2016
Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration
Lin TV, Hsieh L, Kimura T, Malone TJ, Bordey A. Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 11330-11335. PMID: 27647922, PMCID: PMC5056085, DOI: 10.1073/pnas.1605740113.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCell Cycle ProteinsDendritic SpinesEukaryotic Initiation FactorsExcitatory Postsynaptic PotentialsGene Knockdown TechniquesGreen Fluorescent ProteinsMatrix Attachment Region Binding ProteinsMechanistic Target of Rapamycin Complex 1MiceNeurogliaNeuronsPhosphoproteinsProtein BiosynthesisRas Homolog Enriched in Brain ProteinRNA CapsRNA, Small InterferingSignal TransductionTOR Serine-Threonine KinasesTranscription FactorsConceptsBrain cytoarchitectureUpper layer cortical neuronsHyperactive mammalian targetDendritic hypertrophyCortical neuronsCap-dependent translationEctopic placementRadial gliaMammalian targetLate corticogenesisTranslational repressor eukaryotic initiation factor 4EEukaryotic initiation factor 4ENeurodevelopmental disordersProtein 1Rapamycin complex 1Molecular hallmarksInitiation factor 4EMechanisms downstreamCytoarchitectureMolecular identityMisplacementActive mutantHypertrophyGliaOveractivation
2015
Hypoxia-inducible factor-1a contributes to dendritic overgrowth in tuberous sclerosis
Zhang L, Feliciano DM, Huang T, Zhang S, Bordey A. Hypoxia-inducible factor-1a contributes to dendritic overgrowth in tuberous sclerosis. Neuroscience Letters 2015, 612: 43-47. PMID: 26655465, PMCID: PMC4728030, DOI: 10.1016/j.neulet.2015.11.038.Peer-Reviewed Original ResearchConceptsHypoxia-inducible factor 1aTuberous sclerosis complexDendritic complexityOlfactory bulb neuronsNeonatal electroporationBulb neuronsTuberous sclerosisTransgenic miceTSC neuronsDendritic patterningNeurological disordersNeuronsCellular alterationsDendritic overgrowthPathological conditionsMRNA levelsRapamycin complex 1Mechanistic targetCognitive disabilitiesData highlightTranscriptional activityVivoFactor 1AOvergrowthLevel contributes
2012
miR-132 Enhances Dendritic Morphogenesis, Spine Density, Synaptic Integration, and Survival of Newborn Olfactory Bulb Neurons
Pathania M, Torres-Reveron J, Yan L, Kimura T, Lin TV, Gordon V, Teng ZQ, Zhao X, Fulga TA, Van Vactor D, Bordey A. miR-132 Enhances Dendritic Morphogenesis, Spine Density, Synaptic Integration, and Survival of Newborn Olfactory Bulb Neurons. PLOS ONE 2012, 7: e38174. PMID: 22693596, PMCID: PMC3364964, DOI: 10.1371/journal.pone.0038174.Peer-Reviewed Original ResearchConceptsOlfactory bulb neuronsSynaptic integrationMiR-132Bulb neuronsSpine densityFrequency of GABAergicGlutamatergic synaptic inputsSubventricular zone neurogenesisMiR-132 overexpressionMiR-132 expressionMicroRNA miR-132Neonatal SVZTransplanted neuronsDendritic complexityNewborn neuronsNeuronal survivalPostnatal neurogenesisSynaptic inputsTransplant therapyDendritic morphogenesisNeuronsVivo electroporationSurvivalSignificant increasePlasticity program