNF-κB-regulated inflammatory genesGene expression noiseOpen chromatin environmentTranscriptional burst sizeNF-κB target genesNF-κB-regulated genesHistone 3 acetylationChromatin environmentTranscription factor NF-κBTranscriptional noiseExpression noiseTranscriptional burstingTranscript distributionFactor NF-κBGene promoterSubset of cellsIntercellular heterogeneityTNF stimulationCell heterogeneityGenesTNF protein expressionTNF activationProtein expressionTranscriptionBurst size
2020
Assessment of tumor suppressor promoter methylation in healthy individuals
Poduval D, Ognedal E, Sichmanova Z, Valen E, Iversen G, Minsaas L, Lønning P, Knappskog S. Assessment of tumor suppressor promoter methylation in healthy individuals. Clinical Epigenetics 2020, 12: 131. PMID: 32859265, PMCID: PMC7455917, DOI: 10.1186/s13148-020-00920-7.Peer-Reviewed Original ResearchConceptsPromoter methylation statusTumor suppressor geneGene promoterCancer riskSuppressor genePromoter methylation of BRCA1Healthy individualsRisk factorsTumor suppressorMethylation statusTumor suppressor gene promotersMethylation of BRCA1Base-pair resolutionHealthy postmenopausal womenColon cancer riskCancer risk factorsNGS-based approachMethylation landscapePostmenopausal womenDifferential methylationTarget coverageGermline mutationsMethylation profilesPromoter methylationMethylated genesTelomerase Reverse Transcriptase Promoter Mutations Identify a Genomically Defined and Highly Aggressive Human Pleural Mesothelioma Subgroup
Pirker C, Bilecz A, Grusch M, Mohr T, Heidenreich B, Laszlo V, Stockhammer P, Lötsch-Gojo D, Gojo J, Gabler L, Spiegl-Kreinecker S, Dome B, Steindl A, Klikovits T, Hoda MA, Jakopovic M, Samarzija M, Mohorcic K, Kern I, Kiesel B, Brcic L, Oberndorfer F, Müllauer L, Klepetko W, Schmidt WM, Kumar R, Hegedus B, Berger W. Telomerase Reverse Transcriptase Promoter Mutations Identify a Genomically Defined and Highly Aggressive Human Pleural Mesothelioma Subgroup. Clinical Cancer Research 2020, 26: 3819-3830. PMID: 32317288, DOI: 10.1158/1078-0432.ccr-19-3573.Peer-Reviewed Original ResearchMeSH KeywordsAgedBiomarkers, TumorCell Line, TumorCell SurvivalCell Transformation, NeoplasticComparative Genomic HybridizationDisease ProgressionDNA Mutational AnalysisExome SequencingFemaleGene Expression ProfilingHumansKaplan-Meier EstimateMaleMesothelioma, MalignantMiddle AgedMutationPleuraPleural NeoplasmsPrognosisPromoter Regions, GeneticRetrospective StudiesTelomeraseConceptsHuman malignant pleural mesotheliomaMalignant pleural mesotheliomaPromoter mutationsLuciferase promoter assaysGene expression profilingImmortalized cell linesArray comparative genomic hybridizationComparative genomic hybridizationWild-type samplesGene promoterExpression profilingPromoter assaysPromoter activityTelomerase reverse transcriptase gene promoterCell immortalizationMolecular mechanismsMutations/deletionsMalignant transformation processMPM casesSpecific mutation patternsGenomic hybridizationTelomerase activityGenomic alteration patternsMutationsChromosomal alterationsConserved CxnC Motifs in Kaposi’s Sarcoma-Associated Herpesvirus ORF66 Are Required for Viral Late Gene Expression and Are Essential for Its Interaction with ORF34
Didychuk A, Castañeda A, Kushnir L, Huang C, Glaunsinger B. Conserved CxnC Motifs in Kaposi’s Sarcoma-Associated Herpesvirus ORF66 Are Required for Viral Late Gene Expression and Are Essential for Its Interaction with ORF34. Journal Of Virology 2020, 94: 10.1128/jvi.01299-19. PMID: 31578296, PMCID: PMC6955276, DOI: 10.1128/jvi.01299-19.Peer-Reviewed Original ResearchConceptsViral preinitiation complexKaposi's sarcoma-associated herpesvirusC-terminal domainCysteine-rich motifHost transcription machineryPreinitiation complexGene promoterTranscription machinerySarcoma-associated herpesvirusLate genesGene transcriptionViral late gene expressionZinc finger motifsLate gene transcriptionSequence-specific bindingTranscriptional regulatory activityLate gene expressionLate gene promotersInfectious virionsProduction of capsid proteinsRelease of infectious virionsViral replication cycleFinger motifPromoter occupancySequence-specific
