2022
Isotope tracing reveals distinct substrate preference in murine melanoma subtypes with differing anti-tumor immunity
Zhang X, Halberstam A, Zhu W, Leitner B, Thakral D, Bosenberg M, Perry R. Isotope tracing reveals distinct substrate preference in murine melanoma subtypes with differing anti-tumor immunity. Cancer & Metabolism 2022, 10: 21. PMID: 36457136, PMCID: PMC9714036, DOI: 10.1186/s40170-022-00296-7.Peer-Reviewed Original ResearchTumor microenvironmentAnti-tumor immunityPotential prognostic factorsObesity-associated cancersPotential prognostic predictorPatient RNA-seq dataSubset of studiesImmunogenic tumorsCancer Genome AtlasLymphocyte infiltrationMelanoma cell linesPrognostic factorsPrognostic predictorMetabolic therapyMelanoma subtypesMurine modelImmune functionMetabolic gene expressionMelanoma progressionMelanomaSubstrate metabolismMetabolic flux studiesGene expressionGenome AtlasCell lines
2019
Adipocyte alterations in endometriosis: reduced numbers of stem cells and microRNA induced alterations in adipocyte metabolic gene expression
Zolbin MM, Mamillapalli R, Nematian SE, Goetz T, Taylor HS. Adipocyte alterations in endometriosis: reduced numbers of stem cells and microRNA induced alterations in adipocyte metabolic gene expression. Reproductive Biology And Endocrinology 2019, 17: 36. PMID: 30982470, PMCID: PMC6463663, DOI: 10.1186/s12958-019-0480-0.Peer-Reviewed Original ResearchConceptsBody mass indexFat metabolismFat tissueMouse modelAdipose tissueMetabolic gene expressionLower body mass indexOld female C57BL/6 miceAdipocytes of womenMicroRNA let‑7bSerum of womenReproductive-aged womenEffect of endometriosisFemale C57BL/6 miceStem cellsAdipose-derived mesenchymal stem cellsBrown adipocyte differentiationInhibitors of microRNAsStem cell contentMass indexMetabolic abnormalitiesC57BL/6 miceInflammatory disordersIL-6Insulin sensitivityMetabolism and Development during Conidial Germination in Response to a Carbon-Nitrogen-Rich Synthetic or a Natural Source of Nutrition in Neurospora crassa
Wang Z, Miguel-Rojas C, Lopez-Giraldez F, Yarden O, Trail F, Townsend JP. Metabolism and Development during Conidial Germination in Response to a Carbon-Nitrogen-Rich Synthetic or a Natural Source of Nutrition in Neurospora crassa. MBio 2019, 10: 10.1128/mbio.00192-19. PMID: 30914504, PMCID: PMC6437048, DOI: 10.1128/mbio.00192-19.Peer-Reviewed Original ResearchConceptsDevelopmental regulatory genesVegetative growthAsexual reproductionConidial germinationRegulatory genesNutritional environmentLife historyNitrogen metabolismLife-history decisionsMode of reproductionAdaptive life historiesKnockout of genesGenome-wide transcriptomicsEarly life historySexual developmentMetabolic gene expressionReproductive dispersalSexual reproductionDevelopmental genesMetabolic genesNeurospora crassaDiverse ecosystemsNutrient conditionsGene expressionMajor switch
2017
Bisphenol-A exposure in utero programs a sexually dimorphic estrogenic state of hepatic metabolic gene expression
Ilagan Y, Mamillapalli R, Goetz L, Kayani J, Taylor HS. Bisphenol-A exposure in utero programs a sexually dimorphic estrogenic state of hepatic metabolic gene expression. Reproductive Toxicology 2017, 71: 84-94. PMID: 28476547, DOI: 10.1016/j.reprotox.2017.05.001.Peer-Reviewed Original ResearchConceptsBPA exposureGene expressionAdult gene expressionFetal BPA exposureBisphenol A (BPA) exposureMetabolic gene expressionEstrogen receptor alphaExpression of genesBeta gene expressionEstrogenic stateEstrogen treatmentPregnant miceMetabolic disordersE2 stimulationReceptor alphaFetal developmentLipid metabolismDay 9Developmental programmingSexual dimorphismFemale offspringLiverObesityGenesAdult responses
2015
The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming
Phan L, Chou PC, Velazquez-Torres G, Samudio I, Parreno K, Huang Y, Tseng C, Vu T, Gully C, Su CH, Wang E, Chen J, Choi HH, Fuentes-Mattei E, Shin JH, Shiang C, Grabiner B, Blonska M, Skerl S, Shao Y, Cody D, Delacerda J, Kingsley C, Webb D, Carlock C, Zhou Z, Hsieh YC, Lee J, Elliott A, Ramirez M, Bankson J, Hazle J, Wang Y, Li L, Weng S, Rizk N, Wen YY, Lin X, Wang H, Wang H, Zhang A, Xia X, Wu Y, Habra M, Yang W, Pusztai L, Yeung SC, Lee MH. The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming. Nature Communications 2015, 6: 7530. PMID: 26179207, PMCID: PMC4507299, DOI: 10.1038/ncomms8530.Peer-Reviewed Original ResearchMeSH Keywords14-3-3 ProteinsAdultAgedAged, 80 and overBiomarkers, TumorBreast NeoplasmsCell Line, TumorDisease-Free SurvivalEnergy MetabolismExoribonucleasesFemaleGene Expression Regulation, NeoplasticGene Knockout TechniquesGlutamineGlycolysisHCT116 CellsHumansMiddle AgedOrganelle BiogenesisPrognosisProteolysisProto-Oncogene Proteins c-mycUbiquitinationYoung AdultConceptsCancer metabolic reprogrammingMetabolic reprogrammingRecurrence-free survival ratesMetabolic gene expressionBreast cancer patientsCellular energy metabolismHallmarks of cancerMajor metabolic processesTumor glucose uptakeExtensive reprogrammingMetabolic programsMitochondrial biogenesisGene expressionTumorigenic transformationCancer glycolysisMolecular mechanismsReprogrammingCancer patientsMetabolic processesMetabolic shift
