Search results for "Apoptosi"

showing 10 items of 1846 documents

Les IAP au cœur de la signalisation NF-κB

2012

The function of IAP has long been limited to an inhibition of apoptosis through their capacity to bind some caspases. Since the expression of these proteins is altered in some tumor samples, IAPs are targets for anticancer therapy and many small molecules have been designed for their capacity to inhibit IAP-caspase interaction. Unexpectedly, these molecules appeared to significantly affect NF-κB activation. In this review, we will discuss the central role of cIAP1, cIAP2 and XIAP in the regulation of NF-κB activating signaling pathways.

Regulation of gene expressionbiologyGeneral MedicineTransforming growth factor betaNFKB1General Biochemistry Genetics and Molecular BiologyCell biologyXIAPbody regionsApoptosisImmunologybiology.proteinSignal transductionReceptorCaspasemédecine/sciences
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Immunopathology of leishmaniasis: an update.

2007

Leishmaniasis represents a severe, increasing, public health problem. The perspective of its control is highly dependent on research progress, on therapeutic manipulations of the immune system, and on vaccine development. There is a correlation between the clinical outcome of Leishmania infection and the cytokine response profile. While a protective immune response against Leishmania has been clearly identified to be related to the influence of a type-1 response and IFN-γ production, the precise role of T helper (TH) 2 cytokines in non-healing infections requires further exploration. IL-4 and IL-13 (TH2 cytokines) can promote disease progression in cutaneous leishmaniasis, whereas IL-4 woul…

Regulatory T cellImmunopathology; LeishmaniasisengT-LymphocytesImmunologyApoptosisImmunopathology03 medical and health sciences0302 clinical medicineImmune systemCutaneous leishmaniasisImmunopathologyLeishmaniasisengmedicineImmunology and AllergyAnimalsHumansLeishmaniasisPharmacologybiologybusiness.industryLeishmaniasismedicine.diseaseLeishmaniabiology.organism_classificationmedicine.anatomical_structureVisceral leishmaniasis030220 oncology & carcinogenesisImmunologybusinessCD8030215 immunologyInternational journal of immunopathology and pharmacology
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A novel copper compound, CuNV110, induces apoptosis in tumor cells by dissociation of the Hsp60- pro-caspase 3 complex

2015

The biological activity of CuNV1110, a novel copper chemical compound, has been recently studied on cancer cells and it has been showed that it reduces the cell viability, in a dose and time dependent manner, and induces cell apoptosis. In this study we evaluated the possible mechanisms by which CuNV1110 induces cell apoptosis. In particular we looked at its effects on Hsp60 levels and caspase 3 activation. We used an in vitro model of a pulmonary mucoepidermoid carcinoma (NCI-H292 cells). We found that CuNV1110 reduces the cell viability and induces cell apoptosis in a dose/time dependent manner. Then, we found that Hsp60 levels decrease with the increasing concentrations of CuNV110; by co…

Respiratory cells; pulmonary cancer; Hsp60; caspase 3; apoptosis.Respiratory cells pulmonary cancer Hsp60 caspase 3 apoptosis
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A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics

2011

Glutamate excitotoxicity leads to fragmented mitochondria in neurodegenerative diseases, mediated by nitric oxide and S-nitrosylation of dynamin-related protein 1, a mitochondrial outer membrane fission protein. Optic atrophy gene 1 (OPA1) is an inner membrane protein important for mitochondrial fusion. Autosomal dominant optic atrophy (ADOA), caused by mutations in OPA1, is a neurodegenerative disease affecting mainly retinal ganglion cells (RGCs). Here, we showed that OPA1 deficiency in an ADOA model influences N-methyl-D-aspartate (NMDA) receptor expression, which is involved in glutamate excitotoxicity and oxidative stress. Opa1enu/+mice show a slow progressive loss of RGCs, activation …

