2024
Dysregulation of miRNA expression and excitation in MEF2C autism patient hiPSC-neurons and cerebral organoids
Trudler D, Ghatak S, Bula M, Parker J, Talantova M, Luevanos M, Labra S, Grabauskas T, Noveral S, Teranaka M, Schahrer E, Dolatabadi N, Bakker C, Lopez K, Sultan A, Patel P, Chan A, Choi Y, Kawaguchi R, Stankiewicz P, Garcia-Bassets I, Kozbial P, Rosenfeld M, Nakanishi N, Geschwind D, Chan S, Lin W, Schork N, Ambasudhan R, Lipton S. Dysregulation of miRNA expression and excitation in MEF2C autism patient hiPSC-neurons and cerebral organoids. Molecular Psychiatry 2024, 30: 1479-1496. PMID: 39349966, PMCID: PMC11919750, DOI: 10.1038/s41380-024-02761-9.Peer-Reviewed Original ResearchMEF2C haploinsufficiency syndromeLoss-of-function mutationsCerebral organoidsHaploinsufficiency syndromeReceptor antagonistHiPSC-neuronsDecreased neurogenesisSevere formCerebrocortical neuronsAnimal studiesExtrasynaptic activationMEF2CAbnormal phenotypesNeurodevelopmentNeuronsDeficitsOrganoidsTranscription factorsMutationsNitroSynapsinGene networksDysregulation of miRNA expressionSingle‐Cell Patch‐Clamp/Proteomics of Human Alzheimer's Disease iPSC‐Derived Excitatory Neurons Versus Isogenic Wild‐Type Controls Suggests Novel Causation and Therapeutic Targets
Ghatak S, Diedrich J, Talantova M, Bhadra N, Scott H, Sharma M, Albertolle M, Schork N, Yates J, Lipton S. Single‐Cell Patch‐Clamp/Proteomics of Human Alzheimer's Disease iPSC‐Derived Excitatory Neurons Versus Isogenic Wild‐Type Controls Suggests Novel Causation and Therapeutic Targets. Advanced Science 2024, 11: e2400545. PMID: 38773714, PMCID: PMC11304297, DOI: 10.1002/advs.202400545.Peer-Reviewed Original ResearchAbundance of individual proteinsIsogenic wild-type controlsSingle-cell (scHuman AD brainsWild-type controlsSingle-cellAlzheimer's diseaseMulticellular organismsSingle-cell physiologyAD brainTherapeutic targetIndividual proteinsProteomic informationGenetic mutationsProteinProteomicsProtein expressionHiPSC-neuronsExcitatory neuronsElectrophysiological statusDisease statesPhysiologyElectrophysiological dataNeuronsNeuronal level
2021
Soluble α-synuclein–antibody complexes activate the NLRP3 inflammasome in hiPSC-derived microglia
Trudler D, Nazor K, Eisele Y, Grabauskas T, Dolatabadi N, Parker J, Sultan A, Zhong Z, Goodwin M, Levites Y, Golde T, Kelly J, Sierks M, Schork N, Karin M, Ambasudhan R, Lipton S. Soluble α-synuclein–antibody complexes activate the NLRP3 inflammasome in hiPSC-derived microglia. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2025847118. PMID: 33833060, PMCID: PMC8054017, DOI: 10.1073/pnas.2025847118.Peer-Reviewed Original ResearchConceptsHuman microgliaLike receptor family pyrinFibrillar αSynA9 dopaminergic neuronsInterleukin-1β secretionCaspase-1 activationMicroglial activationFamily pyrinAntibody therapyNeuronal deathParkinson's diseaseMicrogliaMouse brainΑ-synucleinDual stimulationMitochondrial damageΑSynAntibodiesInflammationNLRP3Cognate antibodiesHuman brainDiseaseNeuronsStem cells
2014
Differential Effects of Synaptic and Extrasynaptic NMDA Receptors on Aβ-Induced Nitric Oxide Production in Cerebrocortical Neurons
Molokanova E, Akhtar M, Sanz-Blasco S, Nakamura T, Okamoto S, Tu S, Piña-Crespo J, McKercher S, Lipton S. Differential Effects of Synaptic and Extrasynaptic NMDA Receptors on Aβ-Induced Nitric Oxide Production in Cerebrocortical Neurons. Biophysical Journal 2014, 106: 152a. DOI: 10.1016/j.bpj.2013.11.874.Peer-Reviewed Original Research
