2022
Tick tock, tick tock: Mouse culture and tissue aging captured by an epigenetic clock
Minteer C, Morselli M, Meer M, Cao J, Higgins‐Chen A, Lang SM, Pellegrini M, Yan Q, Levine ME. Tick tock, tick tock: Mouse culture and tissue aging captured by an epigenetic clock. Aging Cell 2022, 21: e13553. PMID: 35104377, PMCID: PMC8844113, DOI: 10.1111/acel.13553.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsDNA methylationEpigenetic agingImportant chromatin regulatorsPolycomb group (PcG) factorsAnti-aging interventionsChromatin regulatorsEmbryonic fibroblastsCellular senescenceTissue agingCellular agingEpigenetic clocksMultiple tissuesMouse tissuesCaloric restrictionMechanistic insightsAging changesKidney fibroblastsReduced representationTime pointsPhysiological agingMouse culturesSuch alterationsTick-TockTissue
2021
Mouse Embryonic Fibroblasts Isolated From Nthl1 D227Y Knockin Mice Exhibit Defective DNA Repair and Increased Genome Instability
Marsden CG, Das L, Nottoli TP, Kathe SD, Doublié S, Wallace SS, Sweasy JB. Mouse Embryonic Fibroblasts Isolated From Nthl1 D227Y Knockin Mice Exhibit Defective DNA Repair and Increased Genome Instability. DNA Repair 2021, 109: 103247. PMID: 34826736, PMCID: PMC8787541, DOI: 10.1016/j.dnarep.2021.103247.Peer-Reviewed Original ResearchConceptsGenomic instabilityEmbryonic fibroblastsExogenous DNA damaging agentsBifunctional DNA glycosylaseIncreased genome instabilityGenome editing technologyMurine embryonic fibroblastsDNA damaging agentsMouse embryonic fibroblastsNormal cellular metabolismDefective DNA repairHomozygous stateDNA glycosylase 1Genome instabilityMutant MEFsReplication stressDNA repairCellular phenotypesDNA glycosylaseEditing technologyCellular metabolismDamaging agentsWT proteinOxidative DNA damagePyrimidine lesions
2018
Suppression of dsRNA response genes and innate immunity following Oct4, Stella, and Nanos2 overexpression in mouse embryonic fibroblasts
Farshchian M, Matin M, Armant O, Geerts D, Dastpak M, Nakhaei-Rad S, Tajeran M, Jebelli A, Shahriyari M, Bahrami M, Fallah A, Yaghoobi V, Mirahmadi M, Abbaszadegan M, Bahrami A. Suppression of dsRNA response genes and innate immunity following Oct4, Stella, and Nanos2 overexpression in mouse embryonic fibroblasts. Cytokine 2018, 106: 1-11. PMID: 29501710, DOI: 10.1016/j.cyto.2018.02.021.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCellular ReprogrammingChromosomal Proteins, Non-HistoneDNA Transposable ElementsDown-RegulationEmbryo, MammalianEndogenous RetrovirusesFibroblastsGene Regulatory NetworksHEK293 CellsHumansImmunity, InnateMice, Inbred BALB CModels, BiologicalOctamer Transcription Factor-3Promoter Regions, GeneticRepressor ProteinsRNA-Binding ProteinsRNA, Double-StrandedRNA, Long NoncodingConceptsEmbryonic stem cellsResponse genesGerm cell-specific genesDeep transcriptome analysisGerm cell developmentCell-specific genesStem cellsMouse embryonic fibroblastsTransposon suppressionDsRNA-2Interferon response genesTranscriptome analysisSelf-renewal capacityEndogenous retrotransposonsEmbryonic fibroblastsCell developmentNanos2Antiviral genesGenesInnate immune systemGene cassettesInnate immunityImmune responseCritical pathwaysFirst report
2016
SILAC based protein profiling data of MKK3 knockout mouse embryonic fibroblasts
