Search results for "cell-death"

showing 10 items of 10 documents

Caloric Restriction Mimetics Enhance Anticancer Immunosurveillance

2016

International audience; Caloric restriction mimetics (CRMs) mimic the biochemical effects of nutrient deprivation by reducing lysine acetylation of cellular proteins, thus triggering autophagy. Treatment with the CRM hydroxycitrate, an inhibitor of ATP citrate lyase, induced the depletion of regulatory T cells (which dampen anticancer immunity) from autophagy-competent, but not autophagy-deficient, mutant KRAS-induced lung cancers in mice, thereby improving anticancer immunosurveillance and reducing tumor mass. Short-term fasting or treatment with several chemically unrelated autophagy-inducing CRMs, including hydroxycitrate and spermidine, improved the inhibition of tumor growth by chemoth…

0301 basic medicineCancer ResearchATP citrate lyaseSpermidineBariatric SurgeryimmunosurveillanceT-Lymphocytes RegulatoryAutophagy-Related Protein 5[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compoundMiceregulatory T cellCitrates3. Good healthImmunogenic Cell-DeathImmunosurveillancemedicine.anatomical_structureOncologyBiochemistryDifferentiationembryonic structuresImmunogenic cell deathIn-VivoHumanRegulatory T cell[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyDietary RestrictionNOProto-Oncogene Proteins p21(ras)03 medical and health sciencesMonitoring ImmunologicIn vivoCell Line TumormedicineAutophagyAnimalsHumanscancerChemotherapyBreast-CancerCaloric Restrictioncancer; chemotherapy immunosurveillance regulatory T cellAnimal[ SDV.BC ] Life Sciences [q-bio]/Cellular Biologyregulatory T&nbspAutophagyfungiNeoplasms ExperimentalcellSpermidineMethotrexate030104 developmental biologychemistryAcetylationMutationCancer researchCitrateNeoplasm Transplantation
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Arabidopsis RCD1 coordinates chloroplast and mitochondrial functions through interaction with ANAC transcription factors

2019

Reactive oxygen species (ROS)-dependent signaling pathways from chloroplasts and mitochondria merge at the nuclear protein RADICAL-INDUCED CELL DEATH1 (RCD1). RCD1 interacts in vivo and suppresses the activity of the transcription factors ANAC013 and ANAC017, which mediate a ROS-related retrograde signal originating from mitochondrial complex III. Inactivation of RCD1 leads to increased expression of mitochondrial dysfunction stimulon (MDS) genes regulated by ANAC013 and ANAC017. Accumulating MDS gene products, including alternative oxidases (AOXs), affect redox status of the chloroplasts, leading to changes in chloroplast ROS processing and increased protection of photosynthetic apparatus.…

0106 biological sciences0301 basic medicineretrograde signalingChloroplastsArabidopsisPlant BiologyMitochondrion01 natural sciencesElectron Transport Complex IIIGene Expression Regulation PlantArabidopsisOXIDATIVE STRESS-RESPONSETranscriptional regulationCYCLIC ELECTRON FLOWBiology (General)Nuclear proteinANAC transcription factors1183 Plant biology microbiology virologyreactive oxygen speciesbiologyChemistryRETROGRADE REGULATIONGeneral NeuroscienceQRNuclear Proteinsfood and beveragesGeneral MedicinePlants Genetically Modified:Science::Biological sciences [DRNTU]Cell biologyMitochondriaChloroplastviherhiukkasetMedicineSignal transductionmitochondrial functionsResearch ArticleSignal TransductionQH301-705.5SciencemitokondriotGenetics and Molecular BiologyGeneral Biochemistry Genetics and Molecular BiologyPROTEIN COMPLEXESSIGNALING PATHWAYS03 medical and health scienceschloroplastStress PhysiologicalALTERNATIVE OXIDASESkasvitENZYME-ACTIVITIESredox signalingTranscription factorarabidopsis RCD1General Immunology and MicrobiologybiokemiaArabidopsis Proteinsta1182Biology and Life Sciencesbiology.organism_classification030104 developmental biologyCELL-DEATHPLANT-MITOCHONDRIAA. thalianaGeneral BiochemistryRetrograde signalingGENES-ENCODING MITOCHONDRIALproteiinit010606 plant biology & botanyTranscription Factors
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Free Radicals Mediate Systemic Acquired Resistance

