2021
Cocaine self-administration induces sex-dependent protein expression in the nucleus accumbens
López AJ, Johnson AR, Euston TJ, Wilson R, Nolan SO, Brady LJ, Thibeault KC, Kelly SJ, Kondev V, Melugin P, Kutlu MG, Chuang E, Lam TT, Kiraly DD, Calipari ES. Cocaine self-administration induces sex-dependent protein expression in the nucleus accumbens. Communications Biology 2021, 4: 883. PMID: 34272455, PMCID: PMC8285523, DOI: 10.1038/s42003-021-02358-w.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCocaineFemaleMaleMiceMice, Inbred C57BLNucleus AccumbensProteomeRatsRats, Sprague-DawleySelf AdministrationSex FactorsConceptsProtein expression patternsExpression patternsQuantitative mass spectrometrySubstance use disordersCritical biological variableProteomic functionProtein regulationRegulated proteinsUnique molecular profileNucleus accumbensSexual dimorphismProteomeProtein expressionMolecular substratesDrug-induced plasticityMolecular profileChronic neuropsychiatric conditionsPreclinical evidenceBaseline differencesCocaine administrationReward-associated behaviorsUse disordersMass spectrometryMale subjectsBiological variables
2016
MKK3 influences mitophagy and is involved in cigarette smoke-induced inflammation
Mannam P, Rauniyar N, Lam TT, Luo R, Lee PJ, Srivastava A. MKK3 influences mitophagy and is involved in cigarette smoke-induced inflammation. Free Radical Biology And Medicine 2016, 101: 102-115. PMID: 27717867, DOI: 10.1016/j.freeradbiomed.2016.10.001.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCigarette SmokingGene Expression ProfilingGene Expression RegulationHumansInflammationInterleukin-1betaInterleukin-6MacrophagesMAP Kinase Kinase 3MiceMice, Inbred C57BLMice, KnockoutMitochondriaMitophagyNF-kappa BOxidative PhosphorylationPlant ExtractsPrimary Cell CulturePulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesTobaccoTumor Necrosis Factor-alphaConceptsCigarette smoke extractCigarette smokeCSE treatmentInflammatory responseLung tissueCigarette smoke-induced inflammationWild typeSerum pro-inflammatory cytokinesSmoke-induced inflammationProgression of COPDMitochondrial dysfunctionReactive oxygen speciesPro-inflammatory cytokinesInflammatory cytokine productionPrimary risk factorAssociated inflammatory responsePatient's lung tissueMouse lung tissueMitochondrial functionDual-specificity protein kinaseRespiratory capacitySpare respiratory capacityAirflow obstructionProtein kinase kinase 3CSE exposure
2014
Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation
Shibata S, Arroyo JP, Castañeda-Bueno M, Puthumana J, Zhang J, Uchida S, Stone KL, Lam TT, Lifton RP. Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 15556-15561. PMID: 25313067, PMCID: PMC4217463, DOI: 10.1073/pnas.1418342111.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAmino Acid SequenceAngiotensin IIAnimalsCarrier ProteinsCell LineHumansKidneyMice, Inbred C57BLMicrofilament ProteinsMolecular Sequence DataPhosphorylationPhosphoserineProtein BindingProtein Kinase CProtein Serine-Threonine KinasesProteolysisSignal TransductionConceptsRenal salt reabsorptionAngiotensin IIVolume depletionSalt reabsorptionNormal physiologic responseProtein kinase CAII administrationBlood pressureCardiovascular diseaseGlobal burdenPhysiologic responsesCullin 3Kinase CNaCl cotransporterReabsorptionHuman genetic studiesSecretionHypertensionNormal mechanismsWNK4 degradationMissense mutationsSerine 433WNK4Inverse relationshipCultured cellsInhibitor of the Tyrosine Phosphatase STEP Reverses Cognitive Deficits in a Mouse Model of Alzheimer's Disease
Xu J, Chatterjee M, Baguley TD, Brouillette J, Kurup P, Ghosh D, Kanyo J, Zhang Y, Seyb K, Ononenyi C, Foscue E, Anderson GM, Gresack J, Cuny GD, Glicksman MA, Greengard P, Lam TT, Tautz L, Nairn AC, Ellman JA, Lombroso PJ. Inhibitor of the Tyrosine Phosphatase STEP Reverses Cognitive Deficits in a Mouse Model of Alzheimer's Disease. PLOS Biology 2014, 12: e1001923. PMID: 25093460, PMCID: PMC4122355, DOI: 10.1371/journal.pbio.1001923.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAmino Acid SequenceAnimalsBenzothiepinsCatalytic DomainCell DeathCerebral CortexCognition DisordersCysteineDisease Models, AnimalEnzyme InhibitorsHigh-Throughput Screening AssaysHumansMaleMice, Inbred C57BLMice, KnockoutMolecular Sequence DataNeuronsPhosphorylationPhosphotyrosineProtein Tyrosine Phosphatases, Non-ReceptorSubstrate SpecificityConceptsInhibitors of stepsSpecificity of inhibitorsIsoxazolepropionic acid receptor (AMPAR) traffickingCatalytic cysteinePTP inhibitorsTyrosine phosphataseTyrosine phosphorylationSecondary assaysSTEP KO miceReceptor traffickingFirst large-scale effortN-methyl-D-aspartate receptorsPyk2 activitySTEP inhibitorLarge-scale effortsNovel therapeutic targetSynaptic functionAlzheimer's diseaseNeurodegenerative disordersCortical cellsTherapeutic targetERK1/2Specificity experimentsPhosphataseInhibitors
2013
A Gut Lipid Messenger Links Excess Dietary Fat to Dopamine Deficiency
Tellez LA, Medina S, Han W, Ferreira JG, Licona-Limón P, Ren X, Lam TT, Schwartz GJ, de Araujo IE. A Gut Lipid Messenger Links Excess Dietary Fat to Dopamine Deficiency. Science 2013, 341: 800-802. PMID: 23950538, DOI: 10.1126/science.1239275.Peer-Reviewed Original ResearchConceptsDopamine deficiencyFed miceDietary fatExcess dietary fatBrain dopaminergic functionHigh fat intakeHigh-fat exposureGastrointestinal dysfunctionIntragastric feedingOral intakeDopaminergic functionDopamine releaseExcessive intakeIntakeMiceDeficiencyOleoylethanolamineLipid messengersPhysiological mechanismsFatMotivation deficitsLipid signalingReward sensitivityObesityDysfunction