2024
Plasma Glial Fibrillary Acid Protein and Phosphorated Tau 181 Association with Presynaptic Density-Dependent Tau Pathology at 18F-SynVesT-1 Brain PET Imaging.
Wu J, Li B, Wang J, Huang Q, Chen X, You Z, He K, Guo Q, Li S, Huang Y, Guo T, Dai W, Xiang W, Chen W, Yang D, Zhao J, Guan Y, Xie F. Plasma Glial Fibrillary Acid Protein and Phosphorated Tau 181 Association with Presynaptic Density-Dependent Tau Pathology at 18F-SynVesT-1 Brain PET Imaging. Radiology 2024, 313: e233019. PMID: 39560478, PMCID: PMC11605102, DOI: 10.1148/radiol.233019.Peer-Reviewed Original ResearchConceptsP-tau-181Alzheimer's diseaseAD-related pathologyAmyloid-bPhosphor-tauTau pathologySynaptic densityTau accumulationSynaptic lossTauTau-PETDecreased synaptic densityGlial fibrillary acidic proteinPlasma glial fibrillary acidic proteinCortical thicknessAcidic proteinFibrillary acidic proteinRuijin HospitalProspective studyRelationship of plasmaBlood assayBlood markersPET/MRIBrain PET imagingPET imagingDissecting glial scar formation by spatial point pattern and topological data analysis
Manrique-Castano D, Bhaskar D, ElAli A. Dissecting glial scar formation by spatial point pattern and topological data analysis. Scientific Reports 2024, 14: 19035. PMID: 39152163, PMCID: PMC11329771, DOI: 10.1038/s41598-024-69426-z.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesCicatrixData AnalysisDisease Models, AnimalGlial Fibrillary Acidic ProteinIschemic StrokeMaleMiceMice, Inbred C57BLMicrogliaNeuroglia
2021
Small loci of astroglial glutamine synthetase deficiency in the postnatal brain cause epileptic seizures and impaired functional connectivity
Farina MG, Sandhu MRS, Parent M, Sanganahalli BG, Derbin M, Dhaher R, Wang H, Zaveri HP, Zhou Y, Danbolt NC, Hyder F, Eid T. Small loci of astroglial glutamine synthetase deficiency in the postnatal brain cause epileptic seizures and impaired functional connectivity. Epilepsia 2021, 62: 2858-2870. PMID: 34536233, PMCID: PMC9006438, DOI: 10.1111/epi.17072.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBrainEpilepsyGlial Fibrillary Acidic ProteinGlutamate-Ammonia LigaseGlutamineHumansMetabolic DiseasesMiceSeizuresConceptsPostnatal brainFunctional connectivityContinuous video-electroencephalographic recordingSpontaneous recurrent seizuresPathogenesis of epilepsyGlutamine synthetase deficiencyVideo-electroencephalographic recordingsSpecific animal modelsEx vivo studySeizure thresholdAdult patientsRecurrent seizuresFocal epilepsyAdeno-associated virusHippocampal formationAnimal modelsFocal mannerEpileptic seizuresGS deficiencySmall lociSynthetase deficiencyEpilepsyGradual returnVivo studiesBrainRadial Glial Cells: New Views on Old Questions
Arellano JI, Morozov YM, Micali N, Rakic P. Radial Glial Cells: New Views on Old Questions. Neurochemical Research 2021, 46: 2512-2524. PMID: 33725233, PMCID: PMC8855517, DOI: 10.1007/s11064-021-03296-z.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CycleCell DifferentiationCell Surface ExtensionsEpendymoglial CellsGlial Fibrillary Acidic ProteinMacacaNerve Tissue ProteinsNeuroepithelial CellsNeurogenesisConceptsGlial fibrillary acidic proteinRadial glial cellsNeuroepithelial cellsGFAP expressionFibrillary acidic proteinMigration of neuronsProcess of neurogenesisGlial featuresGlial cellsEmbryonic cerebrumCortical neurogenesisMacaque monkeysPial surfaceAcidic proteinEpithelial featuresBrain developmentNeurogenesisVentricular surfaceTight junctionsCerebrumNeuronsUltrastructural analysisFirst descriptionBrainVertebrate brain
2020
Post-ischemic stroke systemic inflammation: Immunomodulation by progesterone and vitamin D hormone
