2004
JNK activation is critical for Aplidin™-induced apoptosis
Cuadrado A, González L, Suárez Y, Martínez T, Muñoz A. JNK activation is critical for Aplidin™-induced apoptosis. Oncogene 2004, 23: 4673-4680. PMID: 15122339, DOI: 10.1038/sj.onc.1207636.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalAntineoplastic AgentsApoptosisBlotting, WesternBreast NeoplasmsCell DivisionCell Line, TumorCell SurvivalDepsipeptidesEnzyme ActivationFemaleFibroblastsHumansMitogen-Activated Protein KinasesNF-kappa BPeptides, CyclicPhosphorylationPrecipitin TestsProto-Oncogene Proteins c-junTranscription Factor AP-1
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
2001
Dose-dependent effects of lovastatin on cell cycle progression. Distinct requirement of cholesterol and non-sterol mevalonate derivatives
Martı́nez-Botas J, Ferruelo A, Suárez Y, Fernández C, Gómez-Coronado D, Lasunción M. Dose-dependent effects of lovastatin on cell cycle progression. Distinct requirement of cholesterol and non-sterol mevalonate derivatives. Biochimica Et Biophysica Acta 2001, 1532: 185-194. PMID: 11470239, DOI: 10.1016/s1388-1981(01)00125-1.Peer-Reviewed Original ResearchConceptsCell proliferationLow-density lipoprotein cholesterolCell cycle progressionDose-dependent effectCell cycle distributionCell cycleCycle progressionLipoprotein cholesterolConcentrations of lovastatinCholesterol supplyCycle distributionCholesterolLovastatinHuman cell linesCell linesCholesterol biosynthesisCholesterol-free mediumNormal cell cyclingM phaseProgressionProliferationPresent studyHL-60Mevalonate derivativesCell cycling
1999
Impact of different low-density lipoprotein (LDL) receptor mutations on the ability of LDL to support lymphocyte proliferation
Martínez-Botas J, Suárez Y, Reshef A, Carrero P, Ortega H, Gómez-Coronado D, Teruel J, Leitersdorf E, Lasunción M. Impact of different low-density lipoprotein (LDL) receptor mutations on the ability of LDL to support lymphocyte proliferation. Metabolism 1999, 48: 834-839. PMID: 10421221, DOI: 10.1016/s0026-0495(99)90214-7.Peer-Reviewed Original ResearchConceptsLow-density lipoproteinAbility of LDLFamilial hypercholesterolemiaReceptor mutationsLow-density lipoprotein receptor mutationNormal low density lipoproteinHomozygous familial hypercholesterolemiaDifferent LDL receptor mutationsEndogenous cholesterol synthesisLDL receptor mutationsMitogen-stimulated lymphocytesLymphocyte proliferationPeripheral lymphocytesLDL particlesLymphocytesMitogenic effectCytometric analysisCholesterol synthesisLDL bindingCase 2Case 1Similar extentCompound heterozygotesDefective internalizationDifferent phenotypes
1998
Induction of apoptosis in p53-null HL-60 cells by inhibition of lanosterol 14-α demethylase
Martínez-Botas J, Ferruelo A, Suárez Y, Gómez-Coronado D, Lasunción M. Induction of apoptosis in p53-null HL-60 cells by inhibition of lanosterol 14-α demethylase. Biochimie 1998, 80: 887-894. PMID: 9893947, DOI: 10.1016/s0300-9084(00)88884-7.Peer-Reviewed Original Research