2006
Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons
Yuan H, Gerencser A, Liot G, Lipton S, Ellisman M, Perkins G, Bossy-Wetzel E. Mitochondrial fission is an upstream and required event for bax foci formation in response to nitric oxide in cortical neurons. Cell Death & Differentiation 2006, 14: 462-471. PMID: 17053808, DOI: 10.1038/sj.cdd.4402046.Peer-Reviewed Original ResearchConceptsMitochondrial fissionNitric oxideFoci formationCortical neuronsMitochondrial fission machineryBcl-2 familyNitrosative stressAntiapoptotic Bcl-xLNeuronal cell deathFission machineryMitofusin 1Puncta formationBioenergetic crisisBax accumulationMitochondrial inhibitorsNeuronal demiseBcl-xLCell deathMitochondrial dysfunctionMitochondriaNeurodegenerative disordersNO donorNeuronsScission siteFission
2001
Pathways to neuronal injury and apoptosis in HIV-associated dementia
Kaul M, Garden G, Lipton S. Pathways to neuronal injury and apoptosis in HIV-associated dementia. Nature 2001, 410: 988-994. PMID: 11309629, DOI: 10.1038/35073667.Peer-Reviewed Original ResearchConceptsHuman immunodeficiency virus-1Neuronal injuryRelease of macrophageImmunodeficiency virus-1Direct injuryTherapeutic interventionsAlarming occurrenceNeurodegenerative diseasesInjuryVirus 1NeuronsDementiaViral proteinsMacrophagesFree radicalsApoptosisToxinPathwayExcitotoxicityMicrogliaHIVDiseaseBrainIs tissue plasminogen activator a threat to neurons?
Traynelis S, Lipton S. Is tissue plasminogen activator a threat to neurons? Nature Medicine 2001, 7: 17-18. PMID: 11135603, DOI: 10.1038/83289.Peer-Reviewed Original Research
2000
Involvement of Activated Caspase‐3‐Like Proteases in N‐Methyl‐D‐Aspartate‐Induced Apoptosis in Cerebrocortical Neurons
Tenneti L, Lipton S. Involvement of Activated Caspase‐3‐Like Proteases in N‐Methyl‐D‐Aspartate‐Induced Apoptosis in Cerebrocortical Neurons. Journal Of Neurochemistry 2000, 74: 134-142. PMID: 10617114, DOI: 10.1046/j.1471-4159.2000.0740134.x.Peer-Reviewed Original ResearchConceptsCerebrocortical neuronsNeuronal deathNeuronal apoptosisIncubation of neuronsNMDA receptor activationCaspase-3Time-dependent increaseCentral neuronsNMDA stimulationExcessive activationGlutamate receptorsMild insultReceptor activationCaspase-3-like proteasesDouble labelingNeurodegenerative diseasesNMDANeuronsApoptotic cellsConcordant resultsApoptosisPossible activationActivation of caspasesInsultAffinity labeling techniqueHow Are Neuronal Genes Expressed in Neurons? Regulation of NMDA Receptor Subunit Type 1 Gene as a Model
Okamoto S, Sherman K, Lipton S. How Are Neuronal Genes Expressed in Neurons? Regulation of NMDA Receptor Subunit Type 1 Gene as a Model. 2000, 355-360. DOI: 10.1007/978-4-431-66973-9_47.Peer-Reviewed Original ResearchType 1 geneRegulation of expressionGene regulationNeuronal genesEssential subunitDifferentiation proceedsTranscriptional levelFunctional NMDA receptorsNeuronal differentiationGenesVariety of moleculesNR1 geneNeuronal functionRegulationCentral nervous systemNR1ExpressionSynaptic responsesNMDA receptorsNeuronal activityNervous systemSubunitsNeuronsDifferentiationBest model
1999
Chemokines and activated macrophages in HIV gp120-induced neuronal apoptosis
