2024
Increasing the Level of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the <i>CXCR4</i> Locus in the CEM/R5 T Cell Line
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. Increasing the Level of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line. Молекулярная Биология 2024, 58 DOI: 10.31857/s0026898424040044.Peer-Reviewed Original ResearchNuclear localization signalNonhomologous end-joining pathwayEnd-joining pathwayKnock-inKnock-in modelDNA repairDNA-dependent protein kinase inhibitorT cell linesBlock DNA repairGenome editing technologyPeptide fusion inhibitorsTranscription factor NF-kBLocalization signalCXCR4 locusDonor plasmidCas9 nucleaseCas9 proteinDNA modificationsPrimary human cellsProtein kinase inhibitorsHIV-1Transporter sequencesInhibit DNA repairPlasmid transportEffective gene therapy approachIncreasing the Level of Knock-In of the MT-C34-Encoding Construct into the <i>CXCR4</i> Locus by Modifying Donor DNA with Cas9 Target Sites
Shepelev M, Komkov D, Golubev D, Borovikova S, Mazurov D, Kruglova N. Increasing the Level of Knock-In of the MT-C34-Encoding Construct into the CXCR4 Locus by Modifying Donor DNA with Cas9 Target Sites. Молекулярная Биология 2024, 58 DOI: 10.31857/s0026898424040058.Peer-Reviewed Original ResearchKnock-in efficiencyDonor DNADonor plasmidGenetic constructsKnock-inApplication of genome editing technologiesCleavage in vitroDonor plasmid DNACas9 target sitesDouble-strand breaksInduction of double-strand breaksGenome editing technologyPAM sitesDonor sequenceTruncated targetsCell genomeDNA modificationsInduced cleavageIncreased knock-in efficiencyCRISPR/Cas9 systemCas9LociDNAEditing technologyPlasmid DNAEpigenetics-targeted drugs: current paradigms and future challenges
Dai W, Qiao X, Fang Y, Guo R, Bai P, Liu S, Li T, Jiang Y, Wei S, Na Z, Xiao X, Li D. Epigenetics-targeted drugs: current paradigms and future challenges. Signal Transduction And Targeted Therapy 2024, 9: 332. PMID: 39592582, PMCID: PMC11627502, DOI: 10.1038/s41392-024-02039-0.Peer-Reviewed Original ResearchConceptsNon-coding RNA regulationDNA base sequenceRNA modificationsRNA regulationChromatin remodelingHistone modificationsEnhancer of zeste homolog 2Epigenetic landscapeGenetic informationOrganismal developmentDNA methyltransferasesEpigenetic enzymesDNA modificationsBase sequenceHomolog 2Zeste homolog 2Histone deacetylasesHuman diseasesIsocitrate dehydrogenaseDNAPathological contextsRegulatory systemChromatinEnzymeHistoneDonor DNA Modification with Cas9 Targeting Sites Improves the Efficiency of MTC34 Knock-in into the CXCR4 Locus
Shepelev M, Komkov D, Golubev D, Borovikova S, Mazurov D, Kruglova N. Donor DNA Modification with Cas9 Targeting Sites Improves the Efficiency of MTC34 Knock-in into the CXCR4 Locus. Molecular Biology 2024, 58: 672-682. DOI: 10.1134/s0026893324700250.Peer-Reviewed Original ResearchCas9 target sitesDouble-strand breaksKnock-inCell genomeGenetic constructsDNA modificationsDonor DNADonor plasmid DNATarget siteKnock-in efficiencyGenome editing technologyInduce double-strand breaksProximal nucleotidesPAM sitesDonor plasmidDonor sequenceCXCR4 locusGenomeIn vitroInduced cleavageCRISPR/Cas9 systemCas9LociEditing technologyDNAMethods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. Methods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line. Molecular Biology 2024, 58: 658-671. DOI: 10.1134/s0026893324700249.Peer-Reviewed Original ResearchNuclear localization signalNonhomologous End JoiningDNA nuclear targeting sequencesKnock-inCXCR4 locusDNA repairT cell linesNonhomologous end-joining pathwayNuclear targeting sequenceDNA-dependent protein kinase inhibitorBlock DNA repairHIV-1Knock-in efficiencyEffective gene therapy approachGenome editing technologyTranscription factor NF-kBLocalization signalTreat HIV infectionGene therapy approachesTarget sequenceDonor plasmidCas9 nucleaseCas9 proteinEnd joiningDNA modifications[Methods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line].