Atif F, Yousuf S, Espinosa-Garcia C, Harris W, Stein D. Post-ischemic stroke systemic inflammation: Immunomodulation by progesterone and vitamin D hormone. Neuropharmacology 2020, 181: 108327. PMID: 32950558, DOI: 10.1016/j.neuropharm.2020.108327.Peer-Reviewed Original ResearchConceptsPeripheral immune dysfunctionVitamin D hormoneTransient middle cerebral artery occlusion/reperfusionImmune dysfunctionSystemic inflammationInfarct volumeSubsets of immune cellsNeuronal inflammationMeasure infarct volumePost-stroke infectionsInjection of lipopolysaccharideIn-hospital infectionStandard of careFlow cytometric analysisMiddle cerebral artery occlusion/reperfusionCleaved caspase-3Combination therapyInflammation groupImmune cellsAdult ratsIncreased morbidityD hormoneBrain post-strokeImmunomodulatory effectsCombined treatment
2018
Nav1.5 in astrocytes plays a sex‐specific role in clinical outcomes in a mouse model of multiple sclerosis
Pappalardo LW, Samad OA, Liu S, Zwinger PJ, Black JA, Waxman SG. Nav1.5 in astrocytes plays a sex‐specific role in clinical outcomes in a mouse model of multiple sclerosis. Glia 2018, 66: 2174-2187. PMID: 30194875, DOI: 10.1002/glia.23470.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBrainCalcium-Binding ProteinsDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalFemaleGlial Fibrillary Acidic ProteinMaleMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMonocytesMultiple SclerosisNAV1.5 Voltage-Gated Sodium ChannelSex CharacteristicsSpinal CordT-LymphocytesConceptsExperimental autoimmune encephalomyelitisMultiple sclerosisClinical outcomesSex-specific mannerInflammatory infiltrateEAE clinical scoreT cell infiltrationWT littermate controlsAutoimmune encephalomyelitisNeuroinflammatory disordersClinical courseClinical scoresAstroglial responseUnderlying molecular mechanismsSex-specific roleCell infiltrationFemale miceKO miceT cellsImmune responseMurine modelPossible dysregulationMouse modelLittermate controlsTherapeutic targetSelective deletion of glutamine synthetase in the mouse cerebral cortex induces glial dysfunction and vascular impairment that precede epilepsy and neurodegeneration
Zhou Y, Dhaher R, Parent M, Hu QX, Hassel B, Yee SP, Hyder F, Gruenbaum SE, Eid T, Danbolt NC. Selective deletion of glutamine synthetase in the mouse cerebral cortex induces glial dysfunction and vascular impairment that precede epilepsy and neurodegeneration. Neurochemistry International 2018, 123: 22-33. PMID: 30053506, PMCID: PMC8261904, DOI: 10.1016/j.neuint.2018.07.009.Peer-Reviewed Original ResearchConceptsAbnormal glutamate metabolismMouse cerebral cortexCerebral blood vesselsNovel mouse modelPostnatal week threeWeeks of ageProgressive astrogliosisVascular impairmentSpontaneous seizuresCerebral cortexGlial dysfunctionNeurovascular couplingDeficient miceSclerotic areasMouse modelEpileptic patientsApparent malformationsProgressive neurodegenerationSelective deletionGlutamate-ammonia ligaseTissue levelsGlutamate metabolismBlood vesselsWeek threeNeurodegenerationProfiling changes in cortical astroglial cells following chronic stress
Simard S, Coppola G, Rudyk CA, Hayley S, McQuaid RJ, Salmaso N. Profiling changes in cortical astroglial cells following chronic stress. Neuropsychopharmacology 2018, 43: 1961-1971. PMID: 29907879, PMCID: PMC6046043, DOI: 10.1038/s41386-018-0105-x.Peer-Reviewed Original ResearchConceptsChronic variable stressDepressive-like behaviorPerineuronal netsAstroglial cellsAstroglial plasticityCortical astroglial cellsAstroglial cell functionModel of depressionAstroglial contributionNeuroplasticity hypothesisAstroglial changesCortical astrogliaAntidepressant potentialDepressive behaviorSwim testGFAP expressionDepressive phenotypeNeuronal plasticityGlutamate recyclingCorticosterone levelsRibosome affinity purificationSynaptic plasticityGrowth factor signalingChronic stressDegradation of PNNs