Kaul M, Lipton S. Chemokines and activated macrophages in HIV gp120-induced neuronal apoptosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 8212-8216. PMID: 10393974, PMCID: PMC22214, DOI: 10.1073/pnas.96.14.8212.Peer-Reviewed Original ResearchMeSH KeywordsAIDS Dementia ComplexAnimalsApoptosisCells, CulturedCerebral CortexChemokine CCL4Chemokine CCL5Chemokine CXCL12ChemokinesCytokinesEmbryo, MammalianHIV Envelope Protein gp120HIV-1HumansImmunoglobulin FragmentsMacrophage ActivationMacrophage Inflammatory ProteinsMacrophagesNeurogliaNeuronsOligopeptidesRatsRats, Sprague-DawleyRecombinant ProteinsT-LymphocytesConceptsMacrophages/microgliaNeuronal apoptosisChemokine receptorsSDF-1Brain macrophages/microgliaStromal cell-derived factorRat cerebrocortical culturesBeta-chemokines RANTESCell-derived factorNeurotoxic factorsP38 mitogen-activated protein kinase (MAPK) pathwayProportion of cellsInflammatory proteinP38 mitogen-activated protein kinaseGp120SF2Cerebrocortical culturesReceptor CXCR4MicrogliaHuman neuronsHIV gp120CXCR4 receptorMitogen-activated protein kinase pathwayMitogen-activated protein kinaseNeuronsGp120
1998
■ REVIEW : Excitotoxicity, Free Radicals, Necrosis, and Apoptosis
Lipton S, Nicotera P. ■ REVIEW : Excitotoxicity, Free Radicals, Necrosis, and Apoptosis. The Neuroscientist 1998, 4: 345-352. DOI: 10.1177/107385849800400516.Peer-Reviewed Original ResearchNitric oxideMajor excitatory neurotransmitterCentral nervous systemFailure of neuronsFree radicalsNeuronal cell culturesActivation of proteasesNeuronal injuryAIDS dementiaNeuronal necrosisInitial insultExcitatory neurotransmitterNervous systemApoptotic death programAlzheimer's diseaseHuntington's diseaseDiseaseInsultExcitotoxicityMitochondrial membrane potentialNecrosisCell deathDeath programNeuronsApoptosis
1996
Neuronal apoptosis versus necrosis induced by glutamate or free radicals
Nicotera P, Ankarcrona M, Bonfoco E, Orrenius S, Lipton S. Neuronal apoptosis versus necrosis induced by glutamate or free radicals. Apoptosis 1996, 1: 5-10. DOI: 10.1007/bf00142073.Peer-Reviewed Original ResearchMajor excitatory neurotransmitterCentral nervous systemFailure of neuronsFree radicalsNeuronal cell culturesNeuronal injuryExcitatory neurotransmitterNeuronal apoptosisNervous systemApoptotic death programNitric oxideInsultInjuryCell deathDeath programNeuronsGlutamateCell culturesApoptosisExcitotoxinsIschemiaEnergy depletionNecrosisNeurotransmittersProgression
1995
The Coat Protein gp120 of HIV‐1 Inhibits Astrocyte Uptake of Excitatory Amino Acids via Macrophage Arachidonic Acid
Dreyer E, Lipton S. The Coat Protein gp120 of HIV‐1 Inhibits Astrocyte Uptake of Excitatory Amino Acids via Macrophage Arachidonic Acid. European Journal Of Neuroscience 1995, 7: 2502-2507. PMID: 8845955, DOI: 10.1111/j.1460-9568.1995.tb01048.x.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsAmino acidsAstrocyte uptakeNeuronal damageProtein gp120Excitatory amino acid uptakeAmino acid uptakeN-methyl-D-aspartate receptorsArachidonic acidCentral mammalian neuronsMammalian neuronsReleases arachidonic acidNeuronal injuryBrain macrophagesImmunodeficiency syndromeNeurological dysfunctionAcid uptakeExcess glutamateGp120MacrophagesAstrocytesNeuronsInitial activationPresent dataUptakeAn astrocytic binding site for neuronal Thy-1 and its effect on neurite outgrowth.
