2024
X-linked deletion of Crossfirre, Firre, and Dxz4 in vivo uncovers diverse phenotypes and combinatorial effects on autosomes
Hasenbein T, Hoelzl S, Smith Z, Gerhardinger C, Gonner M, Aguilar-Pimentel A, Amarie O, Becker L, Calzada-Wack J, Dragano N, da Silva-Buttkus P, Garrett L, Hölter S, Kraiger M, Östereicher M, Rathkolb B, Sanz-Moreno A, Spielmann N, Wurst W, Gailus-Durner V, Fuchs H, Hrabě de Angelis M, Meissner A, Engelhardt S, Rinn J, Andergassen D. X-linked deletion of Crossfirre, Firre, and Dxz4 in vivo uncovers diverse phenotypes and combinatorial effects on autosomes. Nature Communications 2024, 15: 10631. PMID: 39638999, PMCID: PMC11621363, DOI: 10.1038/s41467-024-54673-5.Peer-Reviewed Original ResearchConceptsAutosomal gene regulationRegions genome-wideAllele-specific analysisSex-specific lociLoci in vivoX-linked genesRandom X-chromosome inactivationX-chromosome inactivationSex-specific phenotypesFirre locusGenome-wideIn vivo roleChromatin structureGene regulationX chromosomeEpigenetic featuresDXZ4Epigenetic profilesKnockout studiesLociDiverse phenotypesLncRNA FIRREFunctional roleCombinatorial effectsFIRREDistinct epigenetic and transcriptional profiles of Epstein-Barr virus-positive and negative primary CNS lymphomas
Hai L, Friedel D, Hinz F, Hoffmann D, Doubrovinskaia S, Rohdjess H, Weidenauer K, Denisova E, Scheffler G, Kessler T, Kourtesakis A, Herold-Mende C, Henegariu O, Baehring J, Dietrich J, Brors B, Wick W, Sahm F, Kaulen L. Distinct epigenetic and transcriptional profiles of Epstein-Barr virus-positive and negative primary CNS lymphomas. Neuro-Oncology 2024, 27: 979-992. PMID: 39575767, PMCID: PMC12083237, DOI: 10.1093/neuonc/noae251.Peer-Reviewed Original ResearchPrimary CNS lymphomaEpstein-Barr virusB cell receptorCNS lymphomaTargeted therapyEpigenetic profilesB cellsDiffuse large B-cell lymphomaLarge B-cell lymphomaB-cell lymphomaPromoter region hypermethylationEBV oncogeneEBV lymphomasEBV- tumorsEPIC methylation arrayWnt/beta-catenin signalingEBV diseaseBiological subtypesUnsupervised cluster analysisInterleukin-10Promoter methylationLymphomaSyk kinase activityBrain tumorsMutational landscape
2023
Babesia duncani multi-omics identifies virulence factors and drug targets
Singh P, Lonardi S, Liang Q, Vydyam P, Khabirova E, Fang T, Gihaz S, Thekkiniath J, Munshi M, Abel S, Ciampossin L, Batugedara G, Gupta M, Lu X, Lenz T, Chakravarty S, Cornillot E, Hu Y, Ma W, Gonzalez L, Sánchez S, Estrada K, Sánchez-Flores A, Montero E, Harb O, Le Roch K, Mamoun C. Babesia duncani multi-omics identifies virulence factors and drug targets. Nature Microbiology 2023, 8: 845-859. PMID: 37055610, PMCID: PMC10159843, DOI: 10.1038/s41564-023-01360-8.Peer-Reviewed Original ResearchConceptsDrug targetsVirulence factorsCandidate virulence factorsRNA-seq dataIntraerythrocytic life cycleAttractive drug targetB. duncaniNuclear genomeGenome annotationApicomplexan parasitesApicomplexan pathogensEpigenetic profilesEpigenetic analysisParasite metabolismMalaria-like diseaseHuman erythrocytesLife cycle stagesBabesia speciesGenomeMetabolic requirementsCycle stagesLife cycleBiologySmall moleculesPotent inhibitor
2021
Prenatal Δ9-Tetrahydrocannabinol Exposure in Males Leads to Motivational Disturbances Related to Striatal Epigenetic Dysregulation
