Search results for " APOPTOSIS"

showing 10 items of 372 documents

Synthesis and antiproliferative activity of 3-(2-chloroethyl)-5-methyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4-(…

2015

Based on the encouraging results found for 3,5-dimethyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4-(3H)-one 7 previously tested by us, as well as the consideration that heterocycle fused tetrazepinones bearing the 2-chloroethyl substituent show a better cytotoxic profile than temozolomide and mitozolomide against human cancer cell lines which express the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT), in this paper we report the multistep synthesis and the biological study of 3-(2-cloroethyl)-5-methyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4-(3H)-one 10. Like compound 7, it was active on P-glycoprotein e…

MethyltransferaseStereochemistryHL60Antineoplastic AgentsApoptosisHL-60 CellsStructure-Activity Relationshipchemistry.chemical_compoundDrug DiscoveryHumansStructure–activity relationshipCell ProliferationPharmacologyTrifluoromethylDose-Response Relationship DrugMolecular StructureChemistryCell growthCell CycleOrganic ChemistryAzepinesGeneral MedicineCell cycleSettore CHIM/08 - Chimica Farmaceutica1235-Tetrazepinones pyrazolo[34-f][1235]-tetrazepinones drug resistance apoptosis antiproliferative activityCell cultureApoptosisPyrazolesDrug Screening Assays AntitumorK562 CellsEuropean Journal of Medicinal Chemistry
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The thiol switch C684 in Mitofusin-2 mediates redox-induced alterations of mitochondrial shape and respiration

2017

Mitofusin-2 (MFN2) is a GTPase in the outer mitochondrial membrane involved in the regulation of mitochondrial fusion and bioenergetics. MFN2 also plays a role in mitochondrial fusion induced by changes in the intracellular redox state. Adding oxidized glutathione (GSSG), the core cellular stress indicator, to mitochondrial preparations stimulates mitochondrial fusion by inducing disulphide bond-mediated oligomer formation of MFN2 and its homolog MFN1 which involve cysteine 684 (C684) of MFN2. Mitochondrial hyperfusion represents an adaptive stress response that confers transient protection by increasing mitochondrial ATP production but how this depends on the thiol switch C684 in MFN2 has …

Mice Knockout0301 basic medicineCell RespirationMFN2Cell BiologyOxidative phosphorylationMitochondrionBiologyMitochondrial apoptosis-induced channelGTP PhosphohydrolasesMitochondriaCell biologyMice03 medical and health sciencesCellular and Molecular NeuroscienceMitofusin-2030104 developmental biologymitochondrial fusionAnimalsMFN1Sulfhydryl CompoundsATP–ADP translocaseCell ShapeOxidation-ReductionCells CulturedNeurochemistry International
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Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species

2010

This review highlights the important role of redox signaling between mitochondria and NADPH oxidases. Besides the definition and general importance of redox signaling, the cross-talk between mitochondrial and Nox-derived reactive oxygen species (ROS) is discussed on the basis of 4 different examples. In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. This concept was supported by observations that ethidium bromide-induced mitochondrial d…

Mitochondrial ROSAgingPotassium ChannelsMyocytes Smooth MuscleBiophysicsIn Vitro TechniquesMitochondrionmedicine.disease_causeMitochondrial Membrane Transport ProteinsModels BiologicalMitochondrial apoptosis-induced channelBiochemistryPeroxynitritechemistry.chemical_compoundmedicineAnimalsHumansMitochondrionFeedback PhysiologicalNADPH oxidasebiologyNADPH oxidaseMitochondrial Permeability Transition PoreSuperoxideAngiotensin IINADPH OxidasesSuperoxideNitric oxideCell BiologyReactive Nitrogen SpeciesMitochondriaCell biologyOxidative StressOxidative protein modificationchemistryMitochondrial permeability transition poreRedox regulationNOX1Hypertensionbiology.proteinReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Bioenergetics
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Insight on [1,3]thiazolo[4,5-e]isoindoles as tubulin polymerization inhibitors

2021

A series of [1,3]thiazolo[4,5-e]isoindoles has been synthesized through a versatile and high yielding multistep sequence. Evaluation of the antiproliferative activity of the new compounds on the full NCI human tumor cell line panel highlighted several compounds that are able to inhibit tumor cell proliferation at micromolar-submicromolar concentrations. The most active derivative 11g was found to cause cell cycle arrest at the G2/M phase and induce apoptosis in HeLa cells, following the mitochondrial pathway, making it a lead compound for the discovery of new antimitotic drugs.