2014

Summary: Systemic acquired resistance (SAR) is a form of resistance that protects plants against a broad spectrum of secondary infections. However, exploiting SAR for the protection of agriculturally important plants warrants a thorough investigation of the mutual interrelationships among the various signals that mediate SAR. Here, we show that nitric oxide (NO) and reactive oxygen species (ROS) serve as inducers of SAR in a concentration-dependent manner. Thus, genetic mutations that either inhibit NO/ROS production or increase NO accumulation (e.g., a mutation in S-nitrosoglutathione reductase [GSNOR]) abrogate SAR. Different ROS function additively to generate the fatty-acid-derived azel…

0106 biological sciences[SDV]Life Sciences [q-bio]ArabidopsisPseudomonas syringaeReductasemedicine.disease_cause01 natural scienceschemistry.chemical_compoundcuticle formationInducerDicarboxylic Acidsskin and connective tissue diseaseslcsh:QH301-705.5chemistry.chemical_classification0303 health sciencesMutationsalicyclic-acidCell biologydefenseGlutathione ReductaseBiochemistryGlycerophosphates[SDE]Environmental Sciencesplant immunitySystemic acquired resistances-nitrosoglutathioneSecondary infectionnitric-oxidearabidopsis-thalianaBiologyNitric OxideGeneral Biochemistry Genetics and Molecular BiologyNitric oxide03 medical and health sciencesmedicine[SDV.BV]Life Sciences [q-bio]/Vegetal Biology030304 developmental biologyReactive oxygen speciesArabidopsis Proteinsfungicell-deathbody regionschemistrylcsh:Biology (General)azelaic-acidresponsesNitric Oxide SynthaseReactive Oxygen SpeciesFunction (biology)010606 plant biology & botanynitric-oxide;plant immunity;arabidopsis-thaliana;s-nitrosoglutathione;cuticle formation;salicyclic-acid;azelaic-acid;cell-death;responses;defenseCell Reports
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Characteristic ERK1/2 signaling dynamics distinguishes necroptosis from apoptosis

2021

International audience; ERK1/2 involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK1/2 dynamics in determining cellular re- sponses. To untangle how ERK1/2 contributes to two cell death programs, we investigated ERK1/2 signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929 cells. We observed that ERK1/2 inhibition sensi- tizes cells to apoptosis while delaying necroptosis. By monitoring ERK1/2 activity by live-cell imaging using an improved ERK1/2 biosensor (EKAR4.0), we reported differential ERK1/2 signaling dynamics between cell survival, apoptosis, and nec- roptosis. We also decrypted a temporally shifted …

Cell biologyProgrammed cell deathScience[SDV]Life Sciences [q-bio]Necroptosis[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsPROTEINMECHANISMSESCRTACTIVATION03 medical and health sciences0302 clinical medicineINFLAMMATIONGene expressionMedicine and Health SciencesKINASEBiology030304 developmental biology0303 health sciencesMultidisciplinaryIDENTIFICATIONChemistryNECROSISQDynamics (mechanics)Biology and Life SciencesErk1 2 signalingCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics[SDV] Life Sciences [q-bio]Biological sciencesBiomolecular engineeringCELL-DEATHApoptosisCell culture030220 oncology & carcinogenesisTumor necrosis factor alphaBIOSENSORSHuman medicineiScience
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Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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Potential anticancer heterometallic Fe-Au and Fe-Pd agents: Initial mechanistic insights

2013

A series of gold(III) and palladium(II) heterometallic complexes with new iminophosphorane ligands derived from ferrocenylphosphanes [{Cp-P(Ph2)═N-Ph}2Fe] (1), [{Cp-P(Ph2)═N-CH2-2-NC5H4}2Fe] (2), and [{Cp-P(Ph2)═N-CH2-2-NC5H4}Fe(Cp)] (3) have been synthesized and structurally characterized. Ligands 2 and 3 afford stable coordination complexes [AuCl2(3)]ClO4, [{AuCl2}2(2)](ClO4)2, [PdCl2(3)], and [{PdCl2}2(2)]. The complexes have been evaluated for their antiproliferative properties in human ovarian cancer cells sensitive and resistant to cisplatin (A2780S/R), in human breast cancer cells (MCF7) and in a nontumorigenic human embryonic kidney cell line (HEK-293T). The highly cytotoxic trimeta…

