2014
MEK-ERK1/2-Dependent FLNA Overexpression Promotes Abnormal Dendritic Patterning in Tuberous Sclerosis Independent of mTOR
Zhang L, Bartley CM, Gong X, Hsieh LS, Lin TV, Feliciano DM, Bordey A. MEK-ERK1/2-Dependent FLNA Overexpression Promotes Abnormal Dendritic Patterning in Tuberous Sclerosis Independent of mTOR. Neuron 2014, 84: 78-91. PMID: 25277454, PMCID: PMC4185153, DOI: 10.1016/j.neuron.2014.09.009.Peer-Reviewed Original ResearchConceptsDendritic complexityFLNA overexpressionDendritic abnormalitiesFLNA expressionDendritic patterningComplex dendritic arborsWild-type neuronsFilamin ADendritic arborsERK1/2-dependent mannerDendritic defectsNeurological defectsMEK-ERK1/2NeuronsMTOR activityNeurodevelopmental disordersNeurodevelopmental diseasesProtein filamin AAbnormalitiesMTOROverexpressionFMRP S499 Is Phosphorylated Independent of mTORC1-S6K1 Activity
Bartley CM, O’Keefe R, Bordey A. FMRP S499 Is Phosphorylated Independent of mTORC1-S6K1 Activity. PLOS ONE 2014, 9: e96956. PMID: 24806451, PMCID: PMC4013076, DOI: 10.1371/journal.pone.0096956.Peer-Reviewed Original Research
2011
Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice
Feliciano DM, Su T, Lopez J, Platel JC, Bordey A. Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice. Journal Of Clinical Investigation 2011, 121: 1596-1607. PMID: 21403402, PMCID: PMC3069783, DOI: 10.1172/jci44909.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBase SequenceCell SizeCerebral CortexDisease Models, AnimalDNA PrimersFemaleGene Knockout TechniquesMiceMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMice, TransgenicPregnancySeizuresTOR Serine-Threonine KinasesTuberous SclerosisTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsConceptsTuberous sclerosis complexSeizure thresholdNeuronal populationsSigns of gliosisLower seizure thresholdContribution of astrocytesDiscrete neuronal populationsAutosomal dominant disorderHeterotopic nodulesCortical hyperexcitabilityCortical tubersCortical lesionsGlial reactivityIntractable seizuresCortical malformationsSoma sizeAnimal modelsTSC1 gene productAffected neuronsDendritic treeGiant cellsUtero electroporationMutant miceLesion formationMammalian target