2015
Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway
Sati L, Zeiss C, Yekkala K, Demir R, McGrath J. Expression of the CTCFL Gene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway. Molecular And Cellular Biology 2015, 35: 3436-3445. PMID: 26169830, PMCID: PMC4561735, DOI: 10.1128/mcb.00381-15.Peer-Reviewed Original ResearchConceptsGrowth factor β pathwayHuman vascular malformationsTestis-expressed genesΒ pathwayParalog of CTCFEmbryonic stem cellsTransforming Growth Factor-β PathwayPrior mouse modelsMouse embryogenesisBioinformatics analysisCancer-testis antigensDownstream targetsES cellsPostnatal lethalityCTCFLEmbryogenesis resultsTGFB pathwayGenesStem cellsVascular defectsPathwayExpressionTransgenic miceEye malformationsPhenotype
2004
Caspase-3 in Postnatal Retinal Development and Degeneration
Zeiss CJ, Neal J, Johnson EA. Caspase-3 in Postnatal Retinal Development and Degeneration. Investigative Ophthalmology & Visual Science 2004, 45: 964-970. PMID: 14985318, DOI: 10.1167/iovs.03-0439.Peer-Reviewed Original ResearchConceptsTerminal dUTP transferase nick end labelingPostnatal retinal developmentCaspase-3Photoreceptor degenerationRod deathMutant miceRetinal developmentInner nuclear layerDouble mutant miceNick end labelingLight microscopic levelRod photoreceptor developmentCell nuclear antigenNeonatal deathRetinal morphometryDysplastic lesionsRetinal dysplasiaNuclear layerPhotoreceptor protectionImmunohistochemical stainingRodent modelsFactor VIICaspase-3 activationNuclear antigenEnd labeling