Srivastava A, Shinn AS, Lam TT, Lee PJ, Mannam P. SILAC based protein profiling data of MKK3 knockout mouse embryonic fibroblasts. Data In Brief 2016, 7: 418-422. PMID: 26977448, PMCID: PMC4782019, DOI: 10.1016/j.dib.2016.02.034.Peer-Reviewed Original ResearchMouse embryonic fibroblastsYale Protein Expression DatabaseIngenuity Pathway AnalysisEmbryonic fibroblastsKnockout mouse embryonic fibroblastsProtein Expression DatabaseWT mouse embryonic fibroblastsQuantitative mass spectrometryWhole cell lysatesTotal proteomeIntegrated DiscoveryMAP kinasePathway analysisAltered pathwaysCell lysatesMass spectrometry dataSILACPhosphopeptide enrichmentProtein levelsExpression databaseProteinSpectrometry dataPathwayFibroblastsMass spectrometry
2015
BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress
Carpio MA, Michaud M, Zhou W, Fisher JK, Walensky LD, Katz SG. BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 7201-7206. PMID: 26015568, PMCID: PMC4466744, DOI: 10.1073/pnas.1421063112.Peer-Reviewed Original ResearchConceptsB-cell lymphoma 2 ovarian killerApoptotic defectsMultidomain proapoptotic proteins BaxApoptotic responseStress stimuliER stressBcl-2 family proteinsER stress agentsUnfolded protein responseMouse embryonic fibroblastsDefective apoptotic responseMitochondrial apoptotic pathwayProapoptotic protein BaxPredominant subcellular localizationThapsigargin-induced apoptosisEndoplasmic reticulum stressFamily proteinsDeath responseSubcellular localizationEmbryonic fibroblastsHigh homologyProtein responseApoptotic pathwayOvert phenotypeProtein BaxPTEN inhibits PREX2-catalyzed activation of RAC1 to restrain tumor cell invasion
Mense SM, Barrows D, Hodakoski C, Steinbach N, Schoenfeld D, Su W, Hopkins BD, Su T, Fine B, Hibshoosh H, Parsons R. PTEN inhibits PREX2-catalyzed activation of RAC1 to restrain tumor cell invasion. Science Signaling 2015, 8: ra32. PMID: 25829446, PMCID: PMC4874664, DOI: 10.1126/scisignal.2005840.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell Line, TumorCell MovementDNA PrimersFluorescent Antibody TechniqueGene Knockout TechniquesGenetic VectorsGuanine Nucleotide Exchange FactorsHumansImmunoblottingImmunoprecipitationLentivirusMiceNeoplasm InvasivenessPolymerase Chain ReactionPTEN Phosphohydrolaserac1 GTP-Binding ProteinRNA, Small InterferingStatistics, NonparametricConceptsLipid phosphatase activityPTEN-mediated inhibitionGEF activityCancer mutantsCell migrationNucleotide exchange assaysPhosphatase activityTumor suppressor PTENMouse embryonic fibroblastsTumor cell invasionPI3K pathwayHuman tumor dataKinase AktSuppressor PTENTail domainEmbryonic fibroblastsGTPase Rac1PREX2 mutationsImmortalized melanocytesMutantsCell invasionHigh PTEN expressionK pathwayRac1Breast cancer cell lines
2014
PIWI Proteins Are Dispensable for Mouse Somatic Development and Reprogramming of Fibroblasts into Pluripotent Stem Cells
Cheng EC, Kang D, Wang Z, Lin H. PIWI Proteins Are Dispensable for Mouse Somatic Development and Reprogramming of Fibroblasts into Pluripotent Stem Cells. PLOS ONE 2014, 9: e97821. PMID: 25238487, PMCID: PMC4169525, DOI: 10.1371/journal.pone.0097821.Peer-Reviewed Original ResearchConceptsPIWI proteinsEmbryonic stem cellsInduced pluripotent stem cellsPluripotent stem cellsIPS cellsPiwi genesGermline stem cell maintenanceStem cellsControl iPS cellsDifferentiated somatic cellsStem cell maintenancePIWI protein familyReprogramming of fibroblastsExpression profiling revealsGermline developmentProtein familyKnockout embryosCell maintenanceFemale fertileSomatic cellsEmbryonic fibroblastsDirect reprogrammingProfiling revealsTeratoma assayGerm layers