2016
Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability
García-Cáceres C, Quarta C, Varela L, Gao Y, Gruber T, Legutko B, Jastroch M, Johansson P, Ninkovic J, Yi CX, Le Thuc O, Szigeti-Buck K, Cai W, Meyer CW, Pfluger PT, Fernandez AM, Luquet S, Woods SC, Torres-Alemán I, Kahn CR, Götz M, Horvath TL, Tschöp MH. Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability. Cell 2016, 166: 867-880. PMID: 27518562, PMCID: PMC8961449, DOI: 10.1016/j.cell.2016.07.028.Peer-Reviewed Original ResearchConceptsBlood-brain barrierSystemic glucose metabolismInsulin receptorGlucose metabolismGlucose uptakeGlial fibrillary acidic proteinBrain glucose uptakePostnatal ablationHypothalamic glucose sensingGlutamate-aspartate transporterFibrillary acidic proteinPositron emission tomographyMelanocortin neuronsKO miceGlucose levelsAstrocyte morphologyNormal responseEmission tomographyGlucose-induced activationAcidic proteinAspartate transporterCircuit connectivityInsulinGlucose availabilityMitochondrial function
2015
Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1−/− Mice
Fink KL, Strittmatter SM, Cafferty WB. Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1−/− Mice. Journal Of Neuroscience 2015, 35: 15403-15418. PMID: 26586827, PMCID: PMC4649010, DOI: 10.1523/jneurosci.3165-15.2015.Peer-Reviewed Original ResearchMeSH KeywordsAmidinesAnalysis of VarianceAnimalsAxonsBiotinCrystallinsDextransDisease Models, AnimalFunctional LateralityGene Expression RegulationGlial Fibrillary Acidic ProteinGPI-Linked ProteinsLuminescent ProteinsMiceMice, Inbred C57BLMice, Transgenicmu-CrystallinsMyelin ProteinsNerve RegenerationNogo Receptor 1Pyramidal TractsReceptors, Cell SurfaceRecovery of FunctionSpinal Cord InjuriesConceptsCorticospinal tractCST axonsTransgenic miceMotor tractsDextran amineFunctional deficitsSpinal cordAxon regenerationSpinal Cord Injury StudySpontaneous axon regenerationSpinal cord traumaNogo receptor 1Permanent functional deficitsPersistent functional deficitsBilateral pyramidotomyDorsal hemisectionMidthoracic cordCord traumaMotor pathwaysAdult CNSCST regenerationInjury studiesLesion siteRegenerating fibersNeural repairCharacterization of cells from patient-derived fibrovascular membranes in proliferative diabetic retinopathy.
Kim LA, Wong LL, Amarnani DS, Bigger-Allen AA, Hu Y, Marko CK, Eliott D, Shah VA, McGuone D, Stemmer-Rachamimov AO, Gai X, D'Amore PA, Arboleda-Velasquez JF. Characterization of cells from patient-derived fibrovascular membranes in proliferative diabetic retinopathy. Molecular Vision 2015, 21: 673-87. PMID: 26120272, PMCID: PMC4462955.Peer-Reviewed Original ResearchConceptsComparative genomic hybridizationDiscovery of cellsPlasma membrane infoldingsSpecific cell populationsCell identityPrimary culturesCell culture modelCharacterization of cellsMajor chromosomal aberrationsMembrane infoldingsCellular constituentsGenomic hybridizationAlpha-smooth muscle actinThrombospondin-1Cell populationsExpression of markersCulture conditionsStromal cellsPerivascular cellsCulture modelUnique resourceGlial fibrillary acidic protein-positive cellsCellsChromosomal aberrationsEndothelial cellsDiffuse and persistent blood–spinal cord barrier disruption after contusive spinal cord injury rapidly recovers following intravenous infusion of bone marrow mesenchymal stem cells
