2015
Limiting Cholesterol Biosynthetic Flux Spontaneously Engages Type I IFN Signaling
York AG, Williams KJ, Argus JP, Zhou QD, Brar G, Vergnes L, Gray EE, Zhen A, Wu NC, Yamada DH, Cunningham CR, Tarling EJ, Wilks MQ, Casero D, Gray DH, Yu AK, Wang ES, Brooks DG, Sun R, Kitchen SG, Wu TT, Reue K, Stetson DB, Bensinger SJ. Limiting Cholesterol Biosynthetic Flux Spontaneously Engages Type I IFN Signaling. Cell 2015, 163: 1716-1729. PMID: 26686653, PMCID: PMC4783382, DOI: 10.1016/j.cell.2015.11.045.Peer-Reviewed Original ResearchConceptsImport of cholesterolI interferonType I IFNsSTING-dependent mannerCholesterol biosynthetic pathwayI IFNsCombination of biosynthesisBiosynthetic fluxBiosynthetic pathwayLong-chain fatty acidsIsotope tracer analysisMetabolic shiftMetabolic pathwaysType I interferonCholesterol biosynthesisLipid requirementsChain fatty acidsInnate immunityBiosynthesisFatty acidsPool sizePathwayMechanistic studiesViral challengeFree cholesterol
2014
Mutation of Nogo-B Receptor, a Subunit of cis-Prenyltransferase, Causes a Congenital Disorder of Glycosylation
Park EJ, Grabińska K, Guan Z, Stránecký V, Hartmannová H, Hodaňová K, Barešová V, Sovová J, Jozsef L, Ondrušková N, Hansíková H, Honzík T, Zeman J, Hůlková H, Wen R, Kmoch S, Sessa WC. Mutation of Nogo-B Receptor, a Subunit of cis-Prenyltransferase, Causes a Congenital Disorder of Glycosylation. Cell Metabolism 2014, 20: 448-457. PMID: 25066056, PMCID: PMC4161961, DOI: 10.1016/j.cmet.2014.06.016.Peer-Reviewed Original ResearchConceptsProtein glycosylationCis-prenyltransferaseGPI anchor biosynthesisDolichol synthesisSynthesis of dolicholO-mannosylationAnchor biosynthesisFirst enzymeGenetic basisC-terminusCongenital disorderFunction mutationsGlycosylationEssential roleEnhanced accumulationMutationsYeastNgBRSubunitsDolicholFibroblastsBiosynthesisTerminusFree cholesterolProtein
2012
Cholesterol and nonalcoholic fatty liver disease: Renewed focus on an old villain
Kerr T, Davidson N, Groszmann R, Iwakiri Y, Taddei T. Cholesterol and nonalcoholic fatty liver disease: Renewed focus on an old villain. Hepatology 2012, 56: 1995-1998. PMID: 23115010, PMCID: PMC3627394, DOI: 10.1002/hep.26088.Peer-Reviewed Original ResearchHMG-CoA reductasePhosphorylation of HMG-CoA reductaseExpression of cholesterol metabolism genesHMG-CoA reductase expressionDysregulated cholesterol metabolismFree cholesterolCholesterol metabolism genesHistological severity of NAFLDMetabolic genesAMP kinaseCoA reductaseLDL receptor expressionCholesterol ester hydrolaseDecreased phosphorylationDisease phenotypeLiver-related mortalitySeverity of NAFLDCholesterol metabolismEster hydrolaseCholesterol synthesisNonalcoholic fatty liver diseaseACAT-2Fatty liver diseaseSirtuin 1Receptor expression
2010
Haloperidol disrupts lipid rafts and impairs insulin signaling in SH-SY5Y cells
Sánchez-Wandelmer J, Dávalos A, de la Peña G, Cano S, Giera M, Canfrán-Duque A, Bracher F, Martín-Hidalgo A, Fernández-Hernando C, Lasunción M, Busto R. Haloperidol disrupts lipid rafts and impairs insulin signaling in SH-SY5Y cells. Neuroscience 2010, 167: 143-153. PMID: 20123000, DOI: 10.1016/j.neuroscience.2010.01.051.Peer-Reviewed Original ResearchConceptsEffects of haloperidolCholesterol contentLipid raft compositionCholesterol biosynthesisCell cholesterol contentSH-SY5Y cellsNeuroblastoma SH-SY5YHL-60 human cell linesDopamine receptorsMetabolic effectsTherapeutic effectHaloperidolInsulin-Akt signalingImpairs insulinCellular cholesterol homeostasisLipid raftsSH-SY5YFree cholesterolCholesterol homeostasisDependent insulinDrug inhibitionHuman cell linesCell linesPhysiological vehicleInsulin
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