Search results for "APOPTOSI"

showing 10 items of 1846 documents

MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal break…

2000

The important regulatory proteins, c-Fos and p53 are induced by exposure of cells to a variety of DNA damaging agents. To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes. We show that c-Fos and p53 deficient fibroblasts are more sensitive than the corresponding wild-type cells as to the induction of chromosomal aberrations and apoptosis. Double knockout fibroblasts lacking both c-Fos and p53 are viable an…

Alkylating AgentsUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisDrug ResistanceMutagenesis (molecular biology technique)ApoptosisBiologyRadiation ToleranceCell LineMicechemistry.chemical_compoundGeneticsAnimalsMolecular BiologyGene knockoutChromosome AberrationsMice KnockoutGenes fosFibroblastsCell cycleGenes p53Molecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Mucosal immunoregulation: transcription factors as possible therapeutic targets.

2005

Much progress has been recently made with regard to our understanding of the mucosal immune system in health and disease. In particular, it has been shown that uncontrolled mucosal immune responses driven by lymphocytes or non-lymphoid cells may lead to immunological diseases such as allergy, hypersensitivity and inflammation. Thus, a more detailed understanding of mucosal immune regulation and decision making at mucosal surfaces is essential for a better understanding of mucosal immune responses in health and disease. Antigen presenting cells and T lymphocytes play a key role in controlling mucosal immune responses. To deal with this key task, T helper cells differentiate into functionally…

AllergyImmunologyInflammationApoptosisSuppressor of Cytokine Signaling ProteinsAllergic inflammationPathogenesisImmune systemImmunitymedicineHypersensitivityImmunology and AllergyAnimalsHumansIL-2 receptorMast CellsAntigen-presenting cellGlucocorticoidsImmunity MucosalPharmacologybusiness.industrymedicine.diseaseInflammatory Bowel DiseasesAsthmaIntestinesSuppressor of Cytokine Signaling 3 ProteinImmunologyCytokinesmedicine.symptombusinessTranscription FactorsCurrent drug targets. Inflammation and allergy
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T cell killing by tolerogenic dendritic cells protects mice from allergy.

2011

It is well established that allergy development can be prevented by repeated low-dose exposure to contact allergens. Exactly which immune mechanisms are responsible for this so-called low zone tolerance (LZT) is not clear, although CD8⁺ suppressor T cells are known to have a role. Here, we show that TNF released by tolerogenic CD11⁺CD8⁺ DCs located in skin-draining lymph nodes is required and sufficient for development of tolerance to contact allergens in mice. DC-derived TNF protected mice from contact allergy by inducing apoptosis in allergen-specific effector CD8⁺ T cells via TNF receptor 2 but did not contribute to the generation and function of