STRUCTURAL-CHARACTERIZATIONARENE-RUTHENIUM COMPLEXESStereochemistryANTITUMOR-ACTIVITYchemistry.chemical_elementGOLD COMPOUNDSAntineoplastic AgentsCYTOTOXIC ACTIVITYArticleCoordination ComplexesCell Line TumorDrug DiscoveryOrganometallic CompoundsmedicineHumansCytotoxic T cellFerrous CompoundsBIOLOGICAL-PROPERTIESGroup 2 organometallic chemistryCisplatinHEK 293 cellsIn vitroPLATINUM(II) COMPLEXESHEK293 CellschemistryCELL-DEATHCell cultureCancer cellMolecular MedicineMETAL-COMPLEXESCisplatinOrganogold CompoundsPalladiumX-RAY-STRUCTUREPalladiummedicine.drug
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Molecular basis of the interaction of novel tributyltin(IV) 2/4-[(E)-2-(aryl)-1-diazenyl] benzoates endowed with an improved cytotoxic profile: Synth…

2010

A series of tributyltin(IV) complexes based on 2/4-[(E)-2-(aryl)-1-diazenyl]benzoate ligands was synthesized, wherein the position of the carboxylate and aryl substituents (methyl, tert-butyl and hydroxyl) varies. The complexes, Bu(3)SnL(1-4)H (1-4), have been structurally characterized by elemental analysis and IR, NMR ((1)H, (13)C, and (119)Sn) and (119)Sn Mossbauer spectroscopy. All have a tetrahedral geometry in solution and a trigonal bipyramidal geometry in the solid-state, except for Bu(3)SnL(4)H (4) that was ascertained to have tetrahedral coordination by X-ray crystallography. Cytotoxicity studies were carried out on human tumor cell lines A498 (renal cancer), EVSA-T (mammary cance…

Models MolecularQuantitative structure–activity relationshipMagnetic Resonance SpectroscopyStereochemistryCell SurvivalANTITUMOR-ACTIVITYHydrophobicityQuantitative Structure-Activity RelationshipAntineoplastic AgentsCrystallography X-RayBiochemistryBenzoatesVALIDATIONInorganic Chemistrychemistry.chemical_compoundAnti-cancer drugCell Line TumorOrganotin CompoundsTRIORGANOTIN(IV) COMPLEXESHumansCRYSTAL-STRUCTURESCarboxylateOPTIMIZATIONArylazobenzoateSpectroscopyX-ray crystallographyMolecular StructureQSARArylTetrahedral molecular geometryNuclear magnetic resonance spectroscopyBenzoatesTributyltin(IV) compoundTrigonal bipyramidal molecular geometryMOSQUITO LARVAEchemistryCELL-DEATHDocking (molecular)Settore CHIM/03 - Chimica Generale E InorganicaDocking studies RIBONUCLEOTIDE REDUCTASE INHIBITORSEMIEMPIRICAL METHODSTrialkyltin CompoundsCell lineAEDES-AEGYPTI
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Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction

2017

In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the U…

0301 basic medicineAgingProgrammed cell deathendocrine systemOxidative phosphorylationReview Articlemedicine.disease_causeEndoplasmic ReticulumBiochemistryINITIATION-FACTOR 2-ALPHA03 medical and health sciencesProgrammed cell-deathSELECTIVE-INHIBITIONProgrammed cell-death;TXNIP/NLRP3 INFLAMMASOME ACTIVATION; MITOCHONDRIAL ELECTRON-TRANSPORT; SPONTANEOUSLY HYPERTENSIVE-RATS; INITIATION-FACTOR 2-ALPHA; CORONARY-ARTERY FUNCTION; ER STRESS; SELECTIVE-INHIBITION; MESSENGER-RNA; TRANSMEMBRANE PROTEINmedicineHumansEndothelial dysfunctionlcsh:QH573-671TXNIP/NLRP3 INFLAMMASOME ACTIVATIONSPONTANEOUSLY HYPERTENSIVE-RATSEndothelial Cellbusiness.industrylcsh:CytologyEndoplasmic reticulumfungiEndothelial CellsOxidative StreCell BiologyGeneral MedicineAdaptive responseMITOCHONDRIAL ELECTRON-TRANSPORTER STRESSmedicine.diseaseCell biologyOxidative Stress030104 developmental biologyProteostasisTRANSMEMBRANE PROTEINUnfolded protein responseUnfolded Protein ResponsebusinessMESSENGER-RNAOxidative stressCORONARY-ARTERY FUNCTIONHumanOxidative Medicine and Cellular Longevity
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Different immunophenotypical apoptotic profiles characterise megakaryocytes of essential thrombocythaemia and primary myelofibrosis.