Matsushita T, Lankford KL, Arroyo EJ, Sasaki M, Neyazi M, Radtke C, Kocsis JD. Diffuse and persistent blood–spinal cord barrier disruption after contusive spinal cord injury rapidly recovers following intravenous infusion of bone marrow mesenchymal stem cells. Experimental Neurology 2015, 267: 152-164. PMID: 25771801, DOI: 10.1016/j.expneurol.2015.03.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, SurfaceBlood-Brain BarrierCell- and Tissue-Based TherapyDisease Models, AnimalEndothelial CellsExploratory BehaviorGlial Fibrillary Acidic ProteinLocomotionMaleMesenchymal Stem CellsMicrovesselsPermeabilityRatsRats, Sprague-DawleyRats, TransgenicReceptor, Platelet-Derived Growth Factor betaSpinal Cord InjuriesTime Factorsvon Willebrand FactorConceptsSpinal cord injuryContusive spinal cord injuryBlood-spinal cord barrierBSCB leakageIntravenous infusionMesenchymal stem cellsVon Willebrand factorMSC infusionCord injurySpinal cordBlood-spinal cord barrier disruptionExperimental spinal cord injuryIntravenous MSC infusionSpinal cord barrierEx vivo optical imagingDissociation of pericytesBone marrow mesenchymal stem cellsStem cellsMarrow mesenchymal stem cellsBSCB integrityBSCB permeabilityLocomotor recoveryPost-SCIBarrier disruptionAntigen expressionPlasticity of Intact Rubral Projections Mediates Spontaneous Recovery of Function after Corticospinal Tract Injury
Siegel CS, Fink KL, Strittmatter SM, Cafferty WB. Plasticity of Intact Rubral Projections Mediates Spontaneous Recovery of Function after Corticospinal Tract Injury. Journal Of Neuroscience 2015, 35: 1443-1457. PMID: 25632122, PMCID: PMC4308593, DOI: 10.1523/jneurosci.3713-14.2015.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDesigner DrugsFunctional LateralityGene Expression RegulationGlial Fibrillary Acidic ProteinLocomotionMaleMiceMice, Inbred C57BLMice, TransgenicMuscle StrengthMyelin ProteinsNeuronal PlasticityNogo ProteinsPsychomotor DisordersPyramidal TractsRaphe NucleiRecovery of FunctionSpinal Cord InjuriesStereotyped BehaviorTime FactorsConceptsSpinal cord injurySpontaneous functional recoveryFunctional recoverySpontaneous recoveryIncomplete spinal cord injuryCorticospinal tract lesionsWeeks of lesionCorticospinal tract injuryNogo receptor 1Nucleus raphe magnusTract injuryRubrospinal projectionsTract lesionsCord injuryRaphe magnusCircuit rearrangementsAdult CNSCircuit plasticityLocomotor functionAdult micePharmacogenetic toolsRed nucleusRubral projectionReceptor 1Extensive sprouting
2014
Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice
Kesby J, Markou A, Semenova S, Grant I, Ellis R, Letendre S, Achim C, Woods S, Carr A, Letendre S, Ellis R, Schrier R, Heaton R, Atkinson J, Cherner M, Marcotte T, Morgan E, Brown G, Jernigan T, Dale A, Liu T, Scadeng M, Fennema-Notestine C, Archibald S, Achim C, Masliah E, Lipton S, Soontornniyomkij V, Gamst A, Cushman C, Abramson I, Vaida F, Deutsch R, Umlauf A, Atkinson J, Marquie-Beck J, Minassian A, Perry W, Geyer M, Henry B, Young J, Grethe A, Paulus M, Ellis R, Morris S, Smith D, Grant I, Semenova S, Markou A, Kesby J, Kaul M. Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice. European Neuropsychopharmacology 2014, 25: 141-150. PMID: 25476577, PMCID: PMC4289653, DOI: 10.1016/j.euroneuro.2014.07.014.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, OcularAnalysis of VarianceAnimalsBody WeightCentral Nervous System StimulantsCognition DisordersDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinHIV Envelope Protein gp120MaleMaze LearningMethamphetamineMiceMice, Inbred C57BLMice, TransgenicReaction TimeRecognition, PsychologyConceptsGp120-tg miceCognitive domainsBarnes mazeMethamphetamine exposureCognitive deficitsSpatial learningAssociative recognition memoryDiscrete cognitive domainsMethamphetamine abuseHuman immunodeficiency virusRecognition memoryExecutive functionBarnes maze testCognitive performanceChronic methamphetamine exposureCognitive functionGp120 expressionAcquisition trialsGreater deficitsHIV infectionPlace testStrategy scoresNeurocognitive outcomesMethamphetamine usersSpatial strategiesLeptin signaling in astrocytes regulates hypothalamic neuronal circuits and feeding