2013
Parvovirus evades interferon-dependent viral control in primary mouse embryonic fibroblasts
Mattei LM, Cotmore SF, Tattersall P, Iwasaki A. Parvovirus evades interferon-dependent viral control in primary mouse embryonic fibroblasts. Virology 2013, 442: 20-27. PMID: 23676303, PMCID: PMC3767977, DOI: 10.1016/j.virol.2013.03.020.Peer-Reviewed Original ResearchConceptsType I IFNsI IFNsI interferonIFN responseAntiviral immune mechanismsType I interferonInnate defense mechanismsMouse embryonic fibroblastsMVMp infectionViral controlImmune mechanismsInnate sensingAntiviral programViral replicationViral sensorsMurine parvovirusPoly (I:C) stimulationVirusEmbryonic fibroblastsType IMiceDefense mechanismsMinute virusMVMpPrimary mouse embryonic fibroblastsTransformation of somatic cells into stem cell‐like cells under a stromal niche
Lee ST, Gong SP, Yum KE, Lee EJ, Lee CH, Choi JH, Kim DY, Han H, Kim K, Hysolli E, Ahn JY, Park I, Han JY, Jeong J, Lim JM. Transformation of somatic cells into stem cell‐like cells under a stromal niche. The FASEB Journal 2013, 27: 2644-2656. PMID: 23580613, PMCID: PMC4050423, DOI: 10.1096/fj.12-223065.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell AggregationCell DedifferentiationCell FusionCells, CulturedChromosome AberrationsCoculture TechniquesEmbryo, MammalianEmbryonic Stem CellsFemaleFibroblastsGene Expression ProfilingInduced Pluripotent Stem CellsKaryotypingMiceMice, Inbred C57BLMice, Inbred CBAMice, Inbred DBAMice, Inbred ICRMicroscopy, Electron, TransmissionOligonucleotide Array Sequence AnalysisOvarySpecies SpecificityStem Cell NicheStem CellsConceptsEmbryonic stem cellsColony-forming fibroblastsParthenogenetic embryonic stem cellsSomatic cellsGenomic single nucleotide polymorphismsAcquisition of pluripotencySomatic cell plasticityPluripotency gene expressionStem cellsInner cell massStem cell-like cellsCell cycle-related proteinsPluripotent stem cellsSomatic genomeCycle-related proteinsGenomic plasticityCell-like cellsSingle nucleotide polymorphismsCell plasticityESC coloniesGenetic manipulationHeterologous recombinationEmbryonic fibroblastsImprinting patternGene expression
2011
Cell organization, growth, and neural and cardiac development require αII-spectrin
Stankewich MC, Cianci CD, Stabach PR, Ji L, Nath A, Morrow JS. Cell organization, growth, and neural and cardiac development require αII-spectrin. Journal Of Cell Science 2011, 124: 3956-3966. PMID: 22159418, PMCID: PMC3244980, DOI: 10.1242/jcs.080374.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsAnkyrinsAxonsBody PatterningCarrier ProteinsCell MembraneCell PolarityCell ProliferationCraniofacial AbnormalitiesEmbryo, MammalianEmbryonic DevelopmentFemaleFibroblastsGene DeletionHeart Defects, CongenitalMaleMiceMice, Inbred C57BLMicrofilament ProteinsNeural Tube DefectsNeuroepithelial CellsPhenotypeProtein StabilityPseudopodiaSpectrinConceptsΑII-spectrinSteady-state protein levelsΒIII spectrinEmbryonic day 12.5Tissue patterningRenal epithelial cellsEmbryonic lethalCortical actinOrgan developmentAnkyrin BExon trappingEmbryonic fibroblastsTranscriptional levelΒ-spectrinCardiac developmentCell organizationCell spreadingAxon formationNeural tubeHeterozygous animalsTargeted disruptionApical membraneNeuroepithelial cellsDay 12.5Cell morphology
2010