2009

Aims: Essential thrombocythaemia (ET) and primary myelofibrosis (PMF) share some clinical and pathological features, but show different biological behaviour and prognosis. The latest contributions to understanding the nature of these disorders have focused on bone marrow microenvironment remodelling and proliferative stress, recognising megakaryocytes (MKCs) as “key-cells”. The aim of this study was to investigate the apoptotic profile of ET and PMF MKCs in order to further characterise the biology of these disorders. Methods: Bone marrow biopsy samples from 30 patients with ET, and 30 patients with PMF, were immunophenotypically studied for the expression of pro-apoptotic (Fas, Fas-L, Bax,…

AdultMalePathologymedicine.medical_specialtyBiopsyIDIOPATHIC MYELOFIBROSISApoptosisPOLYCYTHEMIA-VERASettore MED/08 - Anatomia PatologicaBiologyPathology and Forensic MedicineImmunophenotypingImmunophenotypingMegakaryocyteBone MarrowmedicineIn Situ Nick-End LabelingHumansTelomerase reverse transcriptaseMyelofibrosisMOLECULAR PERSPECTIVEAgedAged 80 and overTUNEL assayEssential thrombocythemiaC-MPLMUTATION STATUSGeneral MedicineMiddle Agedmedicine.diseasePrognosismedicine.anatomical_structureCHRONIC MYELOPROLIFERATIVE DISORDERSCELL-DEATHApoptosisPrimary MyelofibrosisRISK-FACTORSCancer researchBONE-MARROW ANGIOGENESISMYELOID METAPLASIAFemaleBone marrowMegakaryocytesThrombocythemia EssentialJournal of clinical pathology
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Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.

2011

BackgroundIt is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.Methods and resultsBronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between th…

MaleSTRESSPulmonologyChronic Obstructive Pulmonary DiseasesNeutrophilsBiopsyGene ExpressionCD8-Positive T-Lymphocytesmedicine.disease_causeBiochemistryEpitheliumPulmonary function testingPathogenesisACTIVATIONPulmonary Disease Chronic ObstructiveMolecular Cell BiologyLungCOPDMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCOPD Hsp60QRCOPD heat shock proteins inflammationMiddle AgedImmunohistochemistrymedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMedicineFemalemedicine.symptomInflammation MediatorsSPINAL-CORDResearch ArticleEXPRESSIONanimal structuresCOPD; heat shock proteins; inflammationScienceImmunologyMolecular Sequence DataInflammationBronchichemical and pharmacologic phenomenaHEAT-SHOCK-PROTEIN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ACUTE LUNG INJURY SPINAL-CORD CELL-DEATH KAPPA-B HEAT-SHOCK-PROTEIN-60 STRESS EXPRESSION ACTIVATIONKAPPA-BBiologyHEAT-SHOCK-PROTEINMicrobiologycomplex mixturesCell LineACUTE LUNG INJURYMolecular GeneticsIn vivoStress PhysiologicalHeat shock proteinmedicineGeneticsHumansCOPDRNA MessengerBiologyAgedLungMucous MembraneBase SequenceSettore BIO/16 - Anatomia UmanaMacrophagesfungiImmunityTranscription Factor RelAProteinsComputational BiologyChaperonin 60medicine.diseaseChaperone Proteinsrespiratory tract diseasesGene Expression RegulationCELL-DEATHHEAT-SHOCK-PROTEIN-60inflammationImmunologyheat shock proteinsClinical ImmunologyOxidative stressBiomarkers
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