2005
Lovastatin-induced PC-12 cell differentiation is associated with RhoA/RhoA kinase pathway inactivation
Fernández-Hernando C, Suárez Y, Lasunción MA. Lovastatin-induced PC-12 cell differentiation is associated with RhoA/RhoA kinase pathway inactivation. Molecular And Cellular Neuroscience 2005, 29: 591-602. PMID: 15951198, DOI: 10.1016/j.mcn.2005.04.012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCholesterolDiterpenesEnzyme ActivationEnzyme InhibitorsHydroxymethylglutaryl-CoA Reductase InhibitorsIntracellular Signaling Peptides and ProteinsLovastatinNeuritesPC12 CellsPhosphorylationProtein PrenylationProtein Serine-Threonine KinasesRatsRhoA GTP-Binding ProteinRho-Associated KinasesSterolsTerpenesConceptsNeurite outgrowthNon-sterol mevalonate derivativesPC-12 cell differentiationCellular lipid compositionNon-sterol isoprenoidsEffects of geranylgeraniolBiosynthetic pathwayProtein prenylationRole of cholesterolCofilin phosphorylationRhoA signalingMevalonate derivativesA ReductaseRhoA activationCell differentiationCoenzyme A (HMG-CoA) reductaseLovastatin inhibitsPC-12 cellsCholesterol biosynthesisPathway inactivationRhoA kinaseLipid compositionOutgrowthGeranylgeraniolInhibition
2002
AplidinTM Induces Apoptosis in Human Cancer Cells via Glutathione Depletion and Sustained Activation of the Epidermal Growth Factor Receptor, Src, JNK, and p38 MAPK*
Cuadrado A, Garcı́a-Fernández L, González L, Suárez Y, Losada A, Alcaide V, Martı́nez T, Fernández-Sousa J, Sánchez-Puelles J, Muñoz A. AplidinTM Induces Apoptosis in Human Cancer Cells via Glutathione Depletion and Sustained Activation of the Epidermal Growth Factor Receptor, Src, JNK, and p38 MAPK*. Journal Of Biological Chemistry 2002, 278: 241-250. PMID: 12414812, DOI: 10.1074/jbc.m201010200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCell DivisionCell SurvivalCells, CulturedDepsipeptidesEnzyme ActivationEnzyme InhibitorsErbB ReceptorsFemaleFibroblastsFlow CytometryGlutathioneHumansJNK Mitogen-Activated Protein KinasesKidney NeoplasmsMiceMitogen-Activated Protein KinasesP38 Mitogen-Activated Protein KinasesPeptides, CyclicPhosphorylationProto-Oncogene Proteins pp60(c-src)Receptors, Platelet-Derived Growth FactorTumor Cells, CulturedConceptsEpidermal growth factor receptorP38 MAPK activationP38 MAPKNon-receptor protein tyrosine kinase SrcGrowth factor receptorMAPK activationProtein tyrosine kinase SrcStress response programSustained activationFactor receptorCancer cellsMDA-MB-231 breast cancer cellsHuman cancer cellsBenzyloxycarbonyl-VADKinase SrcHuman MDA-MB-231 breast cancer cellsMDA-MB-231 cellsMolecular basisKinase JNKPretreatment of cellsMouse embryosEGFR activationFluoromethyl ketoneGrowth arrestHuman renal cancerDifferential effects of ergosterol and cholesterol on Cdk1 activation and SRE‐driven transcription
Suárez Y, Fernández C, Ledo B, Ferruelo AJ, Martín M, Vega MA, Gómez‐Coronado D, Lasunción MA. Differential effects of ergosterol and cholesterol on Cdk1 activation and SRE‐driven transcription. The FEBS Journal 2002, 269: 1761-1771. PMID: 11895447, DOI: 10.1046/j.1432-1327.2002.02822.x.Peer-Reviewed Original ResearchConceptsHuman cellsCdk1 activationCell cycle machineryCell membrane formationCell cycle progressionCholesterol-free mediumCell cycle arrestG2/M phaseSpecific regulatorsCycle machineryGene constructsYeast sterolCycle progressionCell cycleCell proliferation inhibitionCycle arrestAction of cholesterolUCN-01Cell growthCyclin B1 expressionSKF 104976Cholesterol homeostasisM phaseMembrane formationCell proliferation