2015
Embryonic Stem Cells License a High Level of Dormant Origins to Protect the Genome against Replication Stress
Ge XQ, Han J, Cheng EC, Yamaguchi S, Shima N, Thomas JL, Lin H. Embryonic Stem Cells License a High Level of Dormant Origins to Protect the Genome against Replication Stress. Stem Cell Reports 2015, 5: 185-194. PMID: 26190528, PMCID: PMC4618655, DOI: 10.1016/j.stemcr.2015.06.002.Peer-Reviewed Original ResearchConceptsEmbryonic stem cellsStem/progenitor cellsNeural stem/progenitor cellsStem cellsProgenitor cellsTissue stem/progenitor cellsMCM2-7 complexDNA replication originsTissue-specific stem/progenitor cellsStem cell typesGenome integrityGenomic integrityReplication stressDormant originsReplication forksReplicative stressDNA replicationReplication originsNeural lineagesDNA damageS phaseCell typesAbnormal neurogenesisCellsGenome
2014
Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1
Patterson VL, Zullo AJ, Koenig C, Stoessel S, Jo H, Liu X, Han J, Choi M, DeWan AT, Thomas JL, Kuan CY, Hoh J. Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1. PLOS ONE 2014, 9: e115789. PMID: 25531304, PMCID: PMC4274161, DOI: 10.1371/journal.pone.0115789.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBehavior, AnimalBlotting, WesternCell ProliferationCerebellumFemaleGTP PhosphohydrolasesHigh-Temperature Requirement A Serine Peptidase 2MaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial ProteinsNerve DegenerationNeuronsParkinson DiseaseReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSequence DeletionSerine EndopeptidasesSignal TransductionConceptsNeural-specific deletionStriatal neuronal lossPostnatal day 18Days of ageNeuronal lossNeurological symptomsParkinson's diseaseMouse modelParkinsonian phenotypeSystemic effectsMitochondrial Opa1Day 18Premature deathMutant miceNeural contributionsMiceCerebellar neurodegenerationKey moleculesStructural anomaliesAbnormal activityAbnormal morphologyCerebellumDiseaseComplete penetranceDeath
2007
Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?
Williams A, Piaton G, Aigrot MS, Belhadi A, Théaudin M, Petermann F, Thomas JL, Zalc B, Lubetzki C. Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis? Brain 2007, 130: 2554-2565. PMID: 17855378, DOI: 10.1093/brain/awm202.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsApoptosisCerebral CortexDisease Models, AnimalFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiddle AgedMotor CortexMultiple SclerosisMyelin SheathNerve RegenerationNerve Tissue ProteinsNeurogliaNeuronsRatsRats, WistarRNA, MessengerSemaphorin-3ASignal TransductionUp-RegulationConceptsMultiple sclerosisSemaphorin 3AAbility of plaqueActive demyelinating lesionsNeuronal cell bodiesFailure of repairCentral nervous systemOligodendrocyte precursor cellsOligodendrocyte precursor cell migrationPrecursor cell migrationChronic plaquesDemyelinating lesionsDemyelinated plaquesMyelin repairDemyelinated axonsMS tissueNervous systemCell bodiesExperimental modelPlaquesLesionsPrecursor cellsSclerosisOligodendroglial migrationCell migration