Search results for "Signal"

showing 10 items of 6924 documents

Cytotoxic effects of oxysterols associated with human diseases: Induction of cell death (apoptosis and/or oncosis), oxidative and inflammatory activi…

2009

Oxysterols resulting from spontaneous or enzymatic oxidation of cholesterol are present in numerous foodstuffs and have been identified at increased levels in the plasma and the vascular walls of patients with cardiovascular diseases, especially in atherosclerotic lesions. Consequently, their role in lipid disorders is widely suspected, but they may also contribute to the development of important degenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, osteoporosis, age-related macular degeneration, and cataract. Since these pathologies can be associated with the presence of apoptotic cells, oxidative and inflammatory processes, and lipid disorders, the ab…

Programmed cell deathClinical BiochemistryInflammationApoptosisOxidative phosphorylationPharmacologyBiologyLipidosesBiochemistrychemistry.chemical_compoundMacular DegenerationNeoplasmspolycyclic compoundsmedicineCytotoxic T cellHumansMolecular BiologyKetocholesterolsPhospholipidsPhospholipidosisInflammationCholesterolGeneral MedicineAtherosclerosisHydroxycholesterolsOxidative StresschemistryApoptosisImmunologyMolecular Medicinelipids (amino acids peptides and proteins)Signal transductionmedicine.symptomMolecular aspects of medicine
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DNA damage-induced cell death by apoptosis

2006

Following the induction of DNA damage, a prominent route of cell inactivation is apoptosis. During the last ten years, specific DNA lesions that trigger apoptosis have been identified. These include O6-methylguanine, base N-alkylations, bulky DNA adducts, DNA cross-links and DNA double-strand breaks (DSBs). Repair of these lesions are important in preventing apoptosis. An exception is O6-methylguanine-thymine lesions, which require mismatch repair for triggering apoptosis. Apoptosis induced by many chemical genotoxins is the consequence of blockage of DNA replication, which leads to collapse of replication forks and DSB formation. These DSBs are thought to be crucial downstream apoptosis-tr…

Programmed cell deathDNA RepairDNA repairDNA damageApoptosisp38 Mitogen-Activated Protein KinasesAnimalsHumansE2F1Molecular BiologybiologyCaspase 2DNA replicationDNAProliferating cell nuclear antigenCaspasesbiology.proteinCancer researchMolecular MedicineDNA mismatch repairTumor Suppressor Protein p53biological phenomena cell phenomena and immunityProto-Oncogene Proteins c-aktAtaxia telangiectasia and Rad3 relatedDNA DamageMutagensSignal TransductionTrends in Molecular Medicine
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Apoptosis in liver disease.

2006

The description of the morphological hallmarks of programmed cell death, apoptosis, in 1972 by Kerr, Wyllie and Currie started a field of research that revolutionized our understanding of cellular proliferation, tissue homeostasis and pathophysiology of many diseases. In the following years, a series of proteins involved in signaling and intracellular death pathways were identified and 30 years later the Noble Prize for physiology and medicine was awarded to S. Brenner, H. R. Horvitz and J. E. Sulston for their discoveries related to describing the mechanisms of cell death (apoptosis). The delineation of the signaling pathways that mediate apoptosis changed the paradigms of understanding in…

Programmed cell deathHepatologyLiver DiseasesIntrinsic apoptosisApoptosisBiologymedicine.diseaseCell biologyApoptosismedicineAnimalsHumansSignal transductionCell damageTissue homeostasisIntracellularDeath domainLiver international : official journal of the International Association for the Study of the Liver
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Influence of organophosphate poisoning on human dendritic cells.

