2022
Synaptotagmin rings as high-sensitivity regulators of synaptic vesicle docking and fusion
Zhu J, McDargh ZA, Li F, Krishnakumar SS, Rothman JE, O’Shaughnessy B. Synaptotagmin rings as high-sensitivity regulators of synaptic vesicle docking and fusion. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2208337119. PMID: 36103579, PMCID: PMC9499556, DOI: 10.1073/pnas.2208337119.Peer-Reviewed Original ResearchConceptsVesicle dockingPlasma membrane domainsSynaptic vesiclesCalcium sensor synaptotagminSynaptic vesicle dockingInhibitor of fusionFusion clampSensor synaptotagminMembrane domainsTrigger fusionPlasma membraneC2AB domainAnionic phospholipid bilayersNeuronal synapsesMembrane compositionPhospholipid monolayersATP levelsVesiclesExocytotic releaseDockingPhospholipid bilayersGlutathione-dependent redox balance characterizes the distinct metabolic properties of follicular and marginal zone B cells
Franchina DG, Kurniawan H, Grusdat M, Binsfeld C, Guerra L, Bonetti L, Soriano-Baguet L, Ewen A, Kobayashi T, Farinelle S, Minafra AR, Vandamme N, Carpentier A, Borgmann FK, Jäger C, Chen Y, Kleinewietfeld M, Vasiliou V, Mittelbronn M, Hiller K, Lang PA, Brenner D. Glutathione-dependent redox balance characterizes the distinct metabolic properties of follicular and marginal zone B cells. Nature Communications 2022, 13: 1789. PMID: 35379825, PMCID: PMC8980022, DOI: 10.1038/s41467-022-29426-x.Peer-Reviewed Original ResearchConceptsElectron transport chainMarginal zone B cellsMitochondrial electron transport chainGlutamate-cysteine ligaseCatalytic subunitRedox controlCell-specific ablationRedox balanceTransport chainMetabolic dependenciesCysteine ligaseProtein synthesisMetabolite succinateMTOR activationGlutathione synthesisATP levelsMetabolic propertiesB cellsMetabolic principlesMetabolic featuresDistinct metabolic propertiesMZBCellsActivationLigaseAlpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL
Park HA, Crowe-White KM, Ciesla L, Scott M, Bannerman S, Davis AU, Adhikari B, Burnett G, Broman K, Ferdous KA, Lackey KH, Licznerski P, Jonas EA. Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL. Nutrition Research 2022, 101: 31-42. PMID: 35366596, PMCID: PMC9081260, DOI: 10.1016/j.nutres.2022.02.007.Peer-Reviewed Original ResearchConceptsPrimary hippocampal neuronsControl neuronsHippocampal neuronsAlpha-tocotrienolBcl-xLVitamin E familyCerebral ischemiaNeuronal viabilityMature neuronsB cellsNeurite complexityNeuronal functionMitochondrial energy productionBrain developmentCentral mechanismsNeuronsBeneficial effectsOxidative stressBcl-xL upregulationProtein levelsNeurite branchingTreatmentE familyATP levelsNeurite outgrowth
2020
Roles of Vitamin E in Energy Metabolism During Neurite Outgrowth
Stratton Z, Davis A, Jonas E, Crowe-White K, Park H. Roles of Vitamin E in Energy Metabolism During Neurite Outgrowth. Current Developments In Nutrition 2020, 4: nzaa057_051. PMCID: PMC7259054, DOI: 10.1093/cdn/nzaa057_051.Peer-Reviewed Original ResearchPrimary hippocampal neuronsBrain injuryHippocampal neuronsControl groupNeurite outgrowthNeuronal energy metabolismMaintenance of synapsesVitamin E familyEnergy metabolismNeurite lossNeurobasal mediumVitamin EAlpha-tocotrienolBrain developmentNeuronsOxidative stressNeurite growthBranched neuritesCentral targetMitochondrial inner membrane potentialE familyATP levelsTreatmentNeuritesInjury
2019
Targeting Unique Synthetic Lethal Interactions between PI3K and MYC in B-ALL
Xiao G, Kume K, Geng H, Han T, Klemm L, Müschen M. Targeting Unique Synthetic Lethal Interactions between PI3K and MYC in B-ALL. Blood 2019, 134: 3785. DOI: 10.1182/blood-2019-128719.Peer-Reviewed Original ResearchMYC protein levelsPI3KCell deathMYC overexpressionPTEN deletionRescue effectProtein levelsPI3K hyperactivationMYC protein stabilityTranscription factor Pax5Wild-type MycDegradation of MycSynthetic lethal interactionsGlutamine consumptionGene expression profilesCellular ATP levelsInhibition of glutaminolysisATP levelsPTEN inhibitor SF1670Deletion of PTENMyc mutantsPI3K pathwayPI3K subunitsMyc proteinProtein gene
2018
Protein synthesis controls phosphate homeostasis
Pontes MH, Groisman EA. Protein synthesis controls phosphate homeostasis. Genes & Development 2018, 32: 79-92. PMID: 29437726, PMCID: PMC5828397, DOI: 10.1101/gad.309245.117.Peer-Reviewed Original ResearchConceptsPi starvation responsesStarvation responseProtein synthesisPi transporter genesProtein synthesis controlATP consumptionPi starvationRegulatory connectionsPi homeostasisTransporter geneExtracellular milieuCytoplasmic MgCytoplasmic PiSerovar TyphimuriumPharmacological inhibitionATP levelsRibosomesCytoplasmic magnesiumBacteriumHomeostasisSynthesis controlPhoBSaccharomycesTranscriptionYeast
2017
Optical imaging for the assessment of hepatocyte metabolic state in ischemia and reperfusion injuries.
la Cour M, Mehrvar S, Kim J, Martin A, Zimmerman M, Hong J, Ranji M. Optical imaging for the assessment of hepatocyte metabolic state in ischemia and reperfusion injuries. Biomedical Optics Express 2017, 8: 4419-4426. PMID: 29082074, PMCID: PMC5654789, DOI: 10.1364/boe.8.004419.Peer-Reviewed Original ResearchATP-Dependent Persister Formation in Escherichia coli
Shan Y, Gandt A, Rowe S, Deisinger J, Conlon B, Lewis K, Zgurskaya H, Groisman E. ATP-Dependent Persister Formation in Escherichia coli. MBio 2017, 8: e02267-16. PMID: 28174313, PMCID: PMC5296605, DOI: 10.1128/mbio.02267-16.Peer-Reviewed Original ResearchConceptsChronic infectionFluorescence-activated cell sortingDrug toleranceATP levelsPersister formationDrug-tolerant persistersFluoroquinolone treatmentStress-induced activationSubpopulation of cellsLevels of ATPDormant variantsAntibiotic-tolerant cellsCellular ATP levelsBactericidal antibioticsDim cellsInfectionActivationPersister cellsAntibioticsCell sortingTreatmentSubpopulationsCellsActive toxinToxin activation
2016
Transcriptional Control of Glucose and Energy Supply Prevents Oncogenic Signaling and B Cell Transformation
Chan L, Chen Z, Xiao G, Lee J, Geng H, Christian H, Cazzaniga V, Cazzaniga G, Dickins R, Müschen M. Transcriptional Control of Glucose and Energy Supply Prevents Oncogenic Signaling and B Cell Transformation. Blood 2016, 128: 437. DOI: 10.1182/blood.v128.22.437.437.Peer-Reviewed Original ResearchB-cell transcription factorsTranscription factorsCellular ATP levelsPositive regulatorOncogenic signalingNegative regulatorSurvival fitnessCRISPR/Cas9-mediated deletionWild-type PAX5Glucose uptakeQuantitative chromatin immunoprecipitationEffect of PAX5Regions of genesB cell identityProtein levelsCompetitive growth assaysATP levelsTumor suppressive functionSecondary genetic lesionsB-lineageChIPseq dataTranscriptional controlChromatin immunoprecipitationB-cell transformationPatient-derived preIdentification of the Energy Stress Sensor AMPK As Therapeutic Target in Acute Lymphoblastic Leukemia
Chan L, Lee J, Cosgun K, Geng H, Xiao G, Chen Z, Ernst T, Hochhaus A, Müschen M. Identification of the Energy Stress Sensor AMPK As Therapeutic Target in Acute Lymphoblastic Leukemia. Blood 2016, 128: 2771. DOI: 10.1182/blood.v128.22.2771.2771.Peer-Reviewed Original ResearchChronic myeloid leukemiaAcute lymphoblastic leukemiaMyeloid leukemiaTransplant recipient miceB-cell lineageLKB1/AMPKLymphoblastic leukemiaRecipient miceCML cellsTherapeutic targetLong-term disease-free survivalPhiladelphia chromosome-positive acute lymphoblastic leukemiaB-cell lineage leukemiaPatient-derived preDisease-free survivalInducible deletionNovel therapeutic targetGlycolytic activityBCR-ABL1 tyrosine kinaseNovel therapeutic avenuesATP levelsMitochondrial functionCell deathInitial remissionClinical characteristicsReducing Ribosome Biosynthesis Promotes Translation during Low Mg2+ Stress
Pontes MH, Yeom J, Groisman EA. Reducing Ribosome Biosynthesis Promotes Translation during Low Mg2+ Stress. Molecular Cell 2016, 64: 480-492. PMID: 27746019, PMCID: PMC5500012, DOI: 10.1016/j.molcel.2016.05.008.Peer-Reviewed Original ResearchConceptsSynthesis of ribosomesAmino acid abundanceExpression of proteinsPromotes TranslationAvailability of ATPRibosomal componentsRegulatory circuitsTranslational arrestCytosolic MgRRNA geneProtein synthesisRibosomesATP levelsLevels of ATPATP amountATPDivalent cationsMutantsTranscriptionNegative chargeGenesLow Mg2TranslationProteinAbundanceA painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels
Rolyan H, Liu S, Hoeijmakers JG, Faber CG, Merkies IS, Lauria G, Black JA, Waxman SG. A painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels. Molecular Pain 2016, 12: 1744806916674472. PMID: 27821467, PMCID: PMC5102167, DOI: 10.1177/1744806916674472.Peer-Reviewed Original ResearchConceptsSmall fiber neuropathySmall-diameter axonsTime-dependent degenerationDorsal root ganglion neuronsNerve fiber injuryNervous system disordersPrevious clinical reportsIntracellular calcium levelsMutant Nav1.7 channelsATP levelsAδ nerve fibersHigh altitude sicknessPainful neuropathyTime-dependent increaseFiber injuryClinical onsetGanglion neuronsOxygen species productionSystem disordersCalcium levelsClinical reportsDistal extremitiesIntracellular Ca2NeuropathyNav1.7 channels
2015
When Too Much ATP Is Bad for Protein Synthesis
Pontes MH, Sevostyanova A, Groisman EA. When Too Much ATP Is Bad for Protein Synthesis. Journal Of Molecular Biology 2015, 427: 2586-2594. PMID: 26150063, PMCID: PMC4531837, DOI: 10.1016/j.jmb.2015.06.021.Peer-Reviewed Original ResearchConceptsProtein synthesisStructure of ribosomesEnergy-dependent activitiesATP levelsRibosome productionCellular processesTranslation initiationCytoplasmic membraneEssential enzymeCellular ATPEnergy currencyLiving cellsATPCellsDivalent cationsCrucial roleTriphosphateRibosomesAminoacylationOrganismsNon-physiological increaseCofactorEnzymeBiochemistryCommon divalent cations
2013
A Bacterial Virulence Protein Promotes Pathogenicity by Inhibiting the Bacterium’s Own F1Fo ATP Synthase
Lee EJ, Pontes MH, Groisman EA. A Bacterial Virulence Protein Promotes Pathogenicity by Inhibiting the Bacterium’s Own F1Fo ATP Synthase. Cell 2013, 154: 146-156. PMID: 23827679, PMCID: PMC3736803, DOI: 10.1016/j.cell.2013.06.004.Peer-Reviewed Original Research
2012
Metabolism of the right ventricle and the response to hypertrophy and failure
Altin S, Schulze P. Metabolism of the right ventricle and the response to hypertrophy and failure. Progress In Cardiovascular Diseases 2012, 55: 229-233. PMID: 23009918, PMCID: PMC3766963, DOI: 10.1016/j.pcad.2012.07.010.Peer-Reviewed Original ResearchConceptsRight ventriclePositron emission tomographyRV metabolismRV hypertrophyVolume overloadMetabolic abnormalitiesNon-invasive imagingPharmacologic interventionsClinical trialsCardiac hypertrophyEmission tomographyPathophysiologic stressHypertrophyMolecular targetsEnergetic derangementsMolecular dysfunctionCurrent roleATP levelsVentricleFatty acidsATP generationFailureMetabolismSubsequent failureDerangement
2011
Mitochondria are sources of metabolic sink and arrhythmias
Akar FG, O'Rourke B. Mitochondria are sources of metabolic sink and arrhythmias. Pharmacology & Therapeutics 2011, 131: 287-294. PMID: 21513732, PMCID: PMC3138548, DOI: 10.1016/j.pharmthera.2011.04.005.Peer-Reviewed Original Research
2009
AMP-activated protein kinase: a physiological off switch for murine gastric acid secretion
Sidani S, Kopic S, Socrates T, Kirchhoff P, Föller M, Murek M, Capasso A, Geibel JP. AMP-activated protein kinase: a physiological off switch for murine gastric acid secretion. Pflügers Archiv - European Journal Of Physiology 2009, 459: 39. PMID: 19621238, DOI: 10.1007/s00424-009-0698-3.Peer-Reviewed Original ResearchConceptsProtein kinaseAMPK activationSecretagogue-induced acid secretionCellular ATP levelsPresence of AMPKEnergy-dependent transportersImmunofluorescent localizationParietal cellsGastric glandsCellular ATP consumptionGastric parietal cellsCompound CAMPKProton effluxATP consumptionMetabolic stressRate of intracellularATP levelsKinaseAdenosine monophosphateRegulatorATPLarge abundanceCellsActivation
2007
Slack and Slick KNa Channels Regulate the Accuracy of Timing of Auditory Neurons
Yang B, Desai R, Kaczmarek LK. Slack and Slick KNa Channels Regulate the Accuracy of Timing of Auditory Neurons. Journal Of Neuroscience 2007, 27: 2617-2627. PMID: 17344399, PMCID: PMC6672517, DOI: 10.1523/jneurosci.5308-06.2007.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsAnimals, NewbornAuditory PathwaysBithionolBrain StemComputer SimulationElectric ConductivityElectric StimulationElectrophysiologyIn Vitro TechniquesMiceModels, NeurologicalNerve Tissue ProteinsNeuronsNeurons, AfferentPotassium ChannelsPotassium Channels, Sodium-ActivatedReaction TimeSodium
2006
TCDD decreases ATP levels and increases reactive oxygen production through changes in mitochondrial F0F1-ATP synthase and ubiquinone
Shertzer HG, Genter MB, Shen D, Nebert DW, Chen Y, Dalton TP. TCDD decreases ATP levels and increases reactive oxygen production through changes in mitochondrial F0F1-ATP synthase and ubiquinone. Toxicology And Applied Pharmacology 2006, 217: 363-374. PMID: 17109908, PMCID: PMC1783833, DOI: 10.1016/j.taap.2006.09.014.Peer-Reviewed Original ResearchConceptsReactive oxygen productionATP levelsMitochondria generate ATPMitochondrial glutathione redox stateMitochondrial oxidative DNA damageF0F1-ATP synthaseATP/O ratioGlutathione redox stateOxygen productionATP synthaseGenerate ATPSignal transductionMitochondrial targetsOxidative DNA damageGreater respiratory rateOxidoreductase activityATP synthesisCell deathDNA damageFutile cycleRedox stateCellular pathologyRespiratory control ratioTCDD treatmentATP2‐Deoxyglucose and NMDA inhibit protein synthesis in neurons and regulate phosphorylation of elongation factor‐2 by distinct mechanisms
Maus M, Torrens Y, Gauchy C, Bretin S, Nairn A, Glowinski J, Premont J. 2‐Deoxyglucose and NMDA inhibit protein synthesis in neurons and regulate phosphorylation of elongation factor‐2 by distinct mechanisms. Journal Of Neurochemistry 2006, 96: 815-824. PMID: 16405506, DOI: 10.1111/j.1471-4159.2005.03601.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntimetabolitesBlotting, WesternCalciumCarbonyl Cyanide m-Chlorophenyl HydrazoneCells, CulturedCerebral CortexDeoxyglucoseDose-Response Relationship, DrugDrug InteractionsEmbryo, MammalianEnzyme InhibitorsExcitatory Amino Acid AgonistsIonophoresLeucineMiceModels, BiologicalNeuronsN-MethylaspartateOligomycinsPeptide Elongation Factor 2PhosphorylationProtein KinasesProtein Synthesis InhibitorsPyruvic AcidSodium AzideTime FactorsTOR Serine-Threonine KinasesTritiumConceptsCortical neuronsExcitatory amino acid releaseImine hydrogen maleateNMDA receptor antagonistAMP kinaseAmino acid releaseNeuronal protein synthesisCytosolic free Ca2Protein synthesisCerebral ischaemiaReceptor antagonistBrain damageNeuronal metabolismMetabolic impairmentNMDADistinct mechanismsCytosolic Ca2NeuronsMetabolic deprivationAcid releaseSecondary releaseProtein synthesis inhibitionSynthesis inhibitionElongation factor eEF-2ATP levels
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