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 lesionsJAZF1 heterozygous knockout mice show altered adipose development and metabolism
Jeong J, Jang S, Park S, Kwon W, Kim S, Jang S, Ko J, Park S, Lim S, Yoon D, Yi J, Lee S, Kim M, Choi S, Ryoo Z. JAZF1 heterozygous knockout mice show altered adipose development and metabolism. Cell & Bioscience 2021, 11: 161. PMID: 34407873, PMCID: PMC8375039, DOI: 10.1186/s13578-021-00625-1.Peer-Reviewed Original ResearchHigh-fat dietAdipocyte differentiationNormal dietMetabolic disordersType 2 diabetes mellitusAdipose developmentImpaired adipocyte differentiationImpaired glucose homeostasisBody fat massAdipose tissue massHeterozygous knockout miceRegulation of PPARγKnockout mice showDiabetes mellitusControl miceFat massMouse embryonic fibroblastsGlucose homeostasisKnockout miceConclusionOur findingsTissue massAdipose tissueMice showJAZF1 expressionVivo model
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
BCL6 Is Critical to Overcome Oncogene-Induced Senescence in RAS-Mediated B Cell Transformation
Chan L, Hurtz C, Xiao G, Shojaee S, Caeser R, Geng H, Melnick A, Müschen M. BCL6 Is Critical to Overcome Oncogene-Induced Senescence in RAS-Mediated B Cell Transformation. Blood 2016, 128: 438. DOI: 10.1182/blood.v128.22.438.438.Peer-Reviewed Original ResearchDiffuse large B-cell lymphomaRAS-ERK signalingBCL6 expressionRole of BCL6Recipient micePhiladelphia chromosome-positive acute lymphoblastic leukemiaSTAT5 activityRAS-ERKLarge B-cell lymphomaAbsence of Bcl6Acute lymphoblastic leukemiaNovel mouse modelProto-oncogene Bcl6B-cell lymphomaNovel therapeutic avenuesTransplant recipient miceNovel mechanismMouse embryonic fibroblastsOncogene-Induced SenescenceP53-dependent senescenceB-cell transformationInitial remissionLeukemia relapseOverall survivalImatinib treatmentSILAC 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
MKK3 deletion improves mitochondrial quality
Srivastava A, McGinniss J, Wong Y, Shinn AS, Lam TT, Lee PJ, Mannam P. MKK3 deletion improves mitochondrial quality. Free Radical Biology And Medicine 2015, 87: 373-384. PMID: 26119780, DOI: 10.1016/j.freeradbiomed.2015.06.024.Peer-Reviewed Original ResearchConceptsLPS treatmentMitochondrial membrane potentialIntensive care unitInflammatory cytokine releaseMAP kinase kinase 3Potential therapeutic targetBetter mitochondrial functionMitochondrial functionMitochondrial qualityMouse embryonic fibroblastsCare unitExcessive inflammationCytokine releaseInhibition of mitophagyInflammatory diseasesCytokine secretionInflammatory responseTherapeutic targetLipopolysaccharide (LPS) stimulationSeptic injuryRole of mitophagyMajor causeOxidant productionSevere responseSepsisBCL-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
2013
TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts
Park E, Kim J, Ha T, Choi J, Soo Hong K, Rho J. TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts. Experimental & Molecular Medicine 2013, 45: e35-e35. PMID: 23928855, PMCID: PMC3789259, DOI: 10.1038/emm.2013.67.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsApoptotic cell deathCell deathOxidative stress-induced apoptotic cell deathReactive oxygen speciesPleckstrin homology-like domain familyPromotes oxidative stress-induced apoptosisActivation of caspase-3Stress responseStress-induced cell deathT-cell death-associated genePro-apoptotic functionOxidative stress-induced cell deathOxidative stress-induced apoptosisTDAG51 deficiencyDeath-associated genesStress-induced apoptosisReceptor-mediated cell deathPro-apoptotic genesResponse to oxidative stressCellular stress responseEndoplasmic reticulum stressOxygen speciesProduction of intracellular reactive oxygen speciesIntracellular reactive oxygen speciesParvovirus 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 fibroblasts
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 miceDeletion of the α-Arrestin Protein Txnip in Mice Promotes Adiposity and Adipogenesis While Preserving Insulin Sensitivity
