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 approachMethods 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 inhibitorsThe Role of RAG in V(D)J Recombination
Xiao J, Martin E, Wang K, Schatz D. The Role of RAG in V(D)J Recombination. 2024 DOI: 10.1016/b978-0-128-24465-4.00019-3.Peer-Reviewed Original ResearchRecombination signal sequencesRecombination activating geneV(D)J recombinationDNA cleavageConserved sequence elementsNonhomologous end-joining pathwayLymphoid-specific proteinsAntigen receptor gene segmentsEnd-joining pathwayPair of hairpinsReceptor gene segmentsTransposable elementsDomain architectureSequence elementsLocus structureSignal sequenceTransposition mechanismTranscriptional regulationJawed vertebratesTransposase activityActive genesPosttranslational modificationsEnhancer elementsProtein structureCell cycle
2015
Chapter 2 The Mechanism of V(D)J Recombination
Little A, Matthews A, Oettinger M, Roth D, Schatz D. Chapter 2 The Mechanism of V(D)J Recombination. 2015, 13-34. DOI: 10.1016/b978-0-12-397933-9.00002-3.ChaptersLymphocyte developmentNonhomologous end-joining pathwayRegulation of recombinationAntigen receptor lociEnd-joining pathwayDNA repair proteinsRecombination-activating gene 1RAG proteinsDNA breaksRecombinase machineryFunctional antigen receptorEnd processingReceptor locusGenetic instabilityGene 1Recombinase activityChromosomal translocationsDNA cleavageProtein 1Diverse repertoireRepair stepsBox protein 1Antigen receptorHigh mobility group box protein 1Recombination
2000
The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations
Ferguson D, Sekiguchi J, Chang S, Frank K, Gao Y, DePinho R, Alt F. The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 6630-6633. PMID: 10823907, PMCID: PMC18682, DOI: 10.1073/pnas.110152897.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsEnd-joining pathwayGenomic stabilityNonreciprocal translocationsNonhomologous DNA end-joining pathwayExogenous DNA damaging agentsNonhomologous end-joining pathwayCell cycle checkpoint proteinsDNA-dependent proteinDramatic genomic instabilityDNA ligase IVAlternative repair pathwaysDNA damaging agentsMammalian genomesGenome instabilityLigase IVNonhomologous DNADNA repairGenomic instabilityRepair pathwaysChromosomal fragmentationEmbryonic fibroblastsCheckpoint proteinsDamaging agentsSuppression of translocation
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