Ellis R, Bara A, Vargas C, Frick A, Loh E, Landry J, Uzamere T, Callens J, Martin Q, Rajarajan P, Brennand K, Ramakrishnan A, Shen L, Szutorisz H, Hurd Y. Prenatal Δ9-Tetrahydrocannabinol Exposure in Males Leads to Motivational Disturbances Related to Striatal Epigenetic Dysregulation. Biological Psychiatry 2021, 92: 127-138. PMID: 34895699, PMCID: PMC8957623, DOI: 10.1016/j.biopsych.2021.09.017.Peer-Reviewed Original ResearchConceptsEpigenetic dysregulationNucleus accumbensSimilar transcriptional alterationsExpression of Kmt2aComparison of RNACellular chromatinTranscriptome datasetsPrenatal THC exposureEpigenetic signaturesEpigenetic profilesAdult male offspringHuman major depressive disorderRNA sequencingTranscriptional alterationsSequencing approachPrenatal cannabis exposureMajor depressive disorderΔ9-tetrahydrocannabinol exposurePrincipal psychoactive componentMolecular signaturesUnbiased sequencing approachRat offspringUtero exposureTHC exposureCannabis exposure
2020
Regulatory T Cell-Specific Epigenomic Region Variants Are a Key Determinant of Susceptibility to Common Autoimmune Diseases
Ohkura N, Yasumizu Y, Kitagawa Y, Tanaka A, Nakamura Y, Motooka D, Nakamura S, Okada Y, Sakaguchi S. Regulatory T Cell-Specific Epigenomic Region Variants Are a Key Determinant of Susceptibility to Common Autoimmune Diseases. Immunity 2020, 52: 1119-1132.e4. PMID: 32362325, DOI: 10.1016/j.immuni.2020.04.006.Peer-Reviewed Original ResearchMeSH KeywordsAutoimmune DiseasesBiomarkersCell DifferentiationComputational BiologyCpG IslandsDNA MethylationEpigenesis, GeneticEpigenomicsGene Expression ProfilingGenetic Predisposition to DiseaseGenetic VariationHumansImmunophenotypingPolymorphism, Single NucleotideT-Lymphocyte SubsetsT-Lymphocytes, RegulatoryTranscriptomeConceptsCommon autoimmune diseasesSingle-nucleotide polymorphismsSusceptibility to common autoimmune diseasesCell-specific gene transcriptionGenome-wide epigenetic profilingAssociated with common autoimmune diseasesAssociated with transcriptionPolygenic autoimmune diseasesTreg cellsDemethylated regionCpG hypomethylationSuper-enhancersAutoimmune diseasesDeterminants of susceptibilityEpigenetic modificationsEpigenetic profilesGene transcriptionEpigenetic changesTreg-cell-specific demethylated regionNaive Treg cellsNatural Treg cellsRegional variantsTranscriptionActive stateCells
2019
Integrating 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 linesThe putative Neuronatin imprint control region is an enhancer that also regulates the Blcap gene
Thamban T, Sowpati D, Pai V, Nithianandam V, Abe T, Shioi G, Mishra R, Khosla S. The putative Neuronatin imprint control region is an enhancer that also regulates the Blcap gene. Epigenomics 2019, 11: 251-266. PMID: 30672333, DOI: 10.2217/epi-2018-0060.Peer-Reviewed Original ResearchConceptsImprinting control regionControl regionAllele-specific DNA methylationNnat expressionActive paternal alleleAbstractText Label="MATERIALS &AbstractText Label="AIM">Histone modificationsTranscriptional regulationPaternal alleleDNA methylationIntronRegulatory potentialEpigenetic profilesBLCAPNnatGenesExpressionHistoneAllelesDeletionTranscriptionNeuronatinMiceDomain
2015
The Molecular Taxonomy of Primary Prostate Cancer