Chutkow WA, Birkenfeld AL, Brown JD, Lee HY, Frederick DW, Yoshioka J, Patwari P, Kursawe R, Cushman SW, Plutzky J, Shulman GI, Samuel VT, Lee RT. Deletion of the α-Arrestin Protein Txnip in Mice Promotes Adiposity and Adipogenesis While Preserving Insulin Sensitivity. Diabetes 2010, 59: 1424-1434. PMID: 20299477, PMCID: PMC2874703, DOI: 10.2337/db09-1212.Peer-Reviewed Original ResearchConceptsTxnip knockout miceInsulin resistanceInsulin sensitivityKnockout miceInsulin responsivenessTXNIP expressionSkeletal muscleWild-type littermate control miceStandard chow dietType 2 diabetes pathogenesisHigh-fat dietHigh-fat feedingLittermate control miceGene-deleted miceInhibits glucose uptakeControl miceChow dietAdipose massMore insulinCaloric excessFat massDiabetes pathogenesisMouse embryonic fibroblastsRegulator of adipogenesisPPARgamma expressionBRIT1/MCPH1 Is Essential for Mitotic and Meiotic Recombination DNA Repair and Maintaining Genomic Stability in Mice
Liang Y, Gao H, Lin S, Peng G, Huang X, Zhang P, Goss J, Brunicardi F, Multani A, Chang S, Li K. BRIT1/MCPH1 Is Essential for Mitotic and Meiotic Recombination DNA Repair and Maintaining Genomic Stability in Mice. PLOS Genetics 2010, 6: e1000826. PMID: 20107607, PMCID: PMC2809772, DOI: 10.1371/journal.pgen.1000826.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsDNA double-strand breaksDNA repairGenomic stabilityDNA damage response pathwayBRIT1/MCPH1Meiotic homologous recombinationDNA damage signalingDamage response pathwayRecruitment of RAD51Localization of RAD51Novel key regulatorRAD51 foci formationDouble-strand breaksIrradiation-induced DNA damagePrimary microcephaly patientsBRCT domainMutant spermatocytesBRCA2 complexMCPH1 functionDamage signalingMeiotic chromosomesChromosomal synapsisProphase IResponse pathways
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 pathogenesisA non-Smad mechanism of fibroblast activation by transforming growth factor-β via c-Abl and Egr-1: selective modulation by imatinib mesylate
Bhattacharyya S, Ishida W, Wu M, Wilkes M, Mori Y, Hinchcliff M, Leof E, Varga J. A non-Smad mechanism of fibroblast activation by transforming growth factor-β via c-Abl and Egr-1: selective modulation by imatinib mesylate. Oncogene 2009, 28: 1285-1297. PMID: 19151753, PMCID: PMC4006376, DOI: 10.1038/onc.2008.479.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzamidesBleomycinCells, CulturedCollagenEarly Growth Response Protein 1Extracellular Signal-Regulated MAP KinasesFibroblastsFibrosisHumansImatinib MesylateMiceMice, Inbred BALB CNIH 3T3 CellsPiperazinesProtein Kinase InhibitorsProto-Oncogene Proteins c-ablPyrimidinesSignal TransductionSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaConceptsChronic myelogenous leukemiaFibrotic responseEgr-1Growth factorUpregulated tissue expressionFibrosis of skinNovel therapeutic approachesEarly growth response factor-1Kinase-deficient mutant formC-AblNormal fibroblastsTGF-β stimulationIntracellular signaling mechanismLesional skinStimulation of collagenImatinib mesylateMouse embryonic fibroblastsFibrotic processMyelogenous leukemiaTherapeutic approachesPharmacological targetingTarget of inhibitionTGF-β responseFibroblast activationC-Abl activation
2008
Multimodal evaluation of in vivo magnetic resonance imaging of myocardial restoration by mouse embryonic stem cells
Hendry S, van der Bogt K, Sheikh A, Arai T, Dylla S, Drukker M, McConnell M, Kutschka I, Hoyt G, Cao F, Weissman I, Connolly A, Pelletier M, Wu J, Robbins R, Yang P. Multimodal evaluation of in vivo magnetic resonance imaging of myocardial restoration by mouse embryonic stem cells. Journal Of Thoracic And Cardiovascular Surgery 2008, 136: 1028-1037.e1. PMID: 18954646, DOI: 10.1016/j.jtcvs.2007.12.053.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalEmbryonic Stem CellsFemaleFibroblastsGraft RejectionGraft SurvivalImmunohistochemistryMagnetic Resonance ImagingMiceMice, SCIDMyocardial ContractionMyocardial InfarctionMyocytes, CardiacRandom AllocationReproducibility of ResultsSensitivity and SpecificityStem Cell TransplantationStroke VolumeVentricular RemodelingConceptsEmbryonic stem cellsMagnetic resonance imagingIn vivo magnetic resonance imagingMouse embryonic stem cellsStem cellsResonance imagingMyocardial restorationIn vivo pressure-volume loopsPolymerase chain reactionLeft ventricular ejection fractionBioluminescence imagingSCID-beige miceVentricular ejection fractionEmbryonic stem cell groupStem cell groupMouse embryonic fibroblastsChain reactionIn vivo bioluminescence imagingCoronary artery ligationAssessment of functional recoveryAntifibrotic genesAcute myocardial infarctionDiastolic functionEjection fractionCardiac phenotype
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
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