Retinal Ganglion CellsCancer ResearchReceptor expressionExcitotoxicityApoptosisNeurodegenerativeMitochondrionEyemedicine.disease_causeGTP PhosphohydrolasesMice0302 clinical medicineReceptorsoxidative stressPhosphorylationbcl-2-Associated X Protein0303 health sciencesbiologyGlutamate receptorMitochondriaUp-RegulationCell biologymitochondrial fusionAutosomal DominantOriginal Articlebcl-Associated Death ProteinMitochondrial fissionN-Methyl-D-AspartateBiotechnologymitochondrial fragmentationOncology and CarcinogenesisImmunologybcl-X ProteinSOD2Glutamic AcidReceptors N-Methyl-D-AspartateNMDA receptorsCell Line03 medical and health sciencesCellular and Molecular NeuroscienceBcl-2-associated X proteinOptic Atrophy Autosomal DominantmedicineAnimalsEye Disease and Disorders of Vision030304 developmental biologySuperoxide DismutaseNeurosciencesCell BiologyMolecular biologyeye diseasesOxidative StressOptic AtrophyMutationbiology.proteinOPA1 mutationBiochemistry and Cell Biologysense organsglutamate excitotoxicity030217 neurology & neurosurgeryCell Death & Disease
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Metabolomic changes in the rat retina after optic nerve crush.

2013

Purpose To identify metabolic pathways and metabolites affected by optic nerve crush that can act as predictors of the disease or therapeutic targets. Methods The left optic nerve of adult rats was intraorbitally crushed and retinas were dissected 24 hours or 14 days after the lesion (n = 10 per group). Metabolic profiling analysis was carried out by Metabolon, Inc. A total of 195 metabolites were unambiguously detected. Data were normalized and the regulated metabolites were identified after comparing the different conditions. Metabolite concentration changes were analyzed using single and multivariate statistical analysis to detect discriminatory metabolites. Functional clustering and met…

Retinal Ganglion CellsNerve CrushMetaboliteProtein Array AnalysisApoptosisPharmacologymedicine.disease_causeGas Chromatography-Mass SpectrometryRetinaLesionRats Sprague-Dawleychemistry.chemical_compoundMetabolomicsTandem Mass SpectrometrymedicineAnimalsMetabolomicsAmino AcidsChemistryLipid metabolismAxotomyOptic NerveLipid MetabolismAxonsRatsMetabolic pathwayOxidative StressOptic nerveCarbohydrate MetabolismFemaleMetabolonmedicine.symptomOxidative stressChromatography LiquidSignal TransductionInvestigative ophthalmologyvisual science
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Vesicle transport and photoreceptor death: fishing for molecular links.

2013

Intracellular vesicle transport defects can induce retinal degeneration and photoreceptor cell death, but the molecular connections between these processes remains poorly understood. Reporting in Developmental Cell, Nishiwaki et al. (2013) suggest that a vesicle fusion cis-SNARE complex component translates vesicular transport defects into photoreceptor cell apoptosis.

Retinal degenerationVesicle fusionLipid bilayer fusionIntracellular vesicleApoptosisCell BiologyBiologymedicine.diseaseMembrane FusionGeneral Biochemistry Genetics and Molecular BiologyPhotoreceptor cellCell biologyVesicular transport proteinSoluble N-Ethylmaleimide-Sensitive Factor Attachment Proteinsmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosismedicineRetinal Cone Photoreceptor CellsAnimalsMolecular BiologyDevelopmental BiologyDevelopmental cell
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Phosphodiesterase inhibition induces retinal degeneration, oxidative stress and inflammation in cone-enriched cultures of porcine retina.

2013

nherited retinal degenerations affecting both rod and cone photoreceptors constitute one of the causes 74 of incurable blindness in the developed world. Cyclic guanosine monophosphate (cGMP) is crucial in the 75 phototransduction and, mutations in genes related to its metabolism are responsible for different retinal 76 dystrophies. cGMP-degrading phosphodiesterase 6 (PDE6) mutations cause around 4e5% of the retinitis 77 pigmentosa, a rare form of retinal degeneration. The aim of this study was to evaluate whether phar- 78 macological PDE6 inhibition induced retinal degeneration in cone-enriched cultures of porcine retina 79 similar to that found in murine models. PDE6 inhibition was induced…

