2015
Macrophage-specific de Novo Synthesis of Ceramide Is Dispensable for Inflammasome-driven Inflammation and Insulin Resistance in Obesity*
Camell CD, Nguyen KY, Jurczak MJ, Christian BE, Shulman GI, Shadel GS, Dixit VD. Macrophage-specific de Novo Synthesis of Ceramide Is Dispensable for Inflammasome-driven Inflammation and Insulin Resistance in Obesity*. Journal Of Biological Chemistry 2015, 290: 29402-29413. PMID: 26438821, PMCID: PMC4705943, DOI: 10.1074/jbc.m115.680199.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsBone Marrow CellsCarrier ProteinsCeramidesDiet, High-FatDisease Models, AnimalFatty AcidsFemaleInflammasomesInflammationInsulin ResistanceLipidsMacrophagesMaleMiceMice, TransgenicMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinObesityOxidative StressSerine C-PalmitoyltransferaseConceptsDe novo synthesisNovo synthesisOverexpression of catalaseDietary lipid overloadSynthesis machineryTissue homeostasisCell-specific deletionInflammasome activationAdipose tissue homeostasisNLRP3 inflammasome activationMyeloid cell-specific deletionMetabolic pathwaysCeramide synthesisAlternate metabolic pathwaysCaspase-1 cleavageEnergy homeostasisLipid overloadCeramideLipid metabolismInflammasome-dependent mannerOxidative stressDanger signalsFat diet-induced obesityHomeostasisFatty acids
2014
Mitochondrial remodeling in mice with cardiomyocyte-specific lipid overload
Elezaby A, Sverdlov AL, Tu VH, Soni K, Luptak I, Qin F, Liesa M, Shirihai OS, Rimer J, Schaffer JE, Colucci WS, Miller EJ. Mitochondrial remodeling in mice with cardiomyocyte-specific lipid overload. Journal Of Molecular And Cellular Cardiology 2014, 79: 275-283. PMID: 25497302, PMCID: PMC4301992, DOI: 10.1016/j.yjmcc.2014.12.001.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCarnitineCatalaseCeramidesCyclic AMP Response Element-Binding ProteinDiglyceridesElectron Transport Complex IIFatty Acid Transport ProteinsGene Expression RegulationHydrogen PeroxideLipidsMiceMitochondria, HeartModels, BiologicalMyocardiumMyocytes, CardiacOrgan SpecificityOxygen ConsumptionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphorylationPPAR alphaProtein Kinase CProto-Oncogene Proteins c-aktRNA, MessengerSphingomyelinsTranscription FactorsConceptsMetabolic heart diseaseMitochondrial structureMitochondrial fusion genes Mfn1Mitochondrial-targeted catalaseOverexpression of catalaseMitochondrial oxidative stressStructure/functionPhosphorylation of AktToxic metabolite accumulationTranscriptional regulationMitochondrial structure/functionFatty acid uptakeCardiomyocyte lipid accumulationMitochondrial remodelingMetabolite accumulationDiacylglycerol speciesExcess FAATP synthesisMitochondrial functionMitochondrial dysfunctionLipid speciesFA uptakeMitochondrial sizeHydrogen peroxide productionSubunit B
2012
Reducing Mitochondrial ROS Improves Disease-related Pathology in a Mouse Model of Ataxia-telangiectasia
D'Souza AD, Parish IA, Krause DS, Kaech SM, Shadel GS. Reducing Mitochondrial ROS Improves Disease-related Pathology in a Mouse Model of Ataxia-telangiectasia. Molecular Therapy 2012, 21: 42-48. PMID: 23011031, PMCID: PMC3538311, DOI: 10.1038/mt.2012.203.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCatalaseCD8-Positive T-LymphocytesCell Cycle ProteinsDisease Models, AnimalDNA-Binding ProteinsHematopoiesisImmunologic MemoryLymphomaMiceMice, KnockoutMitochondriaProtein Serine-Threonine KinasesReactive Oxygen SpeciesThymus NeoplasmsTumor Suppressor ProteinsConceptsMitochondrial reactive oxygen speciesReactive oxygen speciesAtaxia telangiectasiaT cell developmental defectsDNA damage responseDisease ataxia telangiectasiaMitochondrial ROS productionOverexpression of catalaseATM kinaseRedox sensingDevelopmental defectsLatter phenotypePartial rescueBone marrow hematopoiesisCancer predispositionNull mouse modelMitochondrial dysfunctionMacrophage differentiationTORC1ROS productionCancer developmentOxygen speciesMouse modelTS pathologyMarrow hematopoiesis
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