Search results for "Mitochondrial Membranes"

showing 10 items of 21 documents

The alkaloid, soyauxinium chloride, displays remarkable cytotoxic effects towards a panel of cancer cells, inducing apoptosis, ferroptosis and necrop…

2020

Abstract The cytotoxic potential of a naturally occurring indoloquinazoline alkaloid, soyauxinium chloride (SCHL), was determined on a broad panel of animal and human cancer cell lines, including various sensitive and drug-resistant phenotypes. The cytotoxicity, SCHL-induced autophagic, ferroptotic, and necroptotic cell death were evaluated by the resazurin reduction assay (RRA). Caspase-Glo assay was used to detect the activity of caspases using spectrophotometric analysis. Flow cytometry was applied for cell cycle analysis (PI staining), apoptosis (annexin V/PI staining), mitochondrial membrane potential (MMP) (JC-1) and reactive oxygen species (ROS) (H2DCFH-DA). SCHL and doxorubicin (ref…

0301 basic medicineProgrammed cell deathNecroptosisAntineoplastic AgentsApoptosisToxicology03 medical and health sciences0302 clinical medicineCell Line TumorCytotoxic T cellFerroptosisHumansRegulated Cell DeathCytotoxicityCaspasebiologyChemistryCell CycleGeneral MedicineMolecular biology030104 developmental biologyCell cultureApoptosis030220 oncology & carcinogenesisCancer cellMitochondrial MembranesNecroptosisbiology.proteinReactive Oxygen SpeciesChemico-biological interactions
researchProduct

Mcl-1 and Bok transmembrane domains : Unexpected players in the modulation of apoptosis

2020

The Bcl-2 protein family comprises both proand antiapoptotic members that control the permeabilization of the mitochondrial outer membrane, a crucial step in the modulation of apoptosis. Recent research has demonstrated that the carboxyl-terminal transmembrane domain (TMD) of some Bcl-2 protein family mem-bers can modulate apoptosis; however, the transmembrane interactome of the antiapoptotic protein Mcl-1 remains largely unexplored. Here, we demonstrate that the Mcl-1 TMD forms homooligomers in the mitochondrial membrane, competes with full-length Mcl-1 protein with regards to its antiapoptotic function, and induces cell death in a Bok-dependent manner. While the Bok TMD oligomers locate p…

0301 basic medicineProtein familyMitochondrionBCL-X(L)Endoplasmic ReticulumInteractome114 Physical sciences03 medical and health sciencesBok0302 clinical medicineProtein DomainsMITOCHONDRIAhemic and lymphatic diseasesAnimalsHumansBcl-2Inner mitochondrial membraneMultidisciplinaryCell DeathChemistryEndoplasmic reticulumapoptosisMcl-1PATHWAYSLOCALIZATIONBiological SciencesTransmembrane protein3. Good healthCell biologytransmembraneTransmembrane domainstomatognathic diseasesGLYCOPHORIN-A DIMERIZATION030104 developmental biologyHELIX PACKINGProto-Oncogene Proteins c-bcl-2BAX030220 oncology & carcinogenesisMitochondrial MembranesPROSURVIVAL BCL-2 PROTEINSMOTIFSURVIVALMyeloid Cell Leukemia Sequence 1 Protein1182 Biochemistry cell and molecular biologyBacterial outer membraneHeLa Cells
researchProduct

Phosphoproteomics of the developing heart identifies PERM1 - An outer mitochondrial membrane protein.

2021

Heart development relies on PTMs that control cardiomyocyte proliferation, differentiation and cardiac morphogenesis. We generated a map of phosphorylation sites during the early stages of cardiac postnatal development in mice; we quantified over 10,000 phosphorylation sites and 5000 proteins that were assigned to different pathways. Analysis of mitochondrial proteins led to the identification of PGC-1- and ERR-induced regulator in muscle 1 (PERM1), which is specifically expressed in skeletal muscle and heart tissue and associates with the outer mitochondrial membrane. We demonstrate PERM1 is subject to rapid changes mediated by the UPS through phosphorylation of its PEST motif by casein ki…

0301 basic medicineProteomicsOrganogenesisMFN2Muscle ProteinsP70-S6 Kinase 1030204 cardiovascular system & hematologyMitochondrionMitochondria Heart03 medical and health sciencesMice0302 clinical medicineCa2+/calmodulin-dependent protein kinaseAnimalsMolecular BiologyMitochondrial transportMice KnockoutChemistryMyocardiumPhosphoproteomicsMembrane ProteinsHeartLipid MetabolismPhosphoproteinsSolute carrier familyCell biology030104 developmental biologyMitochondrial MembranesPhosphorylationCardiology and Cardiovascular MedicineJournal of molecular and cellular cardiology
researchProduct

Characterization of the interaction of the antifungal and cytotoxic cyclic glycolipopeptide hassallidin with sterol-containing lipid membranes.