2013

Organophosphourus compounds (OPC, including nerve agents and pesticides) exhibit acute toxicity by inhibition of acetylcholinesterase. Lung affections are frequent complications and a risk factor for death. In addition, epidemiological studies reported immunological alterations after OPC exposure. In our experiments we investigated the effects of organophosphourus pesticides dimethoate and chlorpyrifos on dendritic cells (DC) that are essential for the initial immune response, especially in the pulmonary system. DC, differentiated from the monocyte cell line THP-1 by using various cytokines (IL-4, GM-CSF, TNF-α, Ionomycin), were exposed to organophosphourus compounds at different concentrat…

Programmed cell deathInsecticidesMAP Kinase Signaling Systemmedicine.medical_treatmentPoison controlPharmacologyToxicologyMonocytesProinflammatory cytokineCell Linechemistry.chemical_compoundOrganophosphate PoisoningmedicineHumansDimethoatePesticidesProtein kinase BCell Deathbusiness.industryMonocyteCell DifferentiationGeneral MedicineDendritic cellDendritic Cellsmedicine.anatomical_structureCytokinechemistryImmunologyIonomycinCytokinesChlorpyrifosbusinessChemico-biological interactions
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Involvement of NO in contact hypersensitivity.

1998

The NO synthases (NOS) generate NO from L-arginine. High concentrations of NO have been shown to be responsible for tissue injury and cell death, while low concentrations of NO induce vasodilatation and other signaling effects. We have investigated the involvement of NO in contact hypersensitivity (CHS) reactions. CHS induced by treatment of BALB/c mice with the contact allergen 2,4-dinitrofluorobenzene (DNFB) was significantly reduced by the NOS inhibitor N-methyl-L-arginine (L-NMA), but not by the stereoisomer D-NMA, as shown by reduced ear swelling responses and evaluation of ear tissue sections. The CHS response was also reduced by aminoguanidine, which is known to preferentially inhibi…

Programmed cell deathLangerhans cellArginineInjections IntradermalT-LymphocytesImmunologyNitric Oxide Synthase Type IIBiologyArginineDermatitis ContactNitric OxideGuanidineschemistry.chemical_compoundMicemedicineImmunology and AllergyAnimalsRNA MessengerEnzyme InhibitorsSkinMice Inbred BALB Cintegumentary systemEpidermis (botany)Histocompatibility Antigens Class IIGeneral MedicineAllergensMolecular biologyPimagedineNitric oxide synthasemedicine.anatomical_structurechemistryLangerhans Cellsbiology.proteinDinitrofluorobenzeneSignal transductionNitric Oxide SynthaseKeratinocyteHaptensInternational immunology
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Targeting Bcl-2 family proteins modulates the sensitivity of B-cell lymphoma to rituximab-induced apoptosis.

2008

The chimeric monoclonal antibody rituximab is the standard of care for patients with B-cell non-Hodgkin lymphoma (B-NHL). Rituximab mediates complementdependent cytotoxicity and antibodydependent cellular cytotoxicity of CD20-positive human B cells. In addition, rituximab sensitizes B-NHL cells to cytotoxic chemotherapy and has direct apoptotic and antiproliferative effects. Whereas expression of the CD20 antigen is a natural prerequisite for rituximab sensitivity, cell-autonomous factors determining the response of B-NHL to rituximab are less defined. To this end, we have studied rituximab-induced apoptosis in human B-NHL models. We find that rituximab directly triggers apoptosis via the m…

Programmed cell deathLymphoma B-CellImmunologyMedizinAntineoplastic AgentsApoptosisMice SCIDBiochemistryPiperazinesNitrophenolsAntibodies Monoclonal Murine-DerivedMicePhosphatidylinositol 3-Kinasesimmune system diseaseshemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansB-cell lymphomaCD20SulfonamidesbiologyBcl-2 familyBiphenyl CompoundsAntibodies MonoclonalCell BiologyHematologymedicine.diseaseAntigens CD20LymphomaGene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2Apoptosisbiology.proteinCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRituximabSignal transductionRituximabNeoplasm Transplantationmedicine.drugSignal TransductionBlood
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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Apoptosis of T cells and the control of inflammatory bowel disease: therapeutic implications.

