2025
S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity
Zhang X, Vlkolinsky R, Wu C, Dolatabadi N, Scott H, Prikhodko O, Zhang A, Blanco M, Lang N, Piña-Crespo J, Nakamura T, Roberto M, Lipton S. S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2418179122. PMID: 40014571, PMCID: PMC11892585, DOI: 10.1073/pnas.2418179122.Peer-Reviewed Original ResearchConceptsActivity-dependent gene expressionGene expressionAlzheimer's diseaseCREB-dependent gene expressionS-nitrosylationNitric oxide (NO)-related speciesTargets of S-nitrosylationNeuronal activity-dependent gene expressionPathogenesis of ADDecreased neurite lengthIncreased neuronal cell deathNeuronal cell deathSynaptic plasticityTranscriptional pathwaysCell deathCRISPR/Cas9 techniqueTranscription coactivator 1AD modelLong-term memory formationIncreased S-nitrosylationLong-term potentiationTherapeutic targetExpressionNeurite lengthCerebrocortical neurons
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 expression
2023
Restorative effect of NitroSynapsin on synaptic plasticity in an animal model of depression
Tse W, Pochwat B, Szewczyk B, Misztak P, Bobula B, Tokarski K, Worch R, Czarnota-Bojarska M, Lipton S, Zaręba-Kozioł M, Bijata M, Wlodarczyk J. Restorative effect of NitroSynapsin on synaptic plasticity in an animal model of depression. Neuropharmacology 2023, 241: 109729. PMID: 37797736, DOI: 10.1016/j.neuropharm.2023.109729.Peer-Reviewed Original ResearchConceptsMedial prefrontal cortexLong-term potentiationChronic restraint stress mouse modelSynaptic plasticityN-methyl-D-aspartate receptor antagonistRestraint stress mouse modelMale C57BL/6J miceAntidepressant-like activityTail suspension testStress mouse modelFunctional synaptic plasticityMajor depressive disorderAntidepressant potentialPharmacological treatmentPsychotomimetic effectsReceptor antagonistC57BL/6J miceDepressive behaviorSucrose preferenceDepressive disorderNitroSynapsinMouse modelSuspension testBehavioral disturbancesCerebrocortical neurons
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
2001
Erythropoietin-mediated neuroprotection involves cross-talk between Jak2 and NF-κB signalling cascades
Digicaylioglu M, Lipton S. Erythropoietin-mediated neuroprotection involves cross-talk between Jak2 and NF-κB signalling cascades. Nature 2001, 412: 641-647. PMID: 11493922, DOI: 10.1038/35088074.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell NucleusCells, CulturedDNAErythropoietinGenes, ReporterJanus Kinase 2N-MethylaspartateNeuronsNeuroprotective AgentsNF-kappa BNitric OxideProtein BindingProtein TransportProtein-Tyrosine KinasesProto-Oncogene ProteinsRatsReceptors, ErythropoietinSignal TransductionSuperoxide DismutaseTumor Necrosis Factor-alphaConceptsHypoxia-inducible factor-1EPO receptorForm of JAK2Transcription factor hypoxia-inducible factor-1NF-κB-dependent transcriptionNF-κB functionActivation of JAK2Subsequent nuclear translocationTranscription factor NF-κBNF-κBFactor NF-κBSignaling cascadesNitric oxideKinase 2NF-κB signaling cascadesHypoxic-ischemic preconditioningNuclear translocationNeuroprotective genesFactor 1JAK2Neuroprotective pathwaysNeuronal apoptosisCerebrocortical neuronsEPO effectsDegenerative damage
2000
Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons
Budd S, Tenneti L, Lishnak T, Lipton S. Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 6161-6166. PMID: 10811898, PMCID: PMC18575, DOI: 10.1073/pnas.100121097.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsApoptosisBongkrekic AcidCaspase 3Caspase 8Caspase 9CaspasesCerebral CortexCytochrome c GroupEnzyme ActivationEnzyme InhibitorsIntracellular MembranesMitochondriaMitochondrial ADP, ATP TranslocasesNerve Tissue ProteinsNeuronsPermeabilityProtein Kinase InhibitorsReceptors, N-Methyl-D-AspartateStaurosporineConceptsAdenine nucleotide translocatorBongkrekic acidCaspase-3 activationMitochondrial adenine nucleotide translocatorCyt cReceptor-mediated apoptosisApoptotic signaling pathwaysMitochondrial permeability transition poreMitochondrial membrane potentialPermeability transition poreStaurosporine-induced activationCellular ATP contentStaurosporine resultsPutative componentsCerebrocortical neuronsNucleotide translocatorCaspase activityCaspase-8Signaling pathwaysTransition poreMitochondrial dysfunctionCytochrome cDistinct pathwaysCultured cerebrocortical neuronsApoptosisCytokine-Stimulated, But Not HIV-Infected, Human Monocyte-Derived Macrophages Produce Neurotoxic Levels of l-Cysteine
Yeh M, Kaul M, Zheng J, Nottet H, Thylin M, Gendelman H, Lipton S. Cytokine-Stimulated, But Not HIV-Infected, Human Monocyte-Derived Macrophages Produce Neurotoxic Levels of l-Cysteine. The Journal Of Immunology 2000, 164: 4265-4270. PMID: 10754324, DOI: 10.4049/jimmunol.164.8.4265.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCerebral CortexCysteineCytokinesDose-Response Relationship, ImmunologicHIV Envelope Protein gp120HIV-1HumansImmune SeraInterleukin 1 Receptor Antagonist ProteinInterleukin-1Macrophage ActivationMacrophagesMonocytesNeuronsRatsRats, Sprague-DawleyReceptors, Interleukin-1Receptors, N-Methyl-D-AspartateSialoglycoproteinsSphingosineTumor Necrosis Factor-alphaConceptsHuman monocyte-derived macrophagesNeuronal injuryTNF-alphaHIV-1N-methyl-D-aspartate (NMDA) subtypeUninfected cellsMacrophages/microgliaCultured rat cerebrocortical neuronsVirus-infected macrophagesRelease of neurotoxinsRat cerebrocortical neuronsEnvelope glycoprotein gp120Monocyte-derived macrophagesDose-dependent mannerNeuropathological symptomsIL-1betaGlutamate receptorsCerebrocortical neuronsHIVGlycoprotein gp120Mononuclear phagocytesNeurotoxic levelsGp120Human monocytesCytokine stimulationInvolvement 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 technique
1998
Role of Caspases in N‐Methyl‐d‐Aspartate‐Induced Apoptosis in Cerebrocortical Neurons
Tenneti L, D'Emilia D, Troy C, Lipton S. Role of Caspases in N‐Methyl‐d‐Aspartate‐Induced Apoptosis in Cerebrocortical Neurons. Journal Of Neurochemistry 1998, 71: 946-959. PMID: 9721720, DOI: 10.1046/j.1471-4159.1998.71030946.x.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid Chloromethyl KetonesAnimalsApoptosisCalciumCaspase 1Cells, CulturedCerebral CortexCysteine EndopeptidasesCysteine Proteinase InhibitorsIntracellular MembranesLipid PeroxidesMembrane PotentialsMitochondriaN-MethylaspartateNeuronsRatsRats, Sprague-DawleyReactive Oxygen SpeciesSignal TransductionConceptsInterleukin-1beta-converting enzymeMitochondrial membrane potentialReactive oxygen speciesRole of caspasesZ-VAD-FMKROS formationMembrane potentialReceptor activationCaspase activationDownstream eventsPseudosubstrate peptideNeuronal apoptosisMitochondrial depolarizationCysteine proteasesLipid peroxidationCaspasesCerebrocortical neuronsSubstrate cleavageIntracellular processesForm of deathN-methyl-D-aspartate (NMDA) receptor activationCortical neuronal apoptosisApoptosisCatalytic siteNMDA receptor activationIncreased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A
Das S, Sasaki Y, Rothe T, Premkumar L, Takasu M, Crandall J, Dikkes P, Conner D, Rayudu P, Cheung W, Chen H, Lipton S, Nakanishi N. Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A. Nature 1998, 393: 377-381. PMID: 9620802, DOI: 10.1038/30748.Peer-Reviewed Original ResearchConceptsNMDA receptorsReceptor subunit NR1Synaptic refinementSpine densityNMDA receptor subunit NR3ANMDA responsesNMDA subclassSmall unitary conductanceNMDAR activitySubunit NR1NMDAR subunitsCerebrocortical neuronsDendritic spinesSynaptic plasticityNR1 subunitMice resultsSingle-channel recordingsGenetic knockoutSynaptic elementsHeteromultimeric channelsNR1NR3AXenopus oocytesUnitary conductanceNMDA
1997
Suppression of neuronal apoptosis by S-nitrosylation of caspases
Tenneti L, D'Emilia D, Lipton S. Suppression of neuronal apoptosis by S-nitrosylation of caspases. Neuroscience Letters 1997, 236: 139-142. PMID: 9406756, DOI: 10.1016/s0304-3940(97)00780-5.Peer-Reviewed Original ResearchConceptsS-nitrosylationInterleukin-1beta-converting enzyme-like proteasesCritical cysteine residuesEnzyme-like proteasesApoptotic cell deathHuman embryonic kidneyTranscription factorsEnzyme familyCysteine residuesG proteinsEmbryonic kidneyCell deathCaspasesIon channelsPrimary cerebrocortical neuronsPhysiological activityEnzyme activityActive siteApoptosisNeuronal apoptosisCerebrocortical neuronsFamilyProteinProteaseEnzyme
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