Dreyer E, Leifer D, Heng J, McConnell J, Gorla M, Levin L, Barnstable C, Lipton S. An astrocytic binding site for neuronal Thy-1 and its effect on neurite outgrowth. Proceedings Of The National Academy Of Sciences Of The United States Of America 1995, 92: 11195-11199. PMID: 7479964, PMCID: PMC40598, DOI: 10.1073/pnas.92.24.11195.Peer-Reviewed Original ResearchConceptsNeurite outgrowthThy-1 functionsNeuronal Thy-1Thy-1Abundant glycoproteinMammalian neuronsNervous systemAnti-idiotype monoclonal antibodyCentral nervous system neuronsMonoclonal antibodiesBinding sitesCentral nervous systemAnti-idiotype antibodiesCertain monoclonal antibodiesBinding assaysCompetitive binding assaysProteinOutgrowthSystem neuronsDendritic developmentAntibodiesNeuronsSitesGlycoproteinCellsGlutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function
Ankarcrona M, Dypbukt J, Bonfoco E, Zhivotovsky B, Orrenius S, Lipton S, Nicotera P. Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function. Neuron 1995, 15: 961-973. PMID: 7576644, DOI: 10.1016/0896-6273(95)90186-8.Peer-Reviewed Original ResearchConceptsIschemic brain injurySubpopulation of neuronsNeuronal cell deathPostsynaptic glutamate receptorsMitochondrial functionEarly necrotic phaseCerebellar granule cellsNeuronal deathBrain injuryGlutamate receptorsGranule cellsIntracellular Ca2Glutamate accumulationEarly necrosisNecrosisMitochondrial membrane potentialApoptotic nucleiIncubation mediumIntracellular debrisCell deathLow molecular weight fragmentsNecrotic phaseNeuronsApoptosisDeath
1994
Greater sensitivity of larger retinal ganglion cells to NMDA-mediated cell death
Dreyer E, Pan Z, Storm S, Lipton S. Greater sensitivity of larger retinal ganglion cells to NMDA-mediated cell death. Neuroreport 1994, 5: 629-631. PMID: 7912962, DOI: 10.1097/00001756-199401000-00024.Peer-Reviewed Original ResearchConceptsLarge retinal ganglion cellsRetinal ganglion cellsGanglion cellsGlutamate-mediated cell deathN-methyl-D-aspartate (NMDA) subtypeIntact rat eyesCell deathNeuronal lossGlutamate toxicityGlutamate receptorsRat eyesPattern of lossNMDAGlaucomaToxic effectsDeathCellsGlutamateTissue cultureGreater sensitivitySubtypesNeuronsSimilar fashionReceptors
1993
hMEF2C gene encodes skeletal muscle- and brain-specific transcription factors.