The telomeric protein SNM1B/Apollo is required for normal cell proliferation and embryonic development
Akhter S, Lam YC, Chang S, Legerski RJ. The telomeric protein SNM1B/Apollo is required for normal cell proliferation and embryonic development. Aging Cell 2010, 9: 1047-1056. PMID: 20854421, PMCID: PMC3719988, DOI: 10.1111/j.1474-9726.2010.00631.x.Peer-Reviewed Original ResearchConceptsMutant mouse embryonic fibroblastsSNM1B/ApolloCell proliferation defectMouse embryonic fibroblastsNormal cell proliferationDevelopmental failureHomozygous null miceEnd fusionsProliferation defectEmbryonic developmentGenomic instabilityEmbryonic fibroblastsTelomeric endDevelopmental defectsCell deathVivo roleCell proliferationImpaired proliferationTelomeresNull miceMutant mice
2009
Maitotoxin converts the plasmalemmal Ca2+ pump into a Ca2+-permeable nonselective cation channel
Sinkins W, Estacion M, Prasad V, Goel M, Shull G, Kunze D, Schilling W. Maitotoxin converts the plasmalemmal Ca2+ pump into a Ca2+-permeable nonselective cation channel. American Journal Of Physiology - Cell Physiology 2009, 297: c1533-c1543. PMID: 19794142, PMCID: PMC2793065, DOI: 10.1152/ajpcell.00252.2009.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsAnimals, Genetically ModifiedCalciumCation Transport ProteinsCationsCell MembraneCells, CulturedDown-RegulationElectric ConductivityFibroblastsHumansIon ChannelsKidneyMarine ToxinsMiceOxocinsPermeabilityPlasma Membrane Calcium-Transporting ATPasesRNA, Small InterferingSpodopteraUp-RegulationConceptsPermeable nonselective cation channelNonselective cation channelsCation channelsSpodoptera frugiperda (Sf9) insect cellsHEK cellsMouse embryonic fibroblastsHuman embryonic kidney 293 cellsEmbryonic kidney 293 cellsKidney 293 cellsInsect cellsEmbryonic fibroblastsWhole-cell membrane currentsMolecular identityCell membrane currentsCell typesPMCACytosolic freeMarine toxinsEnhanced expressionWhole-cell currentsPlasmalemmal Ca2PalytoxinATPaseCellsMaitotoxinCharacterization of DNA damage-dependent cell cycle checkpoints in a menin-deficient model
Kottemann MC, Bale AE. Characterization of DNA damage-dependent cell cycle checkpoints in a menin-deficient model. DNA Repair 2009, 8: 944-952. PMID: 19608464, PMCID: PMC2745199, DOI: 10.1016/j.dnarep.2009.06.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21DNA DamageEmbryo, MammalianFibroblastsG1 PhaseHistone-Lysine N-MethyltransferaseMiceModels, BiologicalMutagensMutationMyeloid-Lymphoid Leukemia ProteinPhenotypePromoter Regions, GeneticProtein BindingProtein Serine-Threonine KinasesProto-Oncogene ProteinsRadiation, IonizingS PhaseTumor Suppressor Protein p53Up-RegulationConceptsP21 promoterDNA damage-dependent mannerPositive transcriptional regulatorDamage-dependent mannerNormal cellular physiologyCell cycle controlLoss of Men1Intra-S checkpointCell cycle checkpointsMouse embryonic fibroblastsCyclin-dependent kinase inhibitorG1/STranscriptional regulationTranscriptional regulatorsCheckpoint responseCellular physiologyCycle checkpointsHistone methyltransferaseDNA repairEmbryonic fibroblastsTranscriptional capacityCycle controlTarget p21MeninCancer pathogenesis
2008
Defective p53 engagement after the induction of DNA damage in cells deficient in topoisomerase 3β