2007

Inflammatory bowel diseases (IBDs) such as Crohn’s disease and ulcerative colitis are the result of an imbalanced mucosal T cell response. Despite the identification of a genetic susceptibility region in the NOD2/CARD15 (nucleotide-binding oligomerisation domain 2/caspase recruitment domain 15) gene, the aetiology is still unclear. Thus, the hunt for disease-initiating factors such as defects in the mucosal barrier or pathogenic microorganisms is ongoing. By contrast, the immunopathogenesis in IBDs is better understood. The identification of cytokines that are involved in T cell and monocyte signalling led to specific therapeutic concepts. Recent data have clearly shown that the most powerf…

Programmed cell deathNecrosisCell Survivalmedicine.medical_treatmentT cellT-LymphocytesApoptosisImmune systemCrohn DiseaseNOD2AzathioprinemedicineHumansIntestinal MucosaMesalamineImmunity Mucosalbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaAnti-Inflammatory Agents Non-SteroidalGastroenterologyRecent Advances in Basic ScienceInflammatory Bowel DiseasesInterleukin-12Immunosuppressive drugmedicine.anatomical_structureApoptosisImmunologyTumor necrosis factor alphamedicine.symptombusinessImmunosuppressive AgentsSignal TransductionGut
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Phospholipidosis and down-regulation of the PI3-K/PDK-1/Akt signalling pathway are vitamin E inhibitable events associated with 7-ketocholesterol-ind…

2007

International audience; Among the oxysterols accumulating in atherosclerotic plaque, 7-ketocholesterol (7KC) is a potent apoptotic inducer, which favours myelin figure formation and polar lipid accumulation. This investigation performed on U937 cells consisted in characterizing the myelin figure formation process; determining the effects of 7KC on the PI3-K/PDK-1/Akt signalling pathway; evaluating the activities of vitamin E (Vit-E) (α-tocopherol) on the formation of myelin figures and the PI3-K/PDK-1/Akt signalling pathway and assessing the effects of PI3-K inhibitors (LY-294002, 3-methyladenine) on the activity of Vit-E on cell death and polar lipid accumulation. The ultrastructural and b…

Programmed cell deathOxysterolEndocrinology Diabetes and MetabolismClinical BiochemistryDown-RegulationApoptosisPyrimidinones[SDV.BC]Life Sciences [q-bio]/Cellular BiologyProtein Serine-Threonine KinasesBiochemistryDephosphorylationPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionOxazinesHumansVitamin EKetocholesterolsMolecular BiologyProtein kinase BPhospholipids030304 developmental biologyPhospholipidosis0303 health sciencesNutrition and DieteticsPhosphoinositide 3-kinasebiologyChemistryPyruvate Dehydrogenase Acetyl-Transferring KinaseU937 CellsProtein phosphatase 2Cell biology030220 oncology & carcinogenesisbiology.proteinBenzimidazolesSignal transductionProto-Oncogene Proteins c-aktSignal TransductionThe Journal of Nutritional Biochemistry
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Calcium in plant defence‐signalling pathways

2006

In plant cells, the calcium ion is a ubiquitous intracellular second messenger involved in numerous signalling pathways. Variations in the cytosolic concentration of Ca2+ ([Ca2+]cyt) couple a large array of signals and responses. Here we concentrate on calcium signalling in plant defence responses, particularly on the generation of the calcium signal and downstream calcium-dependent events participating in the establishment of defence responses with special reference to calcium-binding proteins.

Programmed cell deathPhysiologyGene Expressionchemistry.chemical_elementPlant ScienceBiologyCalciumNitric OxideCytosolPhytoalexinsCalcium-binding proteinCalcium SignalingPhosphorylationPlant DiseasesPlant ProteinsCalcium signalingCell DeathPlant ExtractsTerpenesCalcium-Binding ProteinsPlantsPlant cellElicitorCytosolchemistryBiochemistryCalciumMitogen-Activated Protein KinasesSignal transductionReactive Oxygen SpeciesSesquiterpenesNew Phytologist
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