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 bodiesAdaptationSignalingProteinTransferaseMetabolic Regulation of Gene Expression by Histone Lysine β‐hydroxybutyrylation
Zhang D, Xie Z, Chung D, Tang Z, Huang H, Dai L, Qi S, Li J, Colak G, Chen Y, Peng C, Ruan H, Wang D, Jensen L, Kwon O, Lee S, Pletcher S, Tan M, Lombard D, White K, Zhao H, Li J, Roeder R, Yang X, Zhao Y. Metabolic Regulation of Gene Expression by Histone Lysine β‐hydroxybutyrylation. The FASEB Journal 2017, 31 DOI: 10.1096/fasebj.31.1_supplement.755.2.Peer-Reviewed Original ResearchKetone bodiesNeuro-protective roleDiabetic ketoacidosisAdjunctive treatmentKetogenic dietBrain tumorsPharmacological effectsNeurodegenerative diseasesPathophysiological statesCultured cell linesMedical FoundationLines of evidenceCell linesEpilepsyΒ-hydroxybutyrylationNIHRNA-seq analysisMetabolic regulationRegulatory roleGene expressionShanghai Municipal ScienceMetabolic pathwaysKetoacidosisDiabetesPatients