Network T, Abeshouse A, Ahn J, Akbani R, Ally A, Amin S, Andry C, Annala M, Aprikian A, Armenia J, Arora A, Auman J, Balasundaram M, Balu S, Barbieri C, Bauer T, Benz C, Bergeron A, Beroukhim R, Berrios M, Bivol A, Bodenheimer T, Boice L, Bootwalla M, dos Reis R, Boutros P, Bowen J, Bowlby R, Boyd J, Bradley R, Breggia A, Brimo F, Bristow C, Brooks D, Broom B, Bryce A, Bubley G, Burks E, Butterfield Y, Button M, Canes D, Carlotti C, Carlsen R, Carmel M, Carroll P, Carter S, Cartun R, Carver B, Chan J, Chang M, Chen Y, Cherniack A, Chevalier S, Chin L, Cho J, Chu A, Chuah E, Chudamani S, Cibulskis K, Ciriello G, Clarke A, Cooperberg M, Corcoran N, Costello A, Cowan J, Crain D, Curley E, David K, Demchok J, Demichelis F, Dhalla N, Dhir R, Doueik A, Drake B, Dvinge H, Dyakova N, Felau I, Ferguson M, Frazer S, Freedland S, Fu Y, Gabriel S, Gao J, Gardner J, Gastier-Foster J, Gehlenborg N, Gerken M, Gerstein M, Getz G, Godwin A, Gopalan A, Graefen M, Graim K, Gribbin T, Guin R, Gupta M, Hadjipanayis A, Haider S, Hamel L, Hayes D, Heiman D, Hess J, Hoadley K, Holbrook A, Holt R, Holway A, Hovens C, Hoyle A, Huang M, Hutter C, Ittmann M, Iype L, Jefferys S, Jones C, Jones S, Juhl H, Kahles A, Kane C, Kasaian K, Kerger M, Khurana E, Kim J, Klein R, Kucherlapati R, Lacombe L, Ladanyi M, Lai P, Laird P, Lander E, Latour M, Lawrence M, Lau K, LeBien T, Lee D, Lee S, Lehmann K, Leraas K, Leshchiner I, Leung R, Libertino J, Lichtenberg T, Lin P, Linehan W, Ling S, Lippman S, Liu J, Liu W, Lochovsky L, Loda M, Logothetis C, Lolla L, Longacre T, Lu Y, Luo J, Ma Y, Mahadeshwar H, Mallery D, Mariamidze A, Marra M, Mayo M, McCall S, McKercher G, Meng S, Mes-Masson A, Merino M, Meyerson M, Mieczkowski P, Mills G, Shaw K, Minner S, Moinzadeh A, Moore R, Morris S, Morrison C, Mose L, Mungall A, Murray B, Myers J, Naresh R, Nelson J, Nelson M, Nelson P, Newton Y, Noble M, Noushmehr H, Nykter M, Pantazi A, Parfenov M, Park P, Parker J, Paulauskis J, Penny R, Perou C, Piché A, Pihl T, Pinto P, Prandi D, Protopopov A, Ramirez N, Rao A, Rathmell W, Rätsch G, Ren X, Reuter V, Reynolds S, Rhie S, Rieger-Christ K, Roach J, Robertson A, Robinson B, Rubin M, Saad F, Sadeghi S, Saksena G, Saller C, Salner A, Sanchez-Vega F, Sander C, Sandusky G, Sauter G, Sboner A, Scardino P, Scarlata E, Schein J, Schlomm T, Schmidt L, Schultz N, Schumacher S, Seidman J, Neder L, Seth S, Sharp A, Shelton C, Shelton T, Shen H, Shen R, Sherman M, Sheth M, Shi Y, Shih J, Shmulevich I, Simko J, Simon R, Simons J, Sipahimalani P, Skelly T, Sofia H, Soloway M, Song X, Sorcini A, Sougnez C, Stepa S, Stewart C, Stewart J, Stuart J, Sullivan T, Sun C, Sun H, Tam A, Tan D, Tang J, Tarnuzzer R, Tarvin K, Taylor B, Teebagy P, Tenggara I, Têtu B, Tewari A, Thiessen N, Thompson T, Thorne L, Tirapelli D, Tomlins S, Trevisan F, Troncoso P, True L, Tsourlakis M, Tyekucheva S, Van Allen E, Van Den Berg D, Veluvolu U, Verhaak R, Vocke C, Voet D, Wan Y, Wang Q, Wang W, Wang Z, Weinhold N, Weinstein J, Weisenberger D, Wilkerson M, Wise L, Witte J, Wu C, Wu J, Wu Y, Xu A, Yadav S, Yang L, Yang L, Yau C, Ye H, Yena P, Zeng T, Zenklusen J, Zhang H, Zhang J, Zhang J, Zhang W, Zhong Y, Zhu K, Zmuda E. The Molecular Taxonomy of Primary Prostate Cancer. Cell 2015, 163: 1011-1025. PMID: 26544944, PMCID: PMC4695400, DOI: 10.1016/j.cell.2015.10.025.Peer-Reviewed Original ResearchConceptsPrimary prostate cancerProstate cancerVariable clinical