Kim JG, Suyama S, Koch M, Jin S, Argente-Arizon P, Argente J, Liu ZW, Zimmer MR, Jeong JK, Szigeti-Buck K, Gao Y, Garcia-Caceres C, Yi CX, Salmaso N, Vaccarino FM, Chowen J, Diano S, Dietrich MO, Tschöp MH, Horvath TL. Leptin signaling in astrocytes regulates hypothalamic neuronal circuits and feeding. Nature Neuroscience 2014, 17: 908-910. PMID: 24880214, PMCID: PMC4113214, DOI: 10.1038/nn.3725.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesCell CountEatingExcitatory Postsynaptic PotentialsGlial Fibrillary Acidic ProteinHypothalamusImmunohistochemistryIn Situ HybridizationLeptinMaleMelanocortinsMiceMice, KnockoutMicroscopy, ElectronNerve NetNeuronsPrimary Cell CulturePro-OpiomelanocortinPulmonary Gas ExchangeReal-Time Polymerase Chain ReactionRNA, MessengerSignal TransductionRepeated treatment with electroconvulsive seizures induces HDAC2 expression and down-regulation of NMDA receptor-related genes through histone deacetylation in the rat frontal cortex
Park H, Yu H, Park S, Ahn Y, Kim Y, Kim H. Repeated treatment with electroconvulsive seizures induces HDAC2 expression and down-regulation of NMDA receptor-related genes through histone deacetylation in the rat frontal cortex. The International Journal Of Neuropsychopharmacology 2014, 17: 1487-1500. PMID: 24606669, DOI: 10.1017/s1461145714000248.Peer-Reviewed Original ResearchMeSH KeywordsAcetylationAnalysis of VarianceAnimalsButyric AcidChromatin ImmunoprecipitationDisease Models, AnimalElectroshockFrontal LobeGene Expression RegulationGlial Fibrillary Acidic ProteinHistamine AntagonistsHistone Deacetylase 2MalePhosphopyruvate HydrataseRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateRNA, MessengerSeizuresSignal TransductionConceptsSignaling-related genesHistone deacetylasesHistone modificationsHistone acetylationCalcium/calmodulin-dependent protein kinase II alphaChromatin immunoprecipitation analysisRat frontal cortexEarly growth response 1Transcriptional repressionReceptor-related genesHistone deacetylationH4 proteinN-methyl-D-aspartate 2ATarget genesFrontal cortexImmunoprecipitation analysisElectroconvulsive seizuresGene expressionResponse 1GenesHDAC2 expressionNeuronal cellsECS treatmentClass I HDACsII alphaThe angiotensin type 2 receptor agonist Compound 21 elicits cerebroprotection in endothelin-1 induced ischemic stroke
Joseph JP, Mecca AP, Regenhardt RW, Bennion DM, Rodríguez V, Desland F, Patel NA, Pioquinto DJ, Unger T, Katovich MJ, Steckelings UM, Sumners C. The angiotensin type 2 receptor agonist Compound 21 elicits cerebroprotection in endothelin-1 induced ischemic stroke. Neuropharmacology 2014, 81: 134-141. PMID: 24508710, PMCID: PMC7472595, DOI: 10.1016/j.neuropharm.2014.01.044.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin II Type 2 Receptor BlockersAnimalsBrain InfarctionBrain IschemiaCD11b AntigenCerebrovascular CirculationCytokinesDisease Models, AnimalDose-Response Relationship, DrugEndothelin-1Glial Fibrillary Acidic ProteinImidazolesMaleNitric Oxide Synthase Type IIPeroxidasePyridinesRatsRats, Sprague-DawleyStrokeSulfonamidesThiophenesTime FactorsConceptsMiddle cerebral artery occlusionPost-stroke administrationEndothelin-1Neurological deficitsIschemic strokeCerebroprotective actionCerebral damageCerebral ischemiaAT2R agonistChemokine (C-C) motif ligand 2Inducible nitric oxide synthaseBeneficial effectsCerebral infarct sizeMCAO-induced increaseCerebral artery occlusionAnti-inflammatory effectsCerebral blood flowNitric oxide synthaseSelective AT2R agonistPotential therapeutic valueType 2 mRNAAT2R inhibitorArtery occlusionPeripheral administrationHemorrhagic stroke