Models MolecularCell cycle checkpointIsoindoles1ApoptosisIsoindoles01 natural sciencesPolymerizationTubulin Polymerization InhibitorsCell cycle arrestHeLaStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundTubulinDrug DiscoveryHumansTubulin polymerization inhibitors030304 developmental biologyPharmacology0303 health sciencesDose-Response Relationship DrugMolecular Structurebiology010405 organic chemistry3]thiazolo[4Organic ChemistryGeneral Medicinebiology.organism_classificationTubulin Modulators0104 chemical sciencesBiochemistrychemistryCell cultureApoptosis5-e]isoindoles13]thiazolo[45-e]isoindoles13]thiazolo[45-e]isoindoles; Apoptosis; Cell cycle arrest; Tubulin polymerization inhibitorsLead compoundDerivative (chemistry)HeLa CellsEuropean Journal of Medicinal Chemistry
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Conformational control of Bax localization and apoptotic activity by Pro168.

2004

In healthy cells, Bax resides inactive in the cytosol because its COOH-terminal transmembrane region (TMB) is tucked into a hydrophobic pocket. During apoptosis, Bax undergoes a conformational change involving NH2-terminal exposure and translocates to mitochondria to release apoptogenic factors. How this process is regulated remains unknown. We show that the TMB of Bax is both necessary and sufficient for mitochondrial targeting. However, its availability for targeting depends on Pro168 located within the preceding loop region. Pro168 mutants of Bax lack apoptotic activity, cannot rescue the apoptosis-resistant phenotype of Bax/Bak double knockout cells, and are retained in the cytosol even…

Models MolecularConformational changeProlineCell SurvivalProtein ConformationMutantMolecular Sequence DataApoptosisMitochondrionMitochondrial apoptosis-induced channelArticleCell Line03 medical and health sciencesMice0302 clinical medicineBcl-2-associated X proteinProto-Oncogene ProteinsAnimalsHumansAmino Acid Sequence030304 developmental biologybcl-2-Associated X Proteinapoptosis; Bcl-2 family; NH2-terminal exposure; mitochondria; targeting0303 health sciencesbiologyMembrane ProteinsCell BiologyPeptide FragmentsCell biologyTransport proteinMitochondriaCytosolProtein Transportbcl-2 Homologous Antagonist-Killer ProteinProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisbiology.proteinBcl-2 Homologous Antagonist-Killer ProteinHeLa CellsThe Journal of cell biology
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1,2,4-Oxadiazole Topsentin Analogs with Antiproliferative Activity against Pancreatic Cancer Cells, Targeting GSK3β Kinase.

2021

A new series of topsentin analogs, in which the central imidazole ring of the natural lead was replaced by a 1,2,4- oxadiazole moiety, was efficiently synthesized. All derivatives were pre-screened for antiproliferative activity against the National Cancer Institute (NCI-60) cell lines panel. The five most potent compounds were further investigated in various pancreatic ductal adenocarcinoma (PDAC) cell lines, including SUIT-2, Capan-1, and Panc-1 cells, eliciting EC50 values in the micromolar and sub-micromolar range, associated with significant reduction of cell migration. These remarkable results might be explained by the effects of these new topsentin analogues on epithelial-to-mesenchy…

Models MolecularIndoles124-oxadiazole topsentin analogs; GSK3β kinase; inhibition of migration; PDAC antiproliferative activity; proapoptotic activityApoptosisDrug Screening Assays01 natural sciencesBiochemistrychemistry.chemical_compound124-oxadiazole topsentin analogs; GSK3β kinase; PDAC antiproliferative activity; inhibition of migration; proapoptotic activity; Antineoplastic Agents; Apoptosis; Cell Proliferation; Cell Survival; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; Glycogen Synthase Kinase 3 beta; Humans; Imidazoles; Indoles; Models Molecular; Molecular Structure; Oxadiazoles; Pancreatic Neoplasms; Protein Kinase Inhibitors; Structure-Activity Relationship; Tumor Cells CulturedModelsAnnexinDrug DiscoveryTumor Cells CulturedGSK3β kinaseGeneral Pharmacology Toxicology and Pharmaceutics4-oxadiazole topsentin analogsOxadiazolesCulturedMolecular StructureChemistryKinaseImidazolesCell migrationTumor Cellsinhibition of migrationMolecular MedicineDrugIntracellularPDAC antiproliferative activityproapoptotic activityCell Survival12Antineoplastic AgentsDose-Response RelationshipStructure-Activity RelationshipPancreatic cancermedicineHumansPropidium iodideProtein Kinase InhibitorsCell ProliferationPharmacologyGlycogen Synthase Kinase 3 betaDose-Response Relationship Drug010405 organic chemistryOrganic ChemistryMolecularAntitumormedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaMolecular biology0104 chemical sciencesPancreatic Neoplasms010404 medicinal & biomolecular chemistryApoptosisCell cultureDrug Screening Assays Antitumor124-oxadiazole topsentin analogChemMedChem
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Demyelination patterns in a mathematical model of multiple sclerosis.