Mohanty S, Town T, Yagi T, Scheidig C, Kwan KY, Allore HG, Flavell RA, Shaw AC. Defective p53 engagement after the induction of DNA damage in cells deficient in topoisomerase 3β. Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 5063-5068. PMID: 18367668, PMCID: PMC2278186, DOI: 10.1073/pnas.0801235105.Peer-Reviewed Original ResearchConceptsMurine embryonic fibroblastsDNA damageDependent substrate phosphorylationDNA double-strand breaksType IA topoisomerasesCell cycle checkpointsDNA-damaging agentsS cell cycle checkpointDouble-strand breaksRegulation of totalSubstrate phosphorylationGenomic stabilityDsDNA breaksDNA replicationCycle checkpointsHomologous recombinationDNA repairUnanticipated roleEmbryonic fibroblastsAtaxia telangiectasiaCellular responsesTopoisomerase 3βPhosphorylationRad3Important role
2007
Connective tissue growth factor/CCN2-null mouse embryonic fibroblasts retain intact transforming growth factor-β responsiveness
Mori Y, Hinchcliff M, Wu M, Warner-Blankenship M, Lyons K, Varga J. Connective tissue growth factor/CCN2-null mouse embryonic fibroblasts retain intact transforming growth factor-β responsiveness. Experimental Cell Research 2007, 314: 1094-1104. PMID: 18201696, PMCID: PMC3963386, DOI: 10.1016/j.yexcr.2007.12.010.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCell ProliferationCells, CulturedCollagenCollagen Type IConnective Tissue Growth FactorEmbryo, MammalianExtracellular MatrixFibroblastsFibrosisGene ExpressionImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsMiceSignal TransductionSmad ProteinsTransforming Growth Factor betaConceptsEmbryonic fibroblastsSmad-dependent transcriptional responsesTGF-beta signal transductionMatricellular protein connective tissue growth factorMurine embryonic fibroblastsMouse embryonic fibroblastsProtein connective tissue growth factorWild-type MEFsTransient transfection assaysMyofibroblast transdifferentiationCCN2 expressionRegulation of proliferationCorresponding protein levelsCCN2 functionsCollagen gene expressionTranscriptional responseRT-PCR analysisLoss of CCN2Signal transductionEndogenous CCN2Transfection assaysExtracellular matrix synthesisMouse embryosGene expressionWild type
2006
Multiple Endocrine Neoplasia Type 1 Interacts with Forkhead Transcription Factor CHES1 in DNA Damage Response
Busygina V, Kottemann MC, Scott KL, Plon SE, Bale AE. Multiple Endocrine Neoplasia Type 1 Interacts with Forkhead Transcription Factor CHES1 in DNA Damage Response. Cancer Research 2006, 66: 8397-8403. PMID: 16951149, DOI: 10.1158/0008-5472.can-06-0061.Peer-Reviewed Original ResearchConceptsDNA damage responseDamage responseS-phase checkpoint pathwayDrosophila larval tissuesTranscriptional repressor complexS-phase checkpointMouse embryonic fibroblastsHistone deacetylase 1Cell cycle arrestGenetic screenGenomic integrityInteracting proteinRepressor complexS-phase arrestHuman meninMutant fliesBiochemical functionsLarval tissuesMEN1 proteinCancer susceptibility syndromeEmbryonic fibroblastsCheckpoint pathwayCOOH terminusCHES1Menin
2002
Src Kinase Mediates Phosphatidylinositol 3-Kinase/Akt-dependent Rapid Endothelial Nitric-oxide Synthase Activation by Estrogen*