McDermott J, Cardoso M, Yu Y, Andres V, Leifer D, Krainc D, Lipton S, Nadal-Ginard B. hMEF2C gene encodes skeletal muscle- and brain-specific transcription factors. Molecular And Cellular Biology 1993, 13: 2564-2577. PMID: 8455629, PMCID: PMC359588, DOI: 10.1128/mcb.13.4.2564.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAmino Acid SequenceAnimalsBase SequenceBrainCells, CulturedCloning, MolecularConsensus SequenceDNA-Binding ProteinsGene ExpressionGenesHumansImmunologic TechniquesIn Vitro TechniquesMEF2 Transcription FactorsMiceMolecular Sequence DataMusclesMyogenic Regulatory FactorsNeuronsOligodeoxyribonucleotidesPolymerase Chain ReactionRNA, MessengerSequence AlignmentTissue DistributionTranscription FactorsTranscription, GeneticConceptsSkeletal muscleSubset of neuronsCortical neuronsBrain-specific transcription factorTranscription factorsMRNA levelsPotential targetTrans-activating activityMuscleMEF2 transcription factorsNeuronsBrainBrain transcriptsMEF2 factorsMuscle-specific enhancerExpressionMyogenic differentiationTissue-specific isoformsUbiquitous expressionFactorsTissue-specific patternsGenesNeurogenesishMEF2C Gene Encodes Skeletal Muscle- and Brain-Specific Transcription Factors
McDermott J, Cardoso M, Yu Y, Andres V, Leifer D, Krainc D, Lipton S, Nadal-Ginard B. hMEF2C Gene Encodes Skeletal Muscle- and Brain-Specific Transcription Factors. Molecular And Cellular Biology 1993, 13: 2564-2577. DOI: 10.1128/mcb.13.4.2564-2577.1993.Peer-Reviewed Original ResearchSkeletal muscleSubset of neuronsCortical neuronsBrain-specific transcription factorTranscription factorsMRNA levelsPotential targetTrans-activating activityMuscleMEF2 transcription factorsNeuronsBrainBrain transcriptsMEF2 factorsMuscle-specific enhancerExpressionMyogenic differentiationTissue-specific isoformsUbiquitous expressionFactorsTissue-specific patternsGenesNeurogenesisMEF2C, a MADS/MEF2-family transcription factor expressed in a laminar distribution in cerebral cortex.
Leifer D, Krainc D, Yu Y, McDermott J, Breitbart R, Heng J, Neve R, Kosofsky B, Nadal-Ginard B, Lipton S. MEF2C, a MADS/MEF2-family transcription factor expressed in a laminar distribution in cerebral cortex. Proceedings Of The National Academy Of Sciences Of The United States Of America 1993, 90: 1546-1550. PMID: 7679508, PMCID: PMC45911, DOI: 10.1073/pnas.90.4.1546.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsbeta-GalactosidaseBlotting, NorthernBrainCerebral CortexChloramphenicol O-AcetyltransferaseCloning, MolecularDNADNA-Binding ProteinsFetusGene LibraryGenetic VectorsHumansMADS Domain ProteinsMEF2 Transcription FactorsMolecular Sequence DataMultigene FamilyMyogenic Regulatory FactorsOrgan SpecificityRatsRecombinant Fusion ProteinsRNASequence Homology, Amino AcidTranscription FactorsTransfection
1992
Blockade of NMDA receptor-mediated mobilization of intracellular Ca2+ prevents neurotoxicity
Lei S, Zhang D, Abele A, Lipton S. Blockade of NMDA receptor-mediated mobilization of intracellular Ca2+ prevents neurotoxicity. Brain Research 1992, 598: 196-202. PMID: 1486480, DOI: 10.1016/0006-8993(92)90183-a.Peer-Reviewed Original ResearchConceptsIntracellular Ca2Extracellular Ca2Excessive NMDA receptor stimulationRetinal ganglion cell neuronsNMDA receptor-mediated neurotoxicityGanglion cell neuronsNMDA receptor activationReceptor-mediated mobilizationNMDA receptor stimulationNormal extracellular Ca2Neuronal damagePharmacological interventionsPrevents neurotoxicityReceptor stimulationPresence of EGTAIntracellular storesNMDACell neuronsReceptor activationCultured ratDelayed neurotoxicityDantroleneNeurotoxicityElevated Ca2Neurons
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply