2025
CSF proteomics reveals changes in myelin and synaptic biology after Spectris treatment
Hajós M, Pandey K, Singer A, Duong D, Bitarafan S, Shpokayte M, Malchano Z, Kern R, Lah J, Levey A, Seyfried N. CSF proteomics reveals changes in myelin and synaptic biology after Spectris treatment. Alzheimer's & Dementia: Translational Research & Clinical Interventions 2025, 11: e70051. PMID: 39935616, PMCID: PMC11812123, DOI: 10.1002/trc2.70051.Peer-Reviewed Original ResearchCellular lipid transportLipid transportWeeks of treatmentProteomic changesAlzheimer's diseaseCerebrospinal fluidGamma oscillationsTandem mass tag-mass spectrometryNeuroimmune functionDifferential expression analysisMyelin preservationUnbiased proteomic analysisBiological pathway analysisTreatment of ADSynaptic biologyAffected proteinsProteome modulationPhosphatidylcholine biosynthesisReduced brain volumeCSF proteome changesProtein networkSensory‐evoked gamma oscillationsExpression analysisBiochemical pathwaysBiological pathways
2022
Genomics analysis of Drosophila sechellia response to Morinda citrifolia fruit diet
Drum Z, Lanno S, Gregory S, Shimshak S, Barr W, Gatesman A, Schadt M, Sanford J, Arkin A, Assignon B, Colorado S, Dalgarno C, Devanny T, Ghandour T, Griffin R, Hogan M, Horowitz E, McGhie E, Multer J, O'Halloran H, Ofori-Darko K, Pokushalov D, Richards N, Sagarin K, Taylor N, Thielking A, Towle P, Coolon J. Genomics analysis of Drosophila sechellia response to Morinda citrifolia fruit diet. G3: Genes, Genomes, Genetics 2022, 12: jkac153. PMID: 35736356, PMCID: PMC9526069, DOI: 10.1093/g3journal/jkac153.Peer-Reviewed Original ResearchConceptsGene expression responsesD. sechelliaGenome-wide gene expression responsesExpression responsesTranscription factor prediction analysesNoni fruitDrosophila sechelliaGenomic analysisRegulatory networksIdentified genesHost specialistsToxic fruitsGenetic mechanismsRNA sequencingBiochemical pathwaysToxin resistanceFruit flyFruit dietGenesFruitMorinda citrifoliaAbundant compoundsGeneral responseNoniRegulation
2021
Protein Transnitrosylation Signaling Networks Contribute to Inflammaging and Neurodegenerative Disorders
Nakamura T, Oh C, Zhang X, Tannenbaum S, Lipton S. Protein Transnitrosylation Signaling Networks Contribute to Inflammaging and Neurodegenerative Disorders. Antioxidants And Redox Signaling 2021, 35: 531-550. PMID: 33957758, PMCID: PMC8388249, DOI: 10.1089/ars.2021.0081.Peer-Reviewed Original ResearchConceptsRelated reactive nitrogen speciesS-nitrosylationRedox-based posttranslational modificationProtein S-nitrosylationGlyceraldehyde-3-phosphate dehydrogenaseInhibitor of apoptosisThiol-containing proteinsNeurodegenerative diseasesSignaling networksPosttranslational modificationsReactive nitrogen speciesTransnitrosylation reactionsNuclear proteinsUnderstanding of agingCysteine thiolsTransnitrosylationBiochemical pathwaysChemical biologyMechanisms of diseaseProteinCaspase-3Nitrogen speciesUCH-L1Neurodegenerative disordersPhysiological concentrationsCerebellar Kv3.3 potassium channels activate TANK-binding kinase 1 to regulate trafficking of the cell survival protein Hax-1
Zhang Y, Varela L, Szigeti-Buck K, Williams A, Stoiljkovic M, Šestan-Peša M, Henao-Mejia J, D’Acunzo P, Levy E, Flavell RA, Horvath TL, Kaczmarek LK. Cerebellar Kv3.3 potassium channels activate TANK-binding kinase 1 to regulate trafficking of the cell survival protein Hax-1. Nature Communications 2021, 12: 1731. PMID: 33741962, PMCID: PMC7979925, DOI: 10.1038/s41467-021-22003-8.Peer-Reviewed Original ResearchConceptsTank Binding Kinase 1HAX-1Kv3.3 potassium channelMultivesicular bodiesKinase 1TANK-binding kinase 1Activation of caspasesAnti-apoptotic proteinsPotassium channelsMembrane proteinsBiochemical pathwaysCerebellar neuronsChannels bindCell deathTBK1 activityIon channelsMutant channelsCellular constituentsTraffickingKv3.3 channelsProteinNeuronal survivalMutationsChannel inactivationCaspases
2019
Omics and coagulation disorders in pregnancy
Ornaghi S, Paidas M. Omics and coagulation disorders in pregnancy. 2019, 149-155. DOI: 10.1201/9781315201955-24.Peer-Reviewed Original ResearchFetal growth restrictionOmics technologiesPlacenta-mediated complicationsMaternal thromboembolismSpecific biological sampleCoagulation disordersMolecular basisBiochemical pathwaysRegistry-based studyMessenger RNADifferent clinical conditionsVascular biologyPlacental abruptionFetal lossGrowth restrictionRisk factorsClinical conditionsLarge cohortNonbiased mannerBiomarker developmentThromboembolismPreeclampsiaComplicationsPregnancyRelevant diseases
2018
Reconstructing static and dynamic models of signaling pathways using Modular Response Analysis
Santra T, Rukhlenko O, Zhernovkov V, Kholodenko B. Reconstructing static and dynamic models of signaling pathways using Modular Response Analysis. Current Opinion In Systems Biology 2018, 9: 11-21. DOI: 10.1016/j.coisb.2018.02.003.Peer-Reviewed Original ResearchModular Response AnalysisNetwork reconstruction methodsPhysics-based methodBiochemical pathwaysBiological networksNetwork reconstructionTopological modelDynamic modelResponse analysisNetwork modulesCertain conditionsPathwayReconstruction methodMechanistic modelEntire networkModelCore theoryReformulationPerturbationsTheorySufficient numberNetworkGlobal responseDirection
2006
Riboswitches: Regulators of modern and ancient metabolism
Kim J, Breaker R. Riboswitches: Regulators of modern and ancient metabolism. The Biochemist 2006, 28: 11-15. DOI: 10.1042/bio02802011.Peer-Reviewed Original ResearchComplex biochemical pathwaysPrimitive life formsNucleic acid biochemistryAncient metabolismPrimitive organismsModern cellsLife formsStructured RNAsBiochemical pathwaysBiological processesEfficient enzymeRNARecent findingsMolecular sensorsSpecific receptorsSuch moleculesRiboswitchOrganismsRegulatorEnormous potentialEnzymePathwayBiochemistryMetabolismCellsEndothelial Cell Dysfunction, Injury and Death
Pober JS, Min W. Endothelial Cell Dysfunction, Injury and Death. Handbook Of Experimental Pharmacology 2006, 176/II: 135-156. PMID: 16999227, DOI: 10.1007/3-540-36028-x_5.Peer-Reviewed Original ResearchConceptsTumor necrosis factorCytolytic T lymphocytesEC injuryEndothelial cellsReactive oxygen speciesEndothelial cell dysfunctionMacrophage-derived cytokinesVascular endothelial cellsEndothelial dysfunctionNecrosis factorCell dysfunctionT lymphocytesInjuryCommon mediatorInflammationDysfunctionDeathOxygen speciesCytokinesLymphocytesNeutrophilsDifferent agentsBiochemical pathways
2001
Title Pages
B.Levitan I, Kaczmarek L. Title Pages. 2001, i-iv. DOI: 10.1093/oso/9780195145236.002.0001.Peer-Reviewed Original ResearchElectrical activityAppropriate synaptic connectionsAction of neurotransmittersBiochemical pathwaysMolecular mechanismsMolecular biologyUndifferentiated cellsIon channelsCellular propertiesSynaptic connectionsNerve cellsNeuronsSensory cellsSynaptic junctionsMolecular factorsSingle neuronsFirst courseCellsGenomeBiologyVaried patternsNeurotransmittersHormoneSecretionActivityPreface
