2020
OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance
Yang Y, Li X, Luan HH, Zhang B, Zhang K, Nam JH, Li Z, Fu M, Munk A, Zhang D, Wang S, Liu Y, Albuquerque JP, Ong Q, Li R, Wang Q, Robert ME, Perry RJ, Chung D, Shulman GI, Yang X. OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance. Proceedings Of The National Academy Of Sciences Of The United States Of America 2020, 117: 16616-16625. PMID: 32601203, PMCID: PMC7368321, DOI: 10.1073/pnas.1916121117.Peer-Reviewed Original ResearchConceptsRibosomal protein S6 kinase beta-1Macrophage proinflammatory activationGlcNAc signalingProinflammatory activationUnexpected roleWhole-body metabolismNutrient fluxesLipid accumulationImmune cell activationGlcNAcHomeostatic mechanismsMetabolic disturbancesBeta 1Cell activationDiet-induced metabolic dysfunctionDiet-induced obese miceActivationWhole-body insulin resistanceMacrophage inflammationGlcNAcylationOGTPeripheral tissuesPhosphorylationEnhanced inflammationInsulin resistance
2018
Adipocyte OGT governs diet-induced hyperphagia and obesity
Li MD, Vera NB, Yang Y, Zhang B, Ni W, Ziso-Qejvanaj E, Ding S, Zhang K, Yin R, Wang S, Zhou X, Fang EX, Xu T, Erion DM, Yang X. Adipocyte OGT governs diet-induced hyperphagia and obesity. Nature Communications 2018, 9: 5103. PMID: 30504766, PMCID: PMC6269424, DOI: 10.1038/s41467-018-07461-x.Peer-Reviewed Original ResearchConceptsSerine/threonine residuesN-acetylglucosamine transferaseNutrient cuesThreonine residuesTranscriptional activationO-GlcNAcylationLipid desaturationIntracellular proteinsOGTHigh-fat diet-induced hyperphagiaDevelopment of obesityBaseline food intakeSignaling contributesLipid signalsCB1 signalingBrain axisChronic dysregulationFood intakeMetabolic diseasesPalatable foodPharmacological manipulationHyperphagiaObesityFat sensorSignaling
2017
Calcium-dependent O-GlcNAc signaling drives liver autophagy in adaptation to starvation
Ruan HB, Ma Y, Torres S, Zhang B, Feriod C, Heck RM, Qian K, Fu M, Li X, Nathanson MH, Bennett AM, Nie Y, Ehrlich BE, Yang X. Calcium-dependent O-GlcNAc signaling drives liver autophagy in adaptation to starvation. Genes & Development 2017, 31: 1655-1665. PMID: 28903979, PMCID: PMC5647936, DOI: 10.1101/gad.305441.117.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, BiologicalAnimalsAutophagyAutophagy-Related Protein 5Autophagy-Related Protein-1 HomologCalcium SignalingCalcium-Calmodulin-Dependent Protein Kinase Type 2Cells, CulturedGlucagonHEK293 CellsHeLa CellsHumansInositol 1,4,5-Trisphosphate ReceptorsLiverMice, Inbred C57BLN-AcetylglucosaminyltransferasesNutritional Physiological PhenomenaConceptsAMPK-dependent phosphorylationLiver autophagyN-acetylglucosamine transferaseCalmodulin-dependent kinase IICalcium/calmodulin-dependent kinase IIWhole-body homeostasisULK proteinsNutrient homeostasisKinase IICalcium signalingAutophagic fluxGenetic ablationMetabolic adaptationAutophagyStarvationOGTPhosphorylationHomeostasisMouse liverProduction of glucoseKetone bodiesAdaptationSignalingProteinTransferase
2012
O-GlcNAc Transferase/Host Cell Factor C1 Complex Regulates Gluconeogenesis by Modulating PGC-1α Stability
Ruan HB, Han X, Li MD, Singh JP, Qian K, Azarhoush S, Zhao L, Bennett AM, Samuel VT, Wu J, Yates JR, Yang X. O-GlcNAc Transferase/Host Cell Factor C1 Complex Regulates Gluconeogenesis by Modulating PGC-1α Stability. Cell Metabolism 2012, 16: 226-237. PMID: 22883232, PMCID: PMC3480732, DOI: 10.1016/j.cmet.2012.07.006.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBlotting, WesternChromatin ImmunoprecipitationChromatography, High Pressure LiquidGluconeogenesisHeat-Shock ProteinsHEK293 CellsHep G2 CellsHost Cell Factor C1HumansHyperglycemiaImmunoprecipitationLiverMiceMice, Inbred C57BLMultiprotein ComplexesN-AcetylglucosaminyltransferasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProteomicsReal-Time Polymerase Chain ReactionTandem Mass SpectrometryTranscription FactorsConceptsHCF-1O-GlcNAcylationPGC-1αHost cell factor C1Hexosamine biosynthetic pathwayN-acetylglucosamine (O-GlcNAc) modificationDeubiquitinase BAP1Proteomic approachGlcNAc transferasePosttranslational modificationsNuclear proteinsBiosynthetic pathwayMaster regulatorKey regulatorFactor C1C1 complexOGTGlucose availabilityRegulatorProteinGluconeogenesisHepatic gluconeogenesisGlucose homeostasisComplexesHepatic knockdown
2002
Recruitment of O-GlcNAc Transferase to Promoters by Corepressor mSin3A Coupling Protein O-GlcNAcylation to Transcriptional Repression
Yang X, Zhang F, Kudlow JE. Recruitment of O-GlcNAc Transferase to Promoters by Corepressor mSin3A Coupling Protein O-GlcNAcylation to Transcriptional Repression. Cell 2002, 110: 69-80. PMID: 12150998, DOI: 10.1016/s0092-8674(02)00810-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimal Population GroupsAnimalsCOS CellsGene Expression RegulationGene SilencingGenes, ReporterGlycoproteinsHistone DeacetylasesHumansN-AcetylglucosaminyltransferasesPromoter Regions, GeneticRepressor ProteinsSin3 Histone Deacetylase and Corepressor ComplexTranscription FactorsTranscription, GeneticTumor Cells, CulturedConceptsRNA polymerase IIPolymerase IIGlcNAc transferaseHistone deacetylationTranscription factorsN-acetylglucosamine monosaccharidesHistone deacetylase complexO-GlcNAc modificationProtein O-GlcNAcylationDeacetylase complexTranscriptional repressionThreonine residuesPrecise functional rolePosttranslational modificationsO-GlcNAcylationFunctional roleSpecific mannerMSin3AOGTPromoterDeacetylationTransferaseCorepressorTranscriptionRepression