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. [Methods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line]. Молекулярная Биология 2024, 58: 575-589. PMID: 39709562, DOI: 10.31857/s0026898424040044, edn: incwav.Peer-Reviewed Original ResearchConceptsNuclear localization signalNonhomologous End JoiningDNA nuclear targeting sequencesKnock-inDNA repairNonhomologous end-joining pathwayNuclear targeting sequenceCXCR4 locusDNA-dependent protein kinase inhibitorBlock DNA repairKnock-in efficiencyEffective gene therapy approachGenome editing technologyTranscription factor NF-kBLocalization signalTreat HIV infectionGene therapy approachesTarget sequenceDonor plasmidCas9 nucleaseCas9 proteinEnd joiningDNA modificationsPrimary human cellsProtein kinase inhibitors[Donor DNA Modification with Cas9 Targeting Sites Improves the Efficiency of MTC34 Knock-in into the CXCR4 Locus].
Shepelev M, Komkov D, Golubev D, Borovikova S, Mazurov D, Kruglova N. [Donor DNA Modification with Cas9 Targeting Sites Improves the Efficiency of MTC34 Knock-in into the CXCR4 Locus]. Молекулярная Биология 2024, 58: 590-600. PMID: 39709563, DOI: 10.31857/s0026898424040058, edn: incoyt.Peer-Reviewed Original ResearchConceptsCas9 target sitesDouble-strand breaksCell genomeGenetic constructsDonor DNAKnock-inDonor plasmid DNAKnock-in efficiencyGenome editing technologyInduce double-strand breaksProximal nucleotidesPAM sitesDonor plasmidDonor sequenceDNA modificationsGenomeIn vitroInduced cleavageCRISPR/Cas9 systemCas9Editing technologyDNAPlasmid DNAT cell linesTarget cell genome
2020
N6-methyladenine in DNA antagonizes SATB1 in early development
Li Z, Zhao S, Nelakanti RV, Lin K, Wu TP, Alderman MH, Guo C, Wang P, Zhang M, Min W, Jiang Z, Wang Y, Li H, Xiao AZ. N6-methyladenine in DNA antagonizes SATB1 in early development. Nature 2020, 583: 625-630. PMID: 32669713, PMCID: PMC8596487, DOI: 10.1038/s41586-020-2500-9.Peer-Reviewed Original ResearchConceptsN6-mAN6-methyladenineMouse trophoblast stem cellsLarge chromatin domainsCell fate transitionsLarge-scale chromatinUnexpected molecular mechanismTrophoblast stem cellsEarly embryonic developmentDNA secondary structuresEarly developmentFate transitionsMammalian genomesChromatin domainsEpigenetic landscapeGene regulationChromatin organizerEmbryonic developmentDNA modificationsBiological roleMolecular mechanismsSATB1 functionsMolecular pathwaysCell culture modelSecondary structure
2019
N(6)-Methyladenine in eukaryotes
Alderman MH, Xiao AZ. N(6)-Methyladenine in eukaryotes. Cellular And Molecular Life Sciences 2019, 76: 2957-2966. PMID: 31143960, PMCID: PMC6857450, DOI: 10.1007/s00018-019-03146-w.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsDNA Methylation and Susceptibility to Autism Spectrum Disorder
Tremblay MW, Jiang YH. DNA Methylation and Susceptibility to Autism Spectrum Disorder. Annual Review Of Medicine 2019, 70: 151-166. PMID: 30691368, PMCID: PMC6597259, DOI: 10.1146/annurev-med-120417-091431.Peer-Reviewed Original ResearchConceptsDNA methylationAbnormal DNA methylationDNA methylation reprogrammingGenome-wide changesMethylation-dependent regulationMethylation reprogrammingEpigenetic machineryNext-generation sequencingEmbryonic developmentMolecular basisDNA modificationsMethylationASD etiologyGenetic mutationsAttractive hypothesisRecent advancesReprogrammingEpimutationsTranscriptionASD casesMultiple levelsMachinerySequencingTechnical advancesMutations