2013
Myocardial Loss of IRS1 and IRS2 Causes Heart Failure and Is Controlled by p38α MAPK During Insulin Resistance
Qi Y, Xu Z, Zhu Q, Thomas C, Kumar R, Feng H, Dostal D, White M, Baker K, Guo S. Myocardial Loss of IRS1 and IRS2 Causes Heart Failure and Is Controlled by p38α MAPK During Insulin Resistance. Diabetes 2013, 62: 3887-3900. PMID: 24159000, PMCID: PMC3806607, DOI: 10.2337/db13-0095.Peer-Reviewed Original ResearchConceptsIRS2 proteinGene expressionType 2 diabetesEnergy metabolism gene expressionInsulin resistanceMetabolic gene expressionBox class ODouble knockout miceHeart failureActivation of p38Chronic insulin exposureActivation of p38αMetabolism gene expressionProtein kinaseRole of IRS1Cellular metabolismMolecular mechanismsInsulin receptorNeonatal rat ventricular cardiomyocytesP38α MAPKCause heart failureCellular dysfunctionIRS1Myocardial insulin resistanceClass OAdipose circadian clocks: coordination of metabolic rhythms by clock genes, steroid hormones, and PPARs
Krueger K, Feldman B. Adipose circadian clocks: coordination of metabolic rhythms by clock genes, steroid hormones, and PPARs. Hormone Molecular Biology And Clinical Investigation 2013, 14: 15-24. PMID: 25436716, DOI: 10.1515/hmbci-2013-0011.Peer-Reviewed Original ResearchClock genesTranscriptional feedback regulationExpression of metabolic genesSignal energy statusIntricate feedback mechanismMetabolic gene expressionCentral clockEnergy storage organNuclear hormone receptorsGene loopingClock entrainmentMetabolic genesProtein associationAdipose tissueGene expressionMetabolic homeostasisStorage organsFeedback regulationMetabolic rhythmsFeeding activityGenesPeripheral clocksEnergy statusHormone receptorsSteroid hormones
2012
A highly integrated and complex PPARGC1A transcription factor binding network in HepG2 cells
Charos AE, Reed BD, Raha D, Szekely AM, Weissman SM, Snyder M. A highly integrated and complex PPARGC1A transcription factor binding network in HepG2 cells. Genome Research 2012, 22: 1668-1679. PMID: 22955979, PMCID: PMC3431484, DOI: 10.1101/gr.127761.111.Peer-Reviewed Original ResearchMeSH KeywordsBinding SitesCarrier ProteinsChromatin ImmunoprecipitationCluster AnalysisGene Expression RegulationGene Regulatory NetworksHeat-Shock ProteinsHep G2 CellsHigh-Throughput Nucleotide SequencingHumansNucleotide MotifsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProtein BindingProtein TransportTranscription FactorsTranscription, GeneticConceptsTranscription factorsGenome-wide binding sitesCombinatorial binding patternsHeat shock response pathwayIndividual transcription factorsTranscriptional regulatory networksDNA sequence motifsDifferent transcription factorsShock response pathwayHigh-throughput sequencingMetabolic gene expressionHepG2 cellsTF partnersTranscriptional dynamicsCellular processesChIP-seqSequence motifsRegulatory networksTranscriptional coactivatorResponse pathwaysInterdependent regulationTarget genesChromatin IPRegulatory codeGene expressionDifferential impact of nutrition on developmental and metabolic gene expression during fruiting body development in Neurospora crassa
Wang Z, Lehr N, Trail F, Townsend JP. Differential impact of nutrition on developmental and metabolic gene expression during fruiting body development in Neurospora crassa. Fungal Genetics And Biology 2012, 49: 405-413. PMID: 22469835, PMCID: PMC3397380, DOI: 10.1016/j.fgb.2012.03.004.Peer-Reviewed Original ResearchConceptsCarrot agarPerithecial developmentNeurospora crassaNutritional resourcesCore metabolic genesDifferent fungiSexual developmentDiverse environmental stimuliMetabolic gene expressionKey regulatory roleDevelopmental programMetabolic genesMicroarray hybridizationTranscriptional profilesAnabolic pathwaysExpression patternsGene expressionBody sizeMetabolic differentiationRegulatory roleBody developmentEffects of nutritionNutritional environmentEnvironmental stimuliBody morphology
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