2013
Olfactory ensheathing cells, but not schwann cells, proliferate and migrate extensively within moderately X‐Irradiated juvenile rat brain
Lankford KL, Brown RJ, Sasaki M, Kocsis JD. Olfactory ensheathing cells, but not schwann cells, proliferate and migrate extensively within moderately X‐Irradiated juvenile rat brain. Glia 2013, 62: 52-63. PMID: 24166823, DOI: 10.1002/glia.22583.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAntigensCD11b AntigenCell MovementCell ProliferationCells, CulturedFemaleGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsMaleNeurogliaOlfactory MucosaOligodendrogliaProteoglycansRadiation Injuries, ExperimentalRatsRats, Sprague-DawleySchwann CellsStem Cell TransplantationConceptsJuvenile rat brainAdult spinal cordIntact adult spinal cordSchwann cellsSpinal cordRat brainAdult rat spinal cordSpinal cord lesionsRat spinal cordCord lesionsModerate radiation doseNeuronal repairPoor survivalAdult CNSUnbiased stereologyCordOECsBrainThree weeksNumber of cellsRadiation dosePermissive environmentCell migrationCellsMicrogliaAntiproliferative Effects of PACAP and VIP in Serum-Starved Glioma Cells
D’Amico A, Scuderi S, Saccone S, Castorina A, Drago F, D’Agata V. Antiproliferative Effects of PACAP and VIP in Serum-Starved Glioma Cells. Journal Of Molecular Neuroscience 2013, 51: 503-513. PMID: 23900722, DOI: 10.1007/s12031-013-0076-7.Peer-Reviewed Original ResearchConceptsPituitary adenylate cyclase-activating polypeptideVasoactive intestinal peptideCalorie restrictionGlioma cellsCell proliferationEffects of PACAPAdenylate cyclase-activating polypeptideCyclase-activating polypeptideExpression of p53Expression of nestinFormation of metastasesC6 glioma cellsIntestinal peptideAcute conditionsVIP treatmentPrognostic markerExpression of proteinsCell malignanciesGFAP decreasesTumor microenvironmentAntiproliferative effectsCyclin D1Cancer developmentCancer treatmentCancer cells
2012
Nucleus Accumbens 1, a Pox virus and Zinc finger/Bric-a-brac Tramtrack Broad protein binds to TAR DNA-binding protein 43 and has a potential role in Amyotrophic Lateral Sclerosis
Scofield M, Korutla L, Jackson T, Kalivas P, Mackler S. Nucleus Accumbens 1, a Pox virus and Zinc finger/Bric-a-brac Tramtrack Broad protein binds to TAR DNA-binding protein 43 and has a potential role in Amyotrophic Lateral Sclerosis. Neuroscience 2012, 227: 44-54. PMID: 23022214, PMCID: PMC3505276, DOI: 10.1016/j.neuroscience.2012.09.043.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAspartic AcidCell DeathCholine O-AcetyltransferaseCytoplasmDNA-Binding ProteinsEmbryo, MammalianGene Expression RegulationGlial Fibrillary Acidic ProteinGlutamic AcidImmunoprecipitationNeoplasm ProteinsNeuronsPhosphopyruvate HydrataseProtein BindingRatsRepressor ProteinsSpinal CordTransfectionUbiquitinationConceptsNucleus accumbens-1Amyotrophic lateral sclerosisPOZ/BTB domainUbiquitin-proteasome systemTDP-43Protein 43Lateral sclerosisBTB domainPrimary spinal cord culturesDevelopment of ALSTAR DNA-binding protein 43POZ/BTB proteinDNA-binding protein 43Extracellular glutamate levelsTDP-43 expressionFull-length TDP-43Spinal cord culturesGST pulldown assaysPost-translational modificationsUbiquitinated protein aggregatesCholinergic neuronsGlutamate toxicityCord culturesGlutamate levelsSpinal cord
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