2016
Akt‐mediated foxo1 inhibition is required for liver regeneration
Pauta M, Rotllan N, Fernández-Hernando A, Langhi C, Ribera J, Lu M, Boix L, Bruix J, Jimenez W, Suárez Y, Ford DA, Baldán A, Birnbaum MJ, Morales-Ruiz M, Fernández-Hernando C. Akt‐mediated foxo1 inhibition is required for liver regeneration. Hepatology 2016, 63: 1660-1674. PMID: 26473496, PMCID: PMC5177729, DOI: 10.1002/hep.28286.Peer-Reviewed Original ResearchConceptsAkt/protein kinase BCellular eventsProtein kinase BAkt2-deficient miceAbsence of Akt1Lipid droplet formationContribution of AktAkt2-null miceLiver regenerationAbnormal cellular eventsTranscription factorsAKT-FOXO1Kinase BLiver-specific deletionSuccessful liver regenerationPartial hepatectomyHepatic regenerative capabilityAKT1Chronic liver diseaseFOXO1 inhibitionCell proliferationEssential roleImpaired liver regenerationIntracellular mediatorsEfficient liver regeneration
2015
Neuregulin-activated ERBB4 induces the SREBP-2 cholesterol biosynthetic pathway and increases low-density lipoprotein uptake
Haskins JW, Zhang S, Means RE, Kelleher JK, Cline GW, Canfrán-Duque A, Suárez Y, Stern DF. Neuregulin-activated ERBB4 induces the SREBP-2 cholesterol biosynthetic pathway and increases low-density lipoprotein uptake. Science Signaling 2015, 8: ra111. PMID: 26535009, PMCID: PMC4666504, DOI: 10.1126/scisignal.aac5124.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorCholesterolFemaleHumansHydroxymethylglutaryl CoA ReductasesLipoproteins, LDLMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNeuregulin-1Proto-Oncogene Proteins c-aktReceptor, ErbB-4Receptors, LDLSterol Regulatory Element Binding Protein 2TOR Serine-Threonine KinasesConceptsIntracellular domainEGFR family membersLow-density lipoprotein uptakeCholesterol biosynthesisSREBP target genesRapamycin complex 1ErbB4 intracellular domainSite-1 proteaseCholesterol biosynthesis genesSoluble intracellular domainCholesterol biosynthetic pathwayActivation of ErbB4Mammary epithelial cellsInhibition of AktSterol regulatory elementBiosynthesis genesLipoprotein uptakeRegulatory elementsBiosynthetic pathwayTarget genesDevelopmental processesMetabolic remodelingMature formNeuregulin-1Cellular membranes
2014
Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis
Rodlan N, Chamorro‐Jorganes A, Araldi E, Wanschel AC, Aryal B, Aranda JF, Goedeke L, Salerno AG, Ramírez CM, Sessa WC, Suárez Y, Fernández‐Hernando C. Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis. The FASEB Journal 2014, 29: 597-610. PMID: 25392271, PMCID: PMC4314230, DOI: 10.1096/fj.14-262097.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisBlood GlucoseBone Marrow CellsBone Marrow TransplantationCell MovementCholesterolCytokinesDisease ProgressionInflammationInsulinLeukocytesLipidsLipoproteins, LDLMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalMicroscopy, FluorescencePlaque, AtheroscleroticProto-Oncogene Proteins c-aktReceptors, LDLConceptsProgression of atherosclerosisSerine-threonine protein kinaseBone marrow cellsAkt2-deficient miceInsulin-responsive tissuesWild-type bone marrow cellsProtein kinaseMarrow cellsAkt2 deficiencyAkt2Higher plasma lipidsWild-type miceMice resultsProatherogenic cytokinesObese subjectsPlasma lipidsProinflammatory cytokinesInsulin resistanceInflammatory responseGlucose levelsAtherosclerotic plaquesCholesterol metabolismAtherosclerosisMacrophage migrationMarked reduction
2008
Prohibitin-1 maintains the angiogenic capacity of endothelial cells by regulating mitochondrial function and senescence
Schleicher M, Shepherd BR, Suarez Y, Fernandez-Hernando C, Yu J, Pan Y, Acevedo LM, Shadel GS, Sessa WC. Prohibitin-1 maintains the angiogenic capacity of endothelial cells by regulating mitochondrial function and senescence. Journal Of Cell Biology 2008, 180: 101-112. PMID: 18195103, PMCID: PMC2213620, DOI: 10.1083/jcb.200706072.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaCells, CulturedCellular SenescenceCytoskeletonElectron Transport Complex IEndothelial CellsEndothelium, VascularHumansMiceMice, Inbred StrainsMitochondriaMitochondrial MembranesNeovascularization, PhysiologicNeuropeptidesPhosphatidylinositol 3-KinasesProhibitinsProto-Oncogene Proteins c-aktRac GTP-Binding ProteinsRac1 GTP-Binding ProteinReactive Oxygen SpeciesRepressor ProteinsSignal TransductionConceptsProhibitin 1Mitochondrial functionKnockdown of PHB1Inner mitochondrial membraneEndothelial cell motilityEndothelial cellsCytoskeletal rearrangementsMitochondrial membraneVivo angiogenesis assaysCell motilityAngiogenic capacityCellular senescenceReactive oxygen speciesMitochondrial productionFunctional blood vesselsImportant regulatorSenescenceAngiogenesis assayTube formationOxygen speciesVascular homeostasisCellsVascular systemRac1Yeast
2007
Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease
Fernández-Hernando C, Ackah E, Yu J, Suárez Y, Murata T, Iwakiri Y, Prendergast J, Miao RQ, Birnbaum MJ, Sessa WC. Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease. Cell Metabolism 2007, 6: 446-457. PMID: 18054314, PMCID: PMC3621848, DOI: 10.1016/j.cmet.2007.10.007.Peer-Reviewed Original ResearchMeSH KeywordsAcute Coronary SyndromeAnimalsApolipoproteins EApoptosisAtherosclerosisBone Marrow TransplantationCoronary OcclusionDisease Models, AnimalEndothelial CellsFemaleHumansInflammation MediatorsMacrophagesMaleMiceMice, KnockoutNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktConceptsLoss of Akt1Apolipoprotein E knockout backgroundOcclusive coronary artery diseaseBone marrow transfer experimentsAcute coronary syndromeCoronary artery diseaseLesion expansionCoronary syndromeCoronary atherosclerosisSevere atherosclerosisArtery diseaseInflammatory mediatorsCoronary lesionsVascular protectionVascular originProinflammatory genesENOS phosphorylationCardiovascular systemLesion formationGenetic ablationEndothelial cellsAtherogenesisEnhanced expressionKnockout backgroundVessel wall