Haynes MP, Li L, Sinha D, Russell KS, Hisamoto K, Baron R, Collinge M, Sessa WC, Bender JR. Src Kinase Mediates Phosphatidylinositol 3-Kinase/Akt-dependent Rapid Endothelial Nitric-oxide Synthase Activation by Estrogen*. Journal Of Biological Chemistry 2002, 278: 2118-2123. PMID: 12431978, DOI: 10.1074/jbc.m210828200.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsBlotting, WesternCell LineCells, CulturedElectrophoresis, Polyacrylamide GelEndoplasmic ReticulumEndothelium, VascularEnzyme ActivationEnzyme InhibitorsEstrogensHumansMiceMutationNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesPhosphorylationPrecipitin TestsProtein BindingProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, EstrogenSignal Transductionsrc-Family KinasesTime FactorsTransfectionTyrosineConceptsC-SrcPI3-kinaseAkt phosphorylationSrc kinaseUpstream regulatorKinase-dead c-SrcC-Src associationActive c-SrcC-Src phosphorylationMurine embryonic fibroblastsBasal Akt phosphorylationC-Src expressionCritical upstream regulatorEndothelial nitric oxide synthaseSrc familyActive AktEmbryonic fibroblastsComplex formation resultsEndothelial cellsHuman endothelial cellsAkt activationPhosphorylationKinaseAktPhosphatidylinositolComparative study of the importance of multidrug resistance-associated protein 1 and P-glycoprotein to drug sensitivity in immortalized mouse embryonic fibroblasts.
Lin ZP, Johnson DR, Finch RA, Belinsky MG, Kruh GD, Sartorelli AC. Comparative study of the importance of multidrug resistance-associated protein 1 and P-glycoprotein to drug sensitivity in immortalized mouse embryonic fibroblasts. Molecular Cancer Therapeutics 2002, 1: 1105-14. PMID: 12481434.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnticarcinogenic AgentsAntineoplastic AgentsAntineoplastic Agents, PhytogenicATP Binding Cassette Transporter, Subfamily B, Member 1Biological TransportBlotting, WesternCell SurvivalCells, CulturedChemokines, CCDose-Response Relationship, DrugEtoposideFibroblastsFluoresceinsInhibitory Concentration 50MiceMice, KnockoutPrecipitin TestsReverse Transcriptase Polymerase Chain ReactionRNATime FactorsTransfectionTumor Cells, CulturedVincristineConceptsMultidrug resistance-associated protein 1P-glycoproteinWT fibroblastsDKO fibroblastsCalcein accumulationDrug sensitivityProtein 1Unrelated anticancer agentsAnticancer agentsImmortalized mouse embryonic fibroblastsWestern blot analysisKnockout miceCompensatory mechanismsAccumulation assaysMouse embryonic fibroblastsCompensatory changesEmbryonic fibroblastsMRP1Drug substratesBlot analysisCell viabilityMajor determinantFamily membersFibroblastsFibroblast lines
2000
Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation
Wong K, Chang S, Weiler S, Ganesan S, Chaudhuri J, Zhu C, Artandi S, Rudolph K, Gottlieb G, Chin L, Alt F, DePinho R. Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation. Nature Genetics 2000, 26: 85-88. PMID: 10973255, DOI: 10.1038/79232.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell NucleusCell SurvivalChromosome AberrationsChromosomesDNA FragmentationDNA RepairDose-Response Relationship, RadiationFibroblastsGenotypeIn Situ Nick-End LabelingKineticsMiceMice, TransgenicModels, GeneticRadiation ToleranceRadiation, IonizingTelomereThymus GlandTime FactorsConceptsMouse embryonic fibroblastsTelomere functionOrganismal responsesLinear eukaryotic chromosomesDNA repair machineryTelomerase RNA geneNon-homologous endImpairs DNA repairRole of telomeraseTelomerase-deficient miceEukaryotic chromosomesRNA genesYeast telomeresNucleoprotein complexesRepair machineryDNA repairIntact telomeresCrypt stem cellsEmbryonic fibroblastsTelomere dysfunctionDe novo synthesisChromosomal repairGenetic instabilityPrimary thymocytesRate of apoptosisThe 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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