B.Levitan I, Kaczmarek L. Preface. 2001, vii-viii. DOI: 10.1093/oso/9780195145236.002.0003.Peer-Reviewed Original ResearchElectrical activityBiochemical pathwaysMolecular mechanismsAppropriate synaptic connectionsMolecular biologyUndifferentiated cellsAction of neurotransmittersIon channelsCellular propertiesSensory cellsMolecular factorsSynaptic connectionsNerve cellsNeuronsSynaptic junctionsSingle neuronsCellsFirst courseGenomeBiologyPathwayActivityMechanismVaried patternsAccount of mechanismsPreface to the Second Edition
B.Levitan I, Kaczmarek L. Preface to the Second Edition. 2001, ix-x. DOI: 10.1093/oso/9780195145236.002.0004.Peer-Reviewed Original ResearchElectrical activityAppropriate synaptic connectionsBiochemical pathwaysAction of neurotransmittersMolecular mechanismsMolecular biologyUndifferentiated cellsIon channelsCellular propertiesSensory cellsMolecular factorsSynaptic connectionsNerve cellsNeuronsSynaptic junctionsSingle neuronsCellsFirst courseGenomeBiologyPathwayVaried patternsActivityMechanismNeurotransmittersPreface to the First Edition
B.Levitan I, Kaczmarek L. Preface to the First Edition. 2001, xi-xii. DOI: 10.1093/oso/9780195145236.002.0005.Peer-Reviewed Original ResearchElectrical activityBiochemical pathwaysMolecular mechanismsAppropriate synaptic connectionsAction of neurotransmittersMolecular biologyUndifferentiated cellsIon channelsCellular propertiesSensory cellsMolecular factorsSynaptic connectionsNerve cellsNeuronsSynaptic junctionsSingle neuronsCellsFirst courseGenomeBiologyPathwayActivityMechanismVaried patternsNeurotransmittersThe hedgehog pathway and basal cell carcinomas
Bale A, Yu K. The hedgehog pathway and basal cell carcinomas. Human Molecular Genetics 2001, 10: 757-762. PMID: 11257109, DOI: 10.1093/hmg/10.7.757.Peer-Reviewed Original ResearchConceptsGenetic studiesHereditary basal cell carcinomasDrosophila genesEmbryonic patterningDevelopmental genesDrosophila melanogasterCell fateHuman homologFruit flyHuman congenital anomaliesBiochemical pathwaysRational medical therapyDevelopmental pathwaysHedgehog pathwayGenesCell growthTumor formationPathwayGorlin syndromeBasal cell carcinomaMutationsHereditary diseaseBirth defectsDrosophilaMelanogaster
1998
Identification of morc (microrchidia), a mutation that results in arrest of spermatogenesis at an early meiotic stage in the mouse
Watson M, Zinn A, Inoue N, Hess K, Cobb J, Handel M, Halaban R, Duchene C, Albright G, Moreadith R. Identification of morc (microrchidia), a mutation that results in arrest of spermatogenesis at an early meiotic stage in the mouse. Proceedings Of The National Academy Of Sciences Of The United States Of America 1998, 95: 14361-14366. PMID: 9826705, PMCID: PMC24378, DOI: 10.1073/pnas.95.24.14361.Peer-Reviewed Original ResearchConceptsMammalian germ cell developmentGerm cellsGerm cell developmentNovel biochemical pathwaysEarly meiotic stagesTransgene expressionMale gametogenesisMouse strain transgenicGenomic analysisProphase IMutant animalsTransgene insertionCDNA constructsEye pigmentationBiochemical pathwaysLeptotene stageAbnormal phenotypeCell developmentMeiotic stagesMeiosisMutation resultsArrest of spermatogenesisGenesSpermatogenesisMutationsPROGRAMMED CELL DEATH
Woodle E, Kulkarni S. PROGRAMMED CELL DEATH. Transplantation 1998, 66: 681-691. PMID: 9771830, DOI: 10.1097/00007890-199809270-00001.Peer-Reviewed Original ResearchConceptsCell deathMechanisms of PCDProgrammed Cell DeathCell biologyBiochemical pathwaysPCDIntegral roleBroad implicationsBiology
1997