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 modelGlioblastomaSilencing
2017
DNA Methylation in Schizophrenia
Pries L, Gülöksüz S, Kenis G. DNA Methylation in Schizophrenia. Advances In Experimental Medicine And Biology 2017, 978: 211-236. PMID: 28523549, DOI: 10.1007/978-3-319-53889-1_12.Peer-Reviewed Original ResearchConceptsAberrant DNA modificationsGenome-wide approachesDNA methylation changesCandidate gene studiesHigh heritability estimatesGenetic susceptibility lociHeritable psychiatric conditionEpigenetic mechanismsDNA methylationEpigenetic processesMethylation changesDNA modificationsComplex phenotypesGene studiesSusceptibility lociHeritability estimatesRelevant environmental risk factors
2016
DNA methylation on N6-adenine in mammalian embryonic stem cells
Wu TP, Wang T, Seetin MG, Lai Y, Zhu S, Lin K, Liu Y, Byrum SD, Mackintosh SG, Zhong M, Tackett A, Wang G, Hon LS, Fang G, Swenberg JA, Xiao AZ. DNA methylation on N6-adenine in mammalian embryonic stem cells. Nature 2016, 532: 329-333. PMID: 27027282, PMCID: PMC4977844, DOI: 10.1038/nature17640.Peer-Reviewed Original ResearchMeSH KeywordsAdenineAlkB Homolog 1, Histone H2a DioxygenaseAnimalsCell DifferentiationDNA MethylationDNA Transposable ElementsDNA-(Apurinic or Apyrimidinic Site) LyaseEnhancer Elements, GeneticEpigenesis, GeneticEvolution, MolecularGene SilencingLong Interspersed Nucleotide ElementsMammalsMiceMouse Embryonic Stem CellsUp-RegulationX ChromosomeConceptsLINE-1 transposonsEmbryonic stem cellsN6-methyladenineMammalian genomesEpigenetic silencingDNA methylationX chromosomeMammalian embryonic stem cellsEmbryonic stem cell differentiationMouse embryonic stem cellsStem cellsStem cell differentiationMammalian evolutionTranscriptional silencingEvolutionary ageGene activationDNA modificationsL1 elementsCell differentiationSilencingTransposonN6-adenineGenomeActivation signalsChromosomes
2015
Lin28A Binds Active Promoters and Recruits Tet1 to Regulate Gene Expression
Zeng Y, Yao B, Shin J, Lin L, Kim N, Song Q, Liu S, Su Y, Guo J, Huang L, Wan J, Wu H, Qian J, Cheng X, Zhu H, Ming G, Jin P, Song H. Lin28A Binds Active Promoters and Recruits Tet1 to Regulate Gene Expression. Molecular Cell 2015, 61: 153-160. PMID: 26711009, PMCID: PMC4779955, DOI: 10.1016/j.molcel.2015.11.020.Peer-Reviewed Original ResearchConceptsFunctions of Lin28ADNA sequences in vitroLet-7 miRNA biogenesisGenomic binding sitesTranscription start siteEmbryonic stem cells in vivoRNA-binding proteinsSequences in vitroRegulate gene expressionEpigenetic DNA modificationMRNA translation efficiencyDysregulated DNA methylationChIP-seqGenomic occupancyStart siteRNA-seqTranscriptional regulationTranslational efficiencyDNA methylationMiRNA biogenesisDNA modificationsMammalian systemsTarget genesTET1 knockdownGene expressionGenomic Perspectives of Transcriptional Regulation in Forebrain Development