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 sites
2018
PTEN Regulates Non-Homologous End Joining by Epigenetic Induction of NHEJ1/XLF
Sulkowski PL, Scanlon SE, Oeck S, Glazer PM. PTEN Regulates Non-Homologous End Joining by Epigenetic Induction of NHEJ1/XLF. Molecular Cancer Research 2018, 16: molcanres.0581.2017. PMID: 29739874, PMCID: PMC6072556, DOI: 10.1158/1541-7786.mcr-17-0581.Peer-Reviewed Original ResearchConceptsDNA double-strand breaksKey DNA repair pathwaysCytotoxic DNA lesionsXRCC4-like factorPatient-derived melanomasDNA repair pathwaysDouble-strand breaksNovel regulatory roleTumor suppressor geneSuppression of PTENHistone acetyltransferasesDSB repairGenomic analysisNHEJ defectsNonhomologous endRepair pathwaysGene promoterNovel functionRegulatory acetylationNHEJ deficiencyDNA lesionsRegulatory roleSuppressor geneNHEJ DSB repairNHEJTumor innate immunity primed by specific interferon-stimulated endogenous retroviruses
Cañadas I, Thummalapalli R, Kim J, Kitajima S, Jenkins R, Christensen C, Campisi M, Kuang Y, Zhang Y, Gjini E, Zhang G, Tian T, Sen D, Miao D, Imamura Y, Thai T, Piel B, Terai H, Aref A, Hagan T, Koyama S, Watanabe M, Baba H, Adeni A, Lydon C, Tamayo P, Wei Z, Herlyn M, Barbie T, Uppaluri R, Sholl L, Sicinska E, Sands J, Rodig S, Wong K, Paweletz C, Watanabe H, Barbie D. Tumor innate immunity primed by specific interferon-stimulated endogenous retroviruses. Nature Medicine 2018, 24: 1143-1150. PMID: 30038220, PMCID: PMC6082722, DOI: 10.1038/s41591-018-0116-5.Peer-Reviewed Original ResearchConceptsInnate immune signalingSmall cell lung cancerEndogenous retrovirusesCell lung cancerPro-tumorigenic cytokinesImmune signalingAnalysis of cell linesCancer immunotherapyMesenchymal cell stateIFN-gTumor subpopulationsLung cancerLong terminal repeatHuman tumorsSPARC expressionMesenchymal markersTumorBi-directional transcriptionChromatin-modifying enzymesSTAT1 SignalingCell linesCancerInnate immunityInducible SPARCS expressionGene promoter
2017
Common developmental genome deprogramming in schizophrenia — Role of Integrative Nuclear FGFR1 Signaling (INFS)
Narla S, Lee Y, Benson C, Sarder P, Brennand K, Stachowiak E, Stachowiak M. Common developmental genome deprogramming in schizophrenia — Role of Integrative Nuclear FGFR1 Signaling (INFS). Schizophrenia Research 2017, 185: 17-32. PMID: 28094170, PMCID: PMC5507209, DOI: 10.1016/j.schres.2016.12.012.Peer-Reviewed Original ResearchMeSH KeywordsAdultCell DifferentiationCells, CulturedFemaleGene Expression Regulation, DevelopmentalGene Regulatory NetworksGenomeGenomicsHumansInduced Pluripotent Stem CellsMaleMicroRNAsModels, BiologicalMutationReceptor, Fibroblast Growth Factor, Type 1Receptor, Notch1SchizophreniaSignal TransductionTranscriptomeYoung AdultConceptsMRNA networkMajor developmental pathwaysIntegrative nuclear FGFR1MiRNA-mRNA networkHuman gene promotersCommon developmental genomesMiRNA genesMiRNA transcriptomeGene networksUpregulated genesGene promoterNuclear FGFR1Genomic etiologyGene dysregulationDisease ontogenyNuclear formGlobal dysregulationDevelopmental pathwaysGenesNeuron formationDistinct pathwaysConcerted actionPotential therapeutic targetTranscriptomeGenome
2016
CTCF and CohesinSA-1 Mark Active Promoters and Boundaries of Repressive Chromatin Domains in Primary Human Erythroid Cells