courseAndrogen receptor activityPrimary prostate carcinomasSubtype-specific mannerSubstantial heterogeneityMolecular taxonomyCancer Genome AtlasClinical courseSpecific gene fusionsProstate carcinomaMutant tumorsReceptor activityComprehensive molecular analysisMolecular abnormalitiesCancerDNA repair genesMethylator phenotypeActionable lesionsGenome AtlasPI3KRepair genesEpigenetic profilesTumorsAnalysis of dynamic changes in retinoid-induced transcription and epigenetic profiles of murine Hox clusters in ES cells
De Kumar B, Parrish M, Slaughter B, Unruh J, Gogol M, Seidel C, Paulson A, Li H, Gaudenz K, Peak A, McDowell W, Fleharty B, Ahn Y, Lin C, Smith E, Shilatifard A, Krumlauf R. Analysis of dynamic changes in retinoid-induced transcription and epigenetic profiles of murine Hox clusters in ES cells. Genome Research 2015, 25: 1229-1243. PMID: 26025802, PMCID: PMC4510006, DOI: 10.1101/gr.184978.114.Peer-Reviewed Original ResearchConceptsChromatin modificationsHomeotic clustersHox genesES cellsClustered Hox genesHomeotic gene transcriptionMouse embryonic stem cellsNoncoding RNA genesRetinoid-induced transcriptionGenome-wide approachesCis-regulatory elementsEmbryonic stem cellsTranscription stateChromatin marksHOXB clusterNoncoding genesRNA genesSegmental identityActive transcriptionNoncoding RNAsTranscription factorsEpigenetic profilesGene transcriptionEpigenetic changesBody axis
2014
Epigenetics in the Pathogenesis of Esophageal Adenocarcinoma
Kailasam A, Mittal S, Agrawal D. Epigenetics in the Pathogenesis of Esophageal Adenocarcinoma. Clinical And Translational Science 2014, 8: 394-402. PMID: 25388215, PMCID: PMC4429045, DOI: 10.1111/cts.12242.Peer-Reviewed Original ResearchConceptsHistone acetylationBarrett's esophagus to esophageal adenocarcinomaEsophageal adenocarcinomaCell cycle controlBase pair sequenceDNA base pair sequencesWnt-related genesBarrett's esophagusDNA methylationProapoptotic genesEpigenetic profilesCycle controlPathogenesis of esophageal adenocarcinomaGenetic makeupEpigenetic changesDevelopment of esophageal adenocarcinomaTumor suppressorGenesDevelopment of Barrett's esophagusDown-regulationEpigenetic influencesHistoneTreatment to patientsDNAPremalignant conditionIn Vitro Culture Increases the Frequency of Stochastic Epigenetic Errors at Imprinted Genes in Placental Tissues from Mouse Concepti Produced Through Assisted Reproductive Technologies1
de Waal E, Mak W, Calhoun S, Stein P, Ord T, Krapp C, Coutifaris C, Schultz RM, Bartolomei MS. In Vitro Culture Increases the Frequency of Stochastic Epigenetic Errors at Imprinted Genes in Placental Tissues from Mouse Concepti Produced Through Assisted Reproductive Technologies1. Biology Of Reproduction 2014, 90: 22, 1-12. PMID: 24337315, PMCID: PMC4076403, DOI: 10.1095/biolreprod.113.114785.Peer-Reviewed Original ResearchConceptsEpigenetic errorsEpigenetic defectsART-conceived offspringImprinted genesMammalian embryosDNA methylationEpigenetic profilesPreimplantation developmentEpigenetic abnormalitiesAssisted Reproductive TechnologyMammalian speciesMouse conceptiMouse embryosExpression profilesEmbryonic tissuesAbnormal methylationGenesEmbryosPlacental tissueIVF embryosVitro CultureMethylationHigh oxygen tensionLow birth weightMillions of couples
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