Nord AS, Pattabiraman K, Visel A, Rubenstein JL. Genomic Perspectives of Transcriptional Regulation in Forebrain Development. Neuron 2015, 85: 27-47. PMID: 25569346, PMCID: PMC4438709, DOI: 10.1016/j.neuron.2014.11.011.Peer-Reviewed Original ResearchConceptsCis-acting genomic elementsForebrain developmentGene expression statesGene expression programsAnalysis of chromatinGenomic regulatory mechanismsGenetic circuitryGenomic perspectiveExpression programsGenomic elementsTranscriptional regulationExpression statesHigher-order brain functionsTranscription factorsDNA modificationsGene expressionRegulatory mechanismsHuman neuropsychiatric disordersGenetic defectsCurrent knowledgeChromatinRecent progressEnhancerNeuropsychiatric disordersRegulation
2014
Genome-wide antagonism between 5-hydroxymethylcytosine and DNA methylation in the adult mouse brain
Guo J, Szulwach K, Su Y, Li Y, Yao B, Xu Z, Shin J, Xie B, Gao Y, Ming G, Jin P, Song H. Genome-wide antagonism between 5-hydroxymethylcytosine and DNA methylation in the adult mouse brain. Frontiers In Biology 2014, 9: 66-74. PMID: 25568643, PMCID: PMC4284063, DOI: 10.1007/s11515-014-1295-1.Peer-Reviewed Original ResearchActive DNA demethylationDNA methylomeDNA demethylationDNA methylationGenome-wide distribution of 5hmCGenome-wide distributionGenome-wide comparisonDistribution of 5hmCGranule neurons in vivoGene expression profilesGene bodiesCytosine modificationsNeuronal genomeMammalian nervous systemDNA modificationsGene expressionEmbryonic stem cellsDNAAdult mouse brainFunctional disparityGenesMethylomeCell typesIntegrated analysisGranule neurons
2011
Epigenetic Regulation of Polymerase II Transcription Initiation in Trypanosoma cruzi: Modulation of Nucleosome Abundance, Histone Modification, and Polymerase Occupancy by O-Linked Thymine DNA Glucosylation
Ekanayake D, Sabatini R. Epigenetic Regulation of Polymerase II Transcription Initiation in Trypanosoma cruzi: Modulation of Nucleosome Abundance, Histone Modification, and Polymerase Occupancy by O-Linked Thymine DNA Glucosylation. MSphere 2011, 10: 1465-1472. PMID: 21926332, PMCID: PMC3209055, DOI: 10.1128/ec.05185-11.Peer-Reviewed Original ResearchConceptsPolycistronic transcription unitsBase JPromoter regionTranscription initiationChromatin structureGene expressionRNA polymerase (Pol) IIEpigenetic regulationPolymerase (Pol) IIIncreased Pol II occupancyPol II transcription initiationPol II occupancyRegulate gene expressionThymidine hydroxylasePolymerase occupancyGene organizationTrypanosome genomeTranscription unitHistone modificationsPosttranscriptional processesDNA modificationsTranscription rateHistone H3/H4 acetylationGenesH3/H4 acetylation
2006
LASER MICRODISSECTION OF PLANT TISSUE: What You See Is What You Get
Nelson T, Tausta SL, Gandotra N, Liu T. LASER MICRODISSECTION OF PLANT TISSUE: What You See Is What You Get. Annual Review Of Plant Biology 2006, 57: 181-201. PMID: 16669760, DOI: 10.1146/annurev.arplant.56.032604.144138.Peer-Reviewed Original ResearchConceptsLaser microdissectionCell typesComplex tissuesStable cell wallCell-specific DNAMost cell typesSpecific cell typesPlant cellsPlant tissuesDNA modificationsCell wallCell-specific propertiesTissue organizationMetabolite profilingSpecific cellsPlantsCellsMicrodissectionMetabolite studiesTissueRNAProteinDNAIdentificationProfiling
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