Steiner LA, Schulz V, Makismova Y, Lezon-Geyda K, Gallagher PG. CTCF and CohesinSA-1 Mark Active Promoters and Boundaries of Repressive Chromatin Domains in Primary Human Erythroid Cells. PLOS ONE 2016, 11: e0155378. PMID: 27219007, PMCID: PMC4878738, DOI: 10.1371/journal.pone.0155378.Peer-Reviewed Original ResearchMeSH KeywordsBinding SitesCCCTC-Binding FactorCells, CulturedChromatinChromatin ImmunoprecipitationErythroid CellsErythropoiesisGene Expression ProfilingHematopoietic Stem CellsHigh-Throughput Nucleotide SequencingHumansK562 CellsNuclear ProteinsPromoter Regions, GeneticProtein BindingProtein Interaction MapsRepressor ProteinsSequence Analysis, RNAConceptsPrimary human erythroid cellsRepressive chromatin domainsHuman erythroid cellsChromatin domainsErythroid cellsChromatin architectureGene promoterGene expressionPrimary human hematopoietic stemCell type-specific mannerCritical cellular processesSites of CTCFGenome-wide dataHigh-throughput sequencingMRNA transcriptome analysisHuman hematopoietic stemRepressive chromatinCohesin sitesProtein occupancyInsulator functionRepressive domainsTranscriptional regulationCTCF sitesDomain architectureRelated gene expressionMetabolic Regulation of Gene Expression by Histone Lysine β-Hydroxybutyrylation
Xie Z, Zhang D, Chung D, Tang Z, Huang H, Dai L, Qi S, Li J, Colak G, Chen Y, Xia C, Peng C, Ruan H, Kirkey M, Wang D, Jensen LM, Kwon OK, Lee S, Pletcher SD, Tan M, Lombard DB, White KP, Zhao H, Li J, Roeder RG, Yang X, Zhao Y. Metabolic Regulation of Gene Expression by Histone Lysine β-Hydroxybutyrylation. Molecular Cell 2016, 62: 194-206. PMID: 27105115, PMCID: PMC5540445, DOI: 10.1016/j.molcel.2016.03.036.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesChromatin Assembly and DisassemblyDiabetic KetoacidosisDisease Models, AnimalEnergy MetabolismEpigenesis, GeneticFatty AcidsGene Expression RegulationGlucoseHEK293 CellsHistonesHumansHydroxybutyratesLiverLysineMice, Inbred C57BLPromoter Regions, GeneticProtein Processing, Post-TranslationalStarvationStreptozocinConceptsLysine β-hydroxybutyrylationΒ-hydroxybutyrylationActive gene promotersEpigenetic regulatory marksRNA-seq analysisHistone acetylation sitesChromatin regulationHistone marksChIP-seqAcetylation sitesProtein modificationGene promoterRegulatory marksDiverse functionsGene expressionMetabolic regulationMetabolic pathwaysCultured cellsPathophysiological statesRegulationExpressionNew avenuesKbhbMarksGenesGenome-Wide Studies Reveal that H3K4me3 Modification in Bivalent Genes Is Dynamically Regulated during the Pluripotent Cell Cycle and Stabilized upon Differentiation
Grandy R, Whitfield T, Wu H, Fitzgerald M, VanOudenhove J, Zaidi S, Montecino M, Lian J, van Wijnen A, Stein J, Stein G. Genome-Wide Studies Reveal that H3K4me3 Modification in Bivalent Genes Is Dynamically Regulated during the Pluripotent Cell Cycle and Stabilized upon Differentiation. Molecular And Cellular Biology 2016, 36: 615-627. PMID: 26644406, PMCID: PMC4751694, DOI: 10.1128/mcb.00877-15.Peer-Reviewed Original ResearchMeSH KeywordsCell CycleCell DifferentiationCell LineChromatinDNA MethylationDNA-Binding ProteinsEpigenesis, GeneticGene Expression Regulation, DevelopmentalGenome-Wide Association StudyHistone-Lysine N-MethyltransferaseHistonesHuman Embryonic Stem CellsHumansMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsConceptsHuman embryonic stem cellsBivalent genesHistone modificationsCell cycleCell cycle-dependent fashionPluripotent cell cycleRepressive histone modificationsPosttranslational histone modificationsH3K4me3/H3K27me3Maintenance of pluripotencyHistone modification signaturesMethylation/demethylationLevels of H3K4me3Embryonic stem cellsInduction of differentiationChromatin regulationChromatin modifiersEpigenetic landscapeCell identityModification signaturesLineage commitmentGenomic enrichmentGene promoterProgeny cellsMolecular mechanisms
2015
DNA Methylation Regulates the Differential Expression of CX3CR1 on Human IL-7Rαlow and IL-7Rαhigh Effector Memory CD8+ T Cells with Distinct Migratory Capacities to the Fractalkine