Developmental Genes and Cancer: Role of Patched in Basal Cell Carcinoma of the Skin
Gailani M, Bale A. Developmental Genes and Cancer: Role of Patched in Basal Cell Carcinoma of the Skin. Journal Of The National Cancer Institute 1997, 89: 1103-1109. PMID: 9262247, DOI: 10.1093/jnci/89.15.1103.Peer-Reviewed Original ResearchConceptsHereditary basal cell carcinomasDrosophila genesEmbryonic patterningDevelopmental genesCell fateEmbryonic developmentHuman homologueSporadic basal cell carcinomasBiochemical pathwaysDevelopmental defectsRational medical therapyTumor suppressorGenetic studiesGenesLoss of heterozygosityCell growthChromosome 9q22.3Rare genetic disorderNevoid basal cell carcinoma syndromeBCC formationGenetic disordersBasal cell carcinomaPathwayDrosophilaPatched
1995
Defining control coefficients in non-ideal metabolic pathways
Kholodenko B, Molenaar D, Schuster S, Heinrich R, Westerhoff H. Defining control coefficients in non-ideal metabolic pathways. Biophysical Chemistry 1995, 56: 215-226. PMID: 17023325, DOI: 10.1016/0301-4622(95)00039-z.Peer-Reviewed Original ResearchMetabolic pathwaysFlux control coefficientsHigh enzyme concentrationsMetabolic control analysisBiochemical pathwaysElemental stepsMetabolite channellingMetabolic channellingRelevant pathwaysEnzyme activityPathwayEnzymeControl coefficientsEnzyme concentrationMoiety-conserved cyclesEqual modulationsSpeciesReverse rateElemental processesModulationActivity
1994
Inactivation of a Cdk2 inhibitor during interleukin 2-induced proliferation of human T lymphocytes.
Firpo E, Koff A, Solomon M, Roberts J. Inactivation of a Cdk2 inhibitor during interleukin 2-induced proliferation of human T lymphocytes. Molecular And Cellular Biology 1994, 14: 4889-4901. PMID: 7516474, PMCID: PMC358861, DOI: 10.1128/mcb.14.7.4889.Peer-Reviewed Original ResearchMeSH KeywordsAdultCDC2-CDC28 KinasesCell CycleCells, CulturedCyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsDNAEnzyme ActivationFlow CytometryHumansInterleukin-2KineticsLymphocyte ActivationProtein Kinase InhibitorsProtein KinasesProtein Serine-Threonine KinasesReceptors, Antigen, T-CellReceptors, Interleukin-2Recombinant ProteinsRNASignal TransductionTime FactorsT-LymphocytesConceptsCyclin-dependent kinasesMitogenic signalsCyclin-cdk2 complexesCDK2 inhibitorsNegative growth signalsG1 cyclin-CDK complexesCell cycle commitmentCyclin-CDK complexesCyclin-Cdk inhibitorT cell antigen receptorCell proliferationAntigen receptor stimulationCell cycle proteinsInhibitors of CDK2Mitogenic growth factorsGrowth signalsSimilar proteinsBiochemical pathwaysCell cycleCDK inhibitorsCdk2 activationCycle proteinsRestriction pointS phaseCommon targetInactivation of a Cdk2 Inhibitor during Interleukin 2-Induced Proliferation of Human T Lymphocytes
Firpo E, Koff A, Solomon M, Roberts J. Inactivation of a Cdk2 Inhibitor during Interleukin 2-Induced Proliferation of Human T Lymphocytes. Molecular And Cellular Biology 1994, 14: 4889-4901. DOI: 10.1128/mcb.14.7.4889-4901.1994.Peer-Reviewed Original ResearchCyclin-dependent kinasesMitogenic signalsCyclin-cdk2 complexesCDK2 inhibitorsNegative growth signalsG1 cyclin-CDK complexesCell cycle commitmentCyclin-CDK complexesCyclin-Cdk inhibitorT cell antigen receptorCell proliferationAntigen receptor stimulationCell cycle proteinsInhibitors of CDK2Mitogenic growth factorsGrowth signalsSimilar proteinsBiochemical pathwaysCell cycleCDK inhibitorsCdk2 activationCycle proteinsRestriction pointS phaseCommon target
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