2015
A Dicer-miR-107 Interaction Regulates Biogenesis of Specific miRNAs Crucial for Neurogenesis
Ristori E, Lopez-Ramirez MA, Narayanan A, Hill-Teran G, Moro A, Calvo CF, Thomas JL, Nicoli S. A Dicer-miR-107 Interaction Regulates Biogenesis of Specific miRNAs Crucial for Neurogenesis. Developmental Cell 2015, 32: 546-560. PMID: 25662174, PMCID: PMC8950125, DOI: 10.1016/j.devcel.2014.12.013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell DifferentiationCell ProliferationImmunoenzyme TechniquesIn Situ HybridizationMicroRNAsNeurogenesisNeuronsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRhombencephalonRibonuclease IIIRNA, MessengerTumor Cells, CulturedZebrafishZebrafish ProteinsConceptsSpecific miRNAsDicer levelsBiogenesis of microRNAsNeuronal cellsDicer expression levelsExpression levelsDicer resultsMiRNA biogenesisMiR-107 functionsBiogenesisEctopic accumulationSubstrate selectivityPostmitotic neuronsMiR-107MiR-9MiRNAsHomeostatic levelsPrecise accumulationNeurogenesisDicerCellsAccumulationMicroRNAsRecent reportsProgenitors
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