Shin MS, You S, Kang Y, Lee N, Yoo SA, Park K, Kang KS, Kim SH, Mohanty S, Shaw AC, Montgomery RR, Hwang D, Kang I. DNA Methylation Regulates the Differential Expression of CX3CR1 on Human IL-7Rαlow and IL-7Rαhigh Effector Memory CD8+ T Cells with Distinct Migratory Capacities to the Fractalkine. The Journal Of Immunology 2015, 195: 2861-2869. PMID: 26276874, PMCID: PMC4561204, DOI: 10.4049/jimmunol.1500877.Peer-Reviewed Original ResearchConceptsDNA methylationDifferential expressionGene expressionCellular traitsEpigenetic mechanismsGene promoterGenome-wide DNA methylationDistinct traitsDNA methylation statusIndividual gene expressionMigratory capacityAutocrine amplification loopImportant biological outcomesPotential biological implicationsMammalian cellsMethylationMethylation statusAmplification loopBiological outcomesTraitsBiological implicationsPromoterEffector memoryExpressionT cellsALDH1B1 Is Crucial for Colon Tumorigenesis by Modulating Wnt/β-Catenin, Notch and PI3K/Akt Signaling Pathways
Singh S, Arcaroli J, Chen Y, Thompson DC, Messersmith W, Jimeno A, Vasiliou V. ALDH1B1 Is Crucial for Colon Tumorigenesis by Modulating Wnt/β-Catenin, Notch and PI3K/Akt Signaling Pathways. PLOS ONE 2015, 10: e0121648. PMID: 25950950, PMCID: PMC4423958, DOI: 10.1371/journal.pone.0121648.Peer-Reviewed Original ResearchMeSH KeywordsAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyAldehyde Dehydrogenase, MitochondrialAnimalsCell Line, TumorColonic NeoplasmsGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansMiceNeoplasm TransplantationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, NotchRNA, Small InterferingSignal TransductionSpheroids, CellularWnt Signaling PathwayConceptsWnt/β-cateninPI3K/AktΒ-cateninSW-480 cellsColon cancer tumorigenesisWnt reporter activityPattern of expressionPI3K/Akt Signaling PathwayDual-luciferase reporterPI3K/Akt signal pathwayAkt Signaling PathwayTranscription factorsAkt signal pathwayNude mouse xenograft tumor modelColon tumorigenesisGene promoterColon adenocarcinoma cell lineMouse xenograft tumor modelALDH1B1 expressionAldehyde dehydrogenase 1B1Signaling pathwaysLuciferase reporterSize of spheroidsAdenocarcinoma cell lineXenograft tumor model
2014
Epigenetic regulation of OPA1 sensitizes hepatocellular carcinoma to sorafenib‐induced apoptosis (59.1)
Puszyk W, Dong H, Zhao F, Shisgal P, Cabrera R, Neslon D, Liu C. Epigenetic regulation of OPA1 sensitizes hepatocellular carcinoma to sorafenib‐induced apoptosis (59.1). The FASEB Journal 2014, 28 DOI: 10.1096/fasebj.28.1_supplement.59.1.Peer-Reviewed Original ResearchDNA methylationHepatocellular carcinomaEpigenetic regulationProtein OPA1HCC cellsMitochondrial fragmentationGene promoterC releaseEpigenetic analysisXenograft tumor growthEpigenetic markersSorafenib-induced apoptosisAkt pathwayOPA1HCC xenograft tumor growthHepatocellular carcinoma cellsNovel therapeutic targetExpression levelsTumorigenesis of HCCIdentification of patientsPathogenesis of HCCOPA1 knockdownApoptosisPrimary hepatocytesSensitivity of HCCA new paradigm for transcription factor TFIIB functionality
Gelev V, Zabolotny JM, Lange M, Hiromura M, Yoo SW, Orlando JS, Kushnir A, Horikoshi N, Paquet E, Bachvarov D, Schaffer PA, Usheva A. A new paradigm for transcription factor TFIIB functionality. Scientific Reports 2014, 4: 3664. PMID: 24441171, PMCID: PMC3895905, DOI: 10.1038/srep03664.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnimalsBinding SitesCell CycleCell LineDatasets as TopicGene ExpressionGene Expression ProfilingGene Expression RegulationGene Expression Regulation, ViralGene Knockdown TechniquesGene SilencingGenes, LethalGenome, HumanHerpesvirus 1, HumanHumansOrgan SpecificityProtein BindingRNA Polymerase IITranscription Factor TFIIBTranscription Initiation SiteTranscription, GeneticTranscriptomeConceptsTranscription initiationGene expressionGeneral transcription factor TFIIBTranscription factor TFIIBRNA polymerase IIGlobal gene expressionHuman gene expressionPolymerase IIGene transcriptionBioinformatics analysisBioinformatics studiesGene promoterHuman promotersCellular functionalityMitotic chromatidsTFIIBCell linesTranscriptionPromoterExpression
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