2022
PPARγ phase separates with RXRα at PPREs to regulate target gene expression
Li Z, Luo L, Yu W, Li P, Ou D, Liu J, Ma H, Sun Q, Liang A, Huang C, Chi T, Huang X, Zhang Y. PPARγ phase separates with RXRα at PPREs to regulate target gene expression. Cell Discovery 2022, 8: 37. PMID: 35473936, PMCID: PMC9043196, DOI: 10.1038/s41421-022-00388-0.Peer-Reviewed Original ResearchPPAR response elementNuclear condensatesTranscriptional activationPPRE siteZinc finger motifsDNA binding domainsKey transcription activatorSpecific transcriptional activationTarget gene expressionPPARγ/RXRαRetinoid X receptor αPPARγ target genesFinger motifPhase-separated dropletsTranscription activatorTranscriptional responseObligate heterodimersTarget genesX receptor αBinding domainsGene expressionResponse elementPeroxisome proliferator-activated receptorNovel mechanismProliferator-activated receptor
2018
Deoxypodophyllotoxin in Anthriscus sylvestris alleviates fat accumulation in the liver via AMP-activated protein kinase, impeding SREBP-1c signal
Kim KY, Park KI, Lee SG, Baek SY, Lee EH, Kim S, Kim SH, Park SG, Yu SN, Oh TW, Kim JH, Kim KJ, Ahn SC, Kim Y. Deoxypodophyllotoxin in Anthriscus sylvestris alleviates fat accumulation in the liver via AMP-activated protein kinase, impeding SREBP-1c signal. Chemico-Biological Interactions 2018, 294: 151-157. PMID: 30148990, DOI: 10.1016/j.cbi.2018.08.025.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsApiaceaeBody WeightCholesterolDiet, High-FatDrugs, Chinese HerbalHep G2 CellsHumansHydrocarbons, FluorinatedLipid MetabolismLiverLiver X ReceptorsMaleMiceMice, Inbred C57BLPodophyllotoxinSignal TransductionSterol Regulatory Element Binding Protein 1SulfonamidesTriglyceridesUp-RegulationConceptsSREBP-1c inhibitionLipogenic genesDysregulation of AMPKAnthriscus sylvestrisProtein kinase activationSREBP-1c inductionHigh-fat dietSREBP-1cAcetyl-CoA carboxylaseSterol regulatory elementFatty acid synthaseTranscription factorsProtein kinaseRegulatory elementsStearoyl-CoA desaturase-1X receptor αLiver X receptor αAMPK activationKinase activationRegulatory mechanismsWild chervilOil Red O stainingFat dietAcid synthaseRed O staining
2012
5-Cholesten-3β,25-Diol 3-Sulfate Decreases Lipid Accumulation in Diet-Induced Nonalcoholic Fatty Liver Disease Mouse Model
Xu L, Kim JK, Bai Q, Zhang X, Kakiyama G, Min HK, Sanyal AJ, Pandak WM, Ren S. 5-Cholesten-3β,25-Diol 3-Sulfate Decreases Lipid Accumulation in Diet-Induced Nonalcoholic Fatty Liver Disease Mouse Model. Molecular Pharmacology 2012, 83: 648-658. PMID: 23258548, PMCID: PMC3583496, DOI: 10.1124/mol.112.081505.Peer-Reviewed Original ResearchMeSH KeywordsAcetyl-CoA CarboxylaseAcetyltransferasesAnimalsCholesterol EstersDiet, High-Fatfas ReceptorFatty AcidsFatty LiverFemaleGene ExpressionGlucose Tolerance TestGlycerol-3-Phosphate O-AcyltransferaseHydroxycholesterolsInflammationInsulinInsulin ResistanceInterleukin-1alphaInterleukin-1betaLipid MetabolismLipidsLiverMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSignal TransductionSterol Regulatory Element Binding Protein 1Tumor Necrosis Factor-alphaConceptsNonalcoholic fatty liver diseaseHigh-fat dietLong-term treatmentAcute treatmentTolerance testLipid accumulationMouse modelDiet-induced NAFLD mouse modelNonalcoholic fatty liver disease (NAFLD) mouse modelSREBP-1cLipid homeostasisFatty liver diseaseLiver X receptor αNAFLD mouse modelGlucose tolerance testSerum lipid levelsInsulin tolerance testHepatic lipid accumulationDisease mouse modelDecreases lipid accumulationTumor necrosis factorLipid-induced inflammationAcetyl-CoA carboxylase 1X receptor αSREBP-1c expressionOxysterol sulfation by cytosolic sulfotransferase suppresses liver X receptor/sterol regulatory element binding protein–1c signaling pathway and reduces serum and hepatic lipids in mouse models of nonalcoholic fatty liver disease
Bai Q, Zhang X, Xu L, Kakiyama G, Heuman D, Sanyal A, Pandak WM, Yin L, Xie W, Ren S. Oxysterol sulfation by cytosolic sulfotransferase suppresses liver X receptor/sterol regulatory element binding protein–1c signaling pathway and reduces serum and hepatic lipids in mouse models of nonalcoholic fatty liver disease. Metabolism 2012, 61: 836-845. PMID: 22225954, PMCID: PMC3342481, DOI: 10.1016/j.metabol.2011.11.014.Peer-Reviewed Original ResearchConceptsHepatic lipid levelsOxysterol sulfationSULT2B1b expressionLipid levelsLipid metabolismNonalcoholic fatty liver diseaseWestern blotFatty liver diseaseLiver X receptor αHigh-cholesterol dietReal-time reverse transcriptase-polymerase chain reactionHigh-fat dietReverse transcriptase-polymerase chain reactionTranscriptase-polymerase chain reactionAcetyl-CoA carboxylase 1X receptor αImportant endogenous regulatorLiver diseaseTotal cholesterolHepatic lipidsHepatic steatosisFatty acid synthasePolymerase chain reactionSterol regulatory element-binding proteinLung tissue
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