Retinal degenerationgenetic structuresPurinonesPhosphodiesterase InhibitorsSwineEstrès oxidatiuApoptosisBiologyRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundOrgan Culture TechniquesRetinitis pigmentosamedicineIn Situ Nick-End LabelingAnimalsNeurociènciesCyclic GMPRetinaCalpainCaspase 3Retinal DegenerationPhosphodiesteraseRetinalmedicine.diseaseMolecular biologySensory SystemsOphthalmologyOxidative Stressmedicine.anatomical_structurechemistryBiochemistryRetinal Cone Photoreceptor CellsSwine Miniaturesense organsZaprinastRetinal DystrophiesRetinitis PigmentosaVisual phototransduction
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The role of heat shock proteins in neoplastic processes and the research on their importance in the diagnosis and treatment of cancer

2021

Heat shock proteins (HSPs) are chaperones with highly conservative primary structure, necessary in the processes of protein folding to the most energetically advantageous conformation and maintaining their stability. HSPs perform a number of important functions in various cellular processes and are capable of modulating pathophysiological conditions at the cellular and systemic levels. An example is the high level of HSP expression in neoplastic tissues, which disrupts the apoptosis of transformed cells and promotes the processes of proliferation, invasion, and metastasis. In addition, an increasing amount of information is appearing about the participation of HSPs in the formation of multi…

Review PaperResearch groupsbusiness.industryDisease progressionRapoptosisCancermedicine.diseaseanti-cancer therapy.Cancer treatmentMetastasisOncologyHeat shock proteinheat shock proteinsmedicineCancer researchMedicineNeoplastic ProcessescancerRadiology Nuclear Medicine and imagingProtein foldingbusinessanti-cancer therapyContemporary Oncology
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Heat Shock Protein-60 and Risk for Cardiovascular Disease

2011

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecularchaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60,the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotectivebut a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examplesof specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicatea pathogenic role for HSP60 but also its …

Riskanimal structuresChaperonin Heat shock protein-60 cardiomyocytes heart failure cardiovascular diseases atherosclerosisChaperonin heat shock protein 60 cardiomyocytes heart failure cardiovascular disease atherosclerosis apoptosis microRNAs (miRs) diabetes Atrial fibrillationApoptosischemical and pharmacologic phenomenaDiseaseBioinformaticsAutoimmune DiseasesPathogenesisHeat shock proteinAtrial FibrillationDrug DiscoveryExtracellularAnimalsHumansMyocytes CardiacHeart FailurePharmacologybiologyfungiChaperonin 60AtherosclerosisResponse to treatmentCardiovascular DiseasesReperfusion InjuryChaperone (protein)HypertensionImmunologybiology.proteinHSP60Stress conditionsBiomarkersCurrent Pharmaceutical Design
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Synthesis, computational docking and biological evaluation of celastrol derivatives as dual inhibitors of SERCA and P-glycoprotein in cancer therapy.

2021

Abstract A series of eleven celastrol derivatives was designed, synthesized, and evaluated for their in vitro cytotoxic activities against six human cancer cell lines (A549, HepG2, HepAD38, PC3, DLD-1 Bax-Bak WT and DKO) and three human normal cells (LO2, BEAS-2B, CCD19Lu). To our knowledge, six derivatives were the first example of dipeptide celastrol derivatives. Among them, compound 3 was the most promising derivative, as it exhibited a remarkable anti-proliferative activity and improved selectivity in liver cancer HepAD38 versus human normal hepatocytes, LO2. Compound 6 showed higher selectivity in liver cancer cells against human normal lung fibroblasts, CCD19Lu cell line. The Ca2+ mob…

SERCAAntineoplastic AgentsApoptosisPharmacologySarcoplasmic Reticulum Calcium-Transporting ATPaseschemistry.chemical_compoundStructure-Activity RelationshipCell Line TumorDrug DiscoverymedicineCytotoxic T cellHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinCell ProliferationPharmacologyBinding SitesbiologyOrganic ChemistryCancerGeneral Medicinemedicine.diseaseMolecular Docking SimulationchemistryApoptosisDocking (molecular)CelastrolCell cultureDrug Resistance NeoplasmDrug Designbiology.proteinDrug Screening Assays AntitumorPentacyclic TriterpenesEuropean journal of medicinal chemistry
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