2016

In this paper we derive a reaction-diffusion-chemotaxis model for the dynamics of multiple sclerosis. We focus on the early inflammatory phase of the disease characterized by activated local microglia, with the recruitment of a systemically activated immune response, and by oligodendrocyte apoptosis. The model consists of three equations describing the evolution of macrophages, cytokine and apoptotic oligodendrocytes. The main driving mechanism is the chemotactic motion of macrophages in response to a chemical gradient provided by the cytokines. Our model generalizes the system proposed by Calvez and Khonsari (Math Comput Model 47(7–8):726–742, 2008) and Khonsari and Calvez (PLos ONE 2(1):e…

Multiple Sclerosismedicine.medical_treatmentInflammationApoptosisBiology01 natural sciencesModels BiologicalConcentric ring03 medical and health sciences0302 clinical medicineTuring instabilitymedicineHumansMultiple sclerosi0101 mathematicsSettore MAT/07 - Fisica MatematicaInflammationMicrogliaOligodendrocyte apoptosisPatternMultiple sclerosisTuring instabilityApplied MathematicsChemotaxismedicine.diseaseAgricultural and Biological Sciences (miscellaneous)Magnetic Resonance Imaging010101 applied mathematicsChemotaxis PDE modelCytokinemedicine.anatomical_structureModeling and SimulationImmunologymedicine.symptomNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesJournal of mathematical biology
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Small molecule inhibitors of Apaf-1-related caspase- 3/-9 activation that control mitochondrial-dependent apoptosis

2006

10 pages, 5 figures.-- PMID: 16341125 [PubMed].-- Available online Dec 9, 2005.

Multiprotein complexCytochromeProtein-protein interactionsApoptosisCaspase 3MitochondrionLigandsCell LineChemical librarychemistry.chemical_compoundPeptide LibraryApoptosomesPeptoidHumansCombinatorial libraries inhibitorApoptosomeProtein PrecursorsMolecular BiologybiologyCaspase 3Intrinsic apoptosisCytochromes cCell BiologyCaspase InhibitorsCaspase 9Recombinant ProteinsMitochondriaCell biologyEnzyme ActivationCaspasa-9Apoptotic Protease-Activating Factor 1chemistryBiochemistryN-substituted GlycinesApoptosisCaspasa-3biology.proteinApoptosomeApaf-1Molecular recognitionSmall moleculeProtein BindingCell Death & Differentiation
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Antiproliferative Effects of St. John’s Wort, Its Derivatives, and Other Hypericum Species in Hematologic Malignancies

2021

Hypericumis a widely present plant, and extracts of its leaves, flowers, and aerial elements have been employed for many years as therapeutic cures for depression, skin wounds, and respiratory and inflammatory disorders. Hypericum also displays an ample variety of other biological actions, such as hypotensive, analgesic, anti-infective, anti-oxidant, and spasmolytic abilities. However, recent investigations highlighted that this species could be advantageous for the cure of other pathological situations, such as trigeminal neuralgia, as well as in the treatment of cancer. This review focuses on the in vitro and in vivo antitumor effects of St. John’s Wort (Hypericum perforatum), its derivat…

MyeloidAngiogenesisDrug Evaluation PreclinicalReviewPharmacologylcsh:Chemistrychemistry.chemical_compoundhyperforinDrug InteractionsMyeloid CellsLymphocyteslcsh:QH301-705.5SpectroscopybiologyapoptosisleukemiaHypericum perforatumGeneral MedicineComputer Science ApplicationsHypericinLeukemiamedicine.anatomical_structurephotodynamic therapyHematologic NeoplasmsHypericumHypericumSt. John’s wortlymphomaCatalysisInorganic ChemistryStructure-Activity Relationshipmultidrug resistanceIn vivoCell Line TumormedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyCell ProliferationPlant Extractsbusiness.industryOrganic Chemistry<i>Hypericum</i>biology.organism_classificationmedicine.diseaseAntineoplastic Agents PhytogenicApoptosis; Hyperforin; Hypericin; Hypericum; Leukemia; Lymphoma; Mul-tidrug resistance; Photodynamic therapy; St. John’s wort; Animals; Antineoplastic Agents Phytogenic; Apoptosis; Cell Line Tumor; Cell Proliferation; Drug Evaluation Preclinical; Drug Interactions; Drug Resistance Neoplasm; Hematologic Neoplasms; Humans; Hypericum; Lymphocytes; Myeloid Cells; Plant Extracts; Structure-Activity RelationshipHyperforinchemistrylcsh:Biology (General)lcsh:QD1-999Drug Resistance NeoplasmhypericinbusinessInternational Journal of Molecular Sciences
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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