2019

Hassallidins are cyclic glycolipopeptides produced by cyanobacteria and other prokaryotes. The hassallidin structure consists of a peptide ring of eight amino acids where a fatty acid chain, additional amino acids, and sugar moieties are attached. Hassallidins show antifungal activity against several opportunistic human pathogenic fungi, but does not harbor antibacterial effects. However, they have not been studied on mammalian cells, and the mechanism of action is unknown. We purified hassallidin D from cultured cyanobacterium Anabaena sp. UHCC 0258 and characterized its effect on mammalian and fungal cells. Ultrastructural analysis showed that hassallidin D disrupts cell membranes, causin…

Antifungal AgentskolesteroliPeptideLipopeptide01 natural sciencesBiochemistrychemistry.chemical_compoundSTRUCTURE ELUCIDATIONCandida albicansMARINE CYANOBACTERIAmammalian cellsmembrane1183 Plant biology microbiology virologychemistry.chemical_classification0303 health sciencesCell DeathMembraneGlycopeptidesLipopeptideHERBICOLIN-ADEHYDROPEPTIDE LACTONEAmino acidSterolsCholesterolMembraneBiochemistrysolunsalpaajatMitochondrial Membranesmedicine.symptomBacterial outer membraneBiophysicsmechanismAntineoplastic Agentssaponin digitoninMolecular dynamicsCyanobacteriaITURIN-A03 medical and health sciencesLipopeptidesMembrane LipidsNATURAL-PRODUCTSCell Line TumormedicineHumansPropidium iodidesyanobakteerit030304 developmental biologyantimikrobiset yhdisteet010405 organic chemistryMAJOR COMPONENTCell BiologyluonnonaineetAnabaenaSterol0104 chemical sciencesMechanism of actionchemistrylipopeptidepeptiditMOLECULAR-DYNAMICS1182 Biochemistry cell and molecular biologyDrug Screening Assays AntitumorGlycolipidsBiochimica et biophysica acta. Biomembranes
researchProduct

Artesunate Activates Mitochondrial Apoptosis in Breast Cancer Cells via Iron-catalyzed Lysosomal Reactive Oxygen Species Production

2011

The antimalarial agent artesunate (ART) activates programmed cell death (PCD) in cancer cells in a manner dependent on the presence of iron and the generation of reactive oxygen species. In malaria parasites, ART cytotoxicity originates from interactions with heme-derived iron within the food vacuole. The analogous digestive compartment of mammalian cells, the lysosome, similarly contains high levels of redox-active iron and in response to specific stimuli can initiate mitochondrial apoptosis. We thus investigated the role of lysosomes in ART-induced PCD and determined that in MCF-7 breast cancer cells ART activates lysosome-dependent mitochondrial outer membrane permeabilization. ART impac…

AutophagosomeProgrammed cell deathEndosomeIronArtesunateApoptosisBreast NeoplasmsMitochondrionBiologyBiochemistryPermeabilityAntimalarialsCell Line TumorLysosomemedicineHumansEnzyme InhibitorsMolecular BiologyAutophagyChloroquineCell BiologyArtemisininsMitochondriaCell biologymedicine.anatomical_structureApoptosisMitochondrial MembranesCancer cellFemaleMacrolidesLysosomesReactive Oxygen SpeciesJournal of Biological Chemistry
researchProduct

The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
researchProduct

Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
researchProduct

Anandamide-induced apoptosis in Chang liver cells involves ceramide and JNK/AP-1 pathway

2006

In the present study we demonstrate that anandamide, the most important endogenous cannabinoid, markedly induced apoptosis in Chang liver cells, an immortalized non-tumor cell line derived from normal liver tissue, while it induced only modest effects in a number of hepatoma cell lines. The apoptotic effect was reduced by methyl-beta-cyclodextrin, a membrane cholesterol depletor, suggesting an interaction between anandamide and the membrane microdomains named lipid rafts. Anandamide effects were mediated by the production of ceramide, as demonstrated by experiments performed with the sphingomyelinase inhibitor, desipramine, or with the sphingomyelinase activator, melittin. This conclusion w…

CeramideProgrammed cell deathFas Ligand ProteinCell SurvivalPolyunsaturated AlkamidesLiver cytologyp38 mitogen-activated protein kinasesBlotting WesternApoptosisArachidonic AcidsBiologyCeramidesCell LineMembrane Potentialschemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsGeneticsHumansEnzyme InhibitorsMembrane GlycoproteinsBcl-2-Like Protein 11Dose-Response Relationship DrugDesipramineJNK Mitogen-Activated Protein KinasesMembrane ProteinsFree Radical ScavengersGeneral MedicineAnandamideEndocannabinoid systemAcetylcysteineCell biologyEnzyme ActivationTranscription Factor AP-1cannabinoids apoptosis tumor cells JNK/AP1LiverchemistryApoptosisCaspasesMitochondrial MembranesTumor Necrosis FactorsApoptosis Regulatory ProteinsSphingomyelinEndocannabinoidsSignal TransductionInternational Journal of Molecular Medicine
researchProduct

Cytotoxic Activity of Organotin(IV) Derivatives with Triazolopyrimidine Containing Exocyclic Oxygen Atoms

2020

In this study cytotoxicity of organotin(IV) compounds with 1,2,4-triazolo[1,5-a]pyrimidines, Me3Sn(5tpO) (1), n-Bu3Sn(5tpO) (2), Me3Sn(mtpO) (3), n-Bu3Sn(mtpO) (4), n-Bu3Sn(HtpO2) (5), Ph3Sn(HtpO2) (6) where 5HtpO = 4,5-dihydro-5-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, HmtpO = 4,7-dihydro-5-methyl-7-oxo-[1,2,4]triazolo-[1,5-a]pyrimidine, and H2tpO2 = 4,5,6,7-tetrahydro-5,7- dioxo-[1,2,4]triazolo-[1,5-a]-pyrimidine, was assessed on three different human tumor cell lines: HCT-116 (colorectal carcinoma), HepG2 (hepatocarcinoma) and MCF-7 (breast cancer). While 1 and 3 were inactive, compounds 2, 4, 5 and 6 inhibited the growth of the three tumor cell lines with IC50 values in the submicromolar …

DenticityCellPharmaceutical Science01 natural sciencesAnalytical Chemistrychemistry.chemical_compoundDrug DiscoveryOrganotin CompoundstriazolopyrimidineCytotoxicityMembrane Potential MitochondrialCytotoxinsapoptosisBiological activityHep G2 CellsG2 Phase Cell Cycle CheckpointsGene Expression Regulation Neoplasticmedicine.anatomical_structureChemistry (miscellaneous)Mitochondrial MembranesMCF-7 CellsMolecular MedicineCyclin-Dependent Kinase Inhibitor p21crystal structurein vitro anticancer activityPyrimidineCell SurvivalStereochemistryorganotin(iv)010402 general chemistryArticlelcsh:QD241-441Inhibitory Concentration 50Structure-Activity Relationshiplcsh:Organic chemistrymedicineHumansPhysical and Theoretical ChemistryMetallodrug010405 organic chemistryLigandOrganic ChemistryTriazolesHCT116 CellsapoptosiG1 Phase Cell Cycle Checkpoints0104 chemical sciencesPyrimidineschemistrymetallodrugsCell cultureApoptosisDrug DesignTumor Suppressor Protein p53Reactive Oxygen SpeciesMolecules
researchProduct

As2O3-induced oxidative stress and cycle progression in a human intestinal epithelial cell line (Caco-2)

2007

Foods and drinking water are the main routes for human exposure to inorganic arsenic, the intestinal epithelium being the first barrier against such exogenous toxicants. The present study evaluates the effect of As(III) (0.5-25 microM) upon Caco-2 cells as an intestinal epithelia model. Cell viability, intracellular formation of reactive oxygen species (ROS), mitochondrial membrane potential (Deltapsim) changes, and cell cycle distribution in exposed cultures were evaluated. The intracellular production of ROS was seen to increase in a non-dose dependent manner at all concentrations tested, with impairment of cell mitochondrial enzyme function secondary to a loss of Deltapsim. Concentration…

G2 PhaseCell SurvivalCellTetrazolium SaltsOxidative phosphorylationBiologyToxicologymedicine.disease_causeArsenicalsMembrane PotentialsArsenic TrioxidemedicineHumansViability assaychemistry.chemical_classificationReactive oxygen speciesCell CycleG1 PhaseOxidesGeneral MedicineCell cycleIntestinal epitheliumMitochondriaCell biologyOxidative StressThiazolesmedicine.anatomical_structurechemistryMitochondrial MembranesCaco-2 CellsReactive Oxygen SpeciesOxidative stressIntracellularToxicology in Vitro
researchProduct