2020
Mitochondrial function in women with polycystic ovary syndrome.
Cozzolino M, Seli E. Mitochondrial function in women with polycystic ovary syndrome. Current Opinion In Obstetrics & Gynecology 2020, 32: 205-212. PMID: 32068544, DOI: 10.1097/gco.0000000000000619.Peer-Reviewed Original ResearchConceptsPolycystic ovary syndromeLower mtDNA copy numberOvary syndromePathogenesis of PCOSMitochondrial dysfunctionMtDNA copy numberPotential protective rolePCOS phenotypeInsulin resistancePathophysiological mechanismsCommon findingDiagnostic modalitiesMetabolic milieuFunctional alterationsMitochondrial functional alterationsProtective roleCommon diseaseOxidative stressWomenMitochondrial functionDysfunctionSyndromeCopy numberProtein responseReactive oxygen
2019
Transcriptomic abnormalities in peripheral blood in bipolar disorder, and discrimination of the major psychoses
Hess JL, Tylee DS, Barve R, de Jong S, Ophoff RA, Kumarasinghe N, Tooney P, Schall U, Gardiner E, Beveridge NJ, Scott RJ, Yasawardene S, Perera A, Mendis J, Carr V, Kelly B, Cairns M, Unit T, Tsuang MT, Glatt SJ. Transcriptomic abnormalities in peripheral blood in bipolar disorder, and discrimination of the major psychoses. Schizophrenia Research 2019, 217: 124-135. PMID: 31391148, PMCID: PMC6997041, DOI: 10.1016/j.schres.2019.07.036.Peer-Reviewed Original ResearchConceptsGene modulesSZ casesGene co-expression network analysisCo-expression network analysisGene expression profilesGene expression alterationsChromatin regulationChromatin remodelingNineteen genesGene networksTranscriptomic abnormalitiesDisorder-specific changesGene expressionExpression profilesBiological processesImmune signalingExpression alterationsTranscriptomic signaturesGenesReactive oxygenUnaffected comparison subjectsMajor psychosesOxidative stressBD casesApoptosis
2017
An inflammatory bowel disease–risk variant in INAVA decreases pattern recognition receptor–induced outcomes
Yan J, Hedl M, Abraham C. An inflammatory bowel disease–risk variant in INAVA decreases pattern recognition receptor–induced outcomes. Journal Of Clinical Investigation 2017, 127: 2192-2205. PMID: 28436939, PMCID: PMC5451247, DOI: 10.1172/jci86282.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusCarrier ProteinsCase-Control StudiesCytokinesEnterococcus faecalisGene ExpressionGenetic Association StudiesGenetic Predisposition to DiseaseHEK293 CellsHeterozygoteHumansInflammatory Bowel DiseasesMacrophagesMAP Kinase Signaling SystemMyeloid CellsPolymorphism, Single NucleotidePrimary Cell CultureReceptors, Pattern RecognitionRisk FactorsStaphylococcus aureusConceptsInflammatory bowel diseasePattern recognition receptor signalingDisease risk variantsIntestinal immune homeostasisActivation of MAPKIBD risk lociINAVAPrimary human cellsBacterial clearanceIntestinal myeloid cellsRisk lociAutophagy pathwayProper regulationIntronic regionsHuman cellsImmune homeostasisReceptor signalingDownstream signalsPRR stimulationReactive oxygenIntestinal microbesNF-κB activationGenesNF-κB pathwayMAPKSingle-lung ventilation and oxidative stress
Heerdt PM, Stowe DF. Single-lung ventilation and oxidative stress. Current Opinion In Anaesthesiology 2017, 30: 42-49. PMID: 27783023, DOI: 10.1097/aco.0000000000000410.Peer-Reviewed Original ResearchConceptsSingle-lung ventilationOxidative stressRe-expanded lungHypoxic pulmonary vasoconstrictionRedistribution of bloodLocal tissue hypoxiaPostoperative disruptionPulmonary vasoconstrictionReperfusion responseAtelectatic lungTissue hypoxiaClinical dataReactive oxygenSystemic effectsOrgan functionLungNitrosative stressVentilationNitrogen speciesVasoconstriction
2013
Rapid and Permanent Neuronal Inactivation In Vivo via Subcellular Generation of Reactive Oxygen with the Use of KillerRed
Williams DC, Bejjani RE, Ramirez PM, Coakley S, Kim SA, Lee H, Wen Q, Samuel A, Lu H, Hilliard MA, Hammarlund M. Rapid and Permanent Neuronal Inactivation In Vivo via Subcellular Generation of Reactive Oxygen with the Use of KillerRed. Cell Reports 2013, 5: 553-563. PMID: 24209746, PMCID: PMC3877846, DOI: 10.1016/j.celrep.2013.09.023.Peer-Reviewed Original ResearchConceptsReactive oxygen speciesC. elegansGenetic toolsOrganelle fragmentationPlasma membraneSpecific developmental outcomesSubcellular responsesCell deathKillerRedReactive oxygenOxygen speciesTargeted cellCircuit functionSingle light stimulusSingle animalInactivationElegansCellsVivoCell bodiesSpeciesNeuronal degenerationNeuronsAnimalsNeuronal inactivation
2009
From Reactive Oxygen and Nitrogen Species to Therapy
McKercher S, Nakamura T, Lipton S. From Reactive Oxygen and Nitrogen Species to Therapy. 2009 DOI: 10.1002/9780470015902.a0021989.Peer-Reviewed Original ResearchReactive oxygen speciesProtein misfoldingS-nitrosylationE3 ubiquitin ligase ParkinUbiquitin ligase ParkinProtein disulfide isomeraseMisfolded protein aggregatesCritical cysteine thiolsS-nitrosylation reactionsExcessive reactive oxygen speciesNrf2 transcriptional pathwayProduction of ROSMisfolded proteinsProtein functionTranscriptional pathwaysCysteine thiolsProtein aggregatesMisfoldingReactive oxygenSpeciesPathological productionOxygen speciesGenetic mutationsNitrogen speciesNeurodegenerative diseases
2007
Molecular mechanisms of nitrosative stress-mediated protein misfolding in neurodegenerative diseases
Nakamura T, Lipton S. Molecular mechanisms of nitrosative stress-mediated protein misfolding in neurodegenerative diseases. Cellular And Molecular Life Sciences 2007, 64: 1609-1620. PMID: 17453143, PMCID: PMC11136414, DOI: 10.1007/s00018-007-6525-0.Peer-Reviewed Original ResearchConceptsUbiquitin-proteasome systemNormal protein degradationProtein disulfide isomeraseMolecular chaperonesSpecific chaperonesGlucose-regulated protein 78Proper foldingProtein misfoldingAberrant proteinsProtein foldingUPS proteinsProtein degradationMolecular mechanismsShock proteinsConformational changesExcessive reactive oxygenCell deathNeuronal cell deathProteinChaperonesProtein 78Reactive oxygenMisfoldingNitrogen speciesNitrosative stress
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