2016
Corneal haze phenotype in Aldh3a1-null mice: In vivo confocal microscopy and tissue imaging mass spectrometry
Chen Y, Jester JV, Anderson DM, Marchitti SA, Schey KL, Thompson DC, Vasiliou V. Corneal haze phenotype in Aldh3a1-null mice: In vivo confocal microscopy and tissue imaging mass spectrometry. Chemico-Biological Interactions 2016, 276: 9-14. PMID: 28038895, DOI: 10.1016/j.cbi.2016.12.017.Peer-Reviewed Original ResearchMeSH KeywordsAldehyde DehydrogenaseAnimalsCorneaCorneal DiseasesCorneal StromaDiazepam Binding InhibitorDisease Models, AnimalDynamic Light ScatteringEpitheliumEpithelium, CornealHistonesLens, CrystallineLipidsMiceMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalPhenotypeSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationConceptsImaging mass spectrometryCorneal crystallinsNon-catalytic functionsAcyl-CoA binding proteinFirst genetic animal modelCellular transparencyCorneal epithelial homeostasisCorneal hazeEndogenous proteinsKO miceLipid localizationMixed genetic backgroundKnockout miceCorneal phenotypeEpithelial homeostasisProtein profilesWild-type corneasBinding proteinFunctional roleGenetic backgroundLens cataractMass spectrometryConfocal microscopyMolecular changesPhenotype
2012
Effect of vitamin C deficiency during postnatal development on adult behavior: functional phenotype of Gulo(−/−) knockout mice
Chen Y, Curran C, Nebert D, Patel K, Williams M, Vorhees C. Effect of vitamin C deficiency during postnatal development on adult behavior: functional phenotype of Gulo(−/−) knockout mice. Genes Brain & Behavior 2012, 11: 269-277. PMID: 22296218, PMCID: PMC3325330, DOI: 10.1111/j.1601-183x.2011.00762.x.Peer-Reviewed Original ResearchConceptsGulo-/- miceBiosynthesis of ascorbateImportant cellular antioxidantAscorbate deficiencyL-gulono-γ-lactone oxidaseAmount of ascorbateGULO geneRate-limiting enzymeReactive oxygen speciesAerobic respirationAbnormal behavioral phenotypesMetabolic processesVitamin CCellular antioxidantsSupplemental vitamin CFunctional phenotypeOxygen speciesVitamin C deficiencyWild-type littermatesMild motor deficitsSpeciesBehavioral phenotypesPhenotypeDopamine agonistsMotor deficits
2002
Initial Characterization of the Glutamate-Cysteine Ligase Modifier Subunit Gclm(−/−) Knockout Mouse NOVEL MODEL SYSTEM FOR A SEVERELY COMPROMISED OXIDATIVE STRESS RESPONSE*
Yang Y, Dieter MZ, Chen Y, Shertzer HG, Nebert DW, Dalton TP. Initial Characterization of the Glutamate-Cysteine Ligase Modifier Subunit Gclm(−/−) Knockout Mouse NOVEL MODEL SYSTEM FOR A SEVERELY COMPROMISED OXIDATIVE STRESS RESPONSE*. Journal Of Biological Chemistry 2002, 277: 49446-49452. PMID: 12384496, DOI: 10.1074/jbc.m209372200.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAllelesAnimalsBlotting, NorthernBlotting, SouthernBody WeightCell DeathChromatography, GelCysteineDose-Response Relationship, DrugFibroblastsGenotypeGlutamate-Cysteine LigaseGlutamic AcidGlutathioneHomozygoteHydrogen PeroxideImmunoblottingKidneyKineticsLiverMiceMice, KnockoutModels, GeneticMutagenesis, Site-DirectedOxidative StressOxygenPhenotypePolymerase Chain ReactionProtein Structure, TertiaryTime FactorsTissue DistributionConceptsGlutamate-cysteine ligaseModifier subunitGSH biosynthesis pathwayGlutamate-cysteine ligase modifier subunitOxidative stress responseGCL holoenzymeHigher eukaryotesBiosynthesis pathwayCellular functionsCatalytic subunitNovel model systemRate-limiting enzymeNumerous pathophysiological conditionsNull allelesStress responseOvert phenotypeGCL activityOxidant insultSubunitsFetal fibroblastsChronic GSH depletionInitial characterizationHoloenzymeGSH inhibitionGSH depletion