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
2017
ATP-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 pre
2010
Lymphocytes Accelerate Epithelial Tight Junction Assembly: Role of AMP-Activated Protein Kinase (AMPK)
Tang XX, Chen H, Yu S, Zhang L, Caplan MJ, Chan HC. Lymphocytes Accelerate Epithelial Tight Junction Assembly: Role of AMP-Activated Protein Kinase (AMPK). PLOS ONE 2010, 5: e12343. PMID: 20808811, PMCID: PMC2925955, DOI: 10.1371/journal.pone.0012343.Peer-Reviewed Original ResearchConceptsTJ assemblyActivation of AMPKProtein kinaseEpithelial cellsCalcium switch experimentsEpithelial cell polaritySuppression of AMPKTight junction assemblyRole of AMPMadin-Darby canine kidney cellsCellular ATP levelsCanine kidney cellsTight junctionsCell polarityApicolateral borderJunction assemblyModel cell lineAMPK activationProper formationAdjacent epithelial cellsTJ formationChemical inhibitorsCalu-3 human airway epithelial cellsHuman airway epithelial cellsMDCK cells
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
2003
Hsp27 associates with actin and limits injury in energy depleted renal epithelia.
Van Why SK, Mann AS, Ardito T, Thulin G, Ferris S, Macleod MA, Kashgarian M, Siegel NJ. Hsp27 associates with actin and limits injury in energy depleted renal epithelia. Journal Of The American Society Of Nephrology 2003, 14: 98-106. PMID: 12506142, DOI: 10.1097/01.asn.0000038687.24289.83.Peer-Reviewed Original ResearchConceptsGreen fluorescence proteinFluorescence energy transferATP depletionF-actinRenal epitheliumSpecific intracellular domainsCellular ATP levelsHsp27 interactionHsp27 associatesIntracellular domainLLC-PK1 cellsFluorescence proteinLateral cell boundariesHuman HSP27Phalloidin fluorescenceActinHSP27K-ATPaseCytoskeletonControl cellsATP levelsEnergy depletionCell bodiesG cellsCells
1995
ATP depletion and inactivation of an ATP-sensitive taurine channel by classic ion channel blockers.
Ballatori N, Truong A, Jackson P, Strange K, Boyer J. ATP depletion and inactivation of an ATP-sensitive taurine channel by classic ion channel blockers. Molecular Pharmacology 1995, 48: 472-476. PMID: 7565627, DOI: 10.1016/s0026-895x(25)10495-1.Peer-Reviewed Original ResearchConceptsIon channel blockersChannel blockersVolume-activated anion channelsATP levelsATP contentActivity of ATPPhysiologic alterationsIntracellular ATP levelsCellular ATPTaurine effluxBlockersIntracellular ATP contentTaurine channelCellular ATP levelsATP/ADP ratioIntracellular organic osmolytesSkate hepatocytesIntracellular ATPATP depletionCell volume regulationDifferent cell typesEffluxCellular ATP concentrationMetabolic poisonsCell types
1991
Redistribution of cellular energy following renal ischemia
Gaudio K, Thulin G, Ardito T, Kashgarian M, Siegel N. Redistribution of cellular energy following renal ischemia. Pediatric Nephrology 1991, 5: 591-596. PMID: 1911145, DOI: 10.1007/bf00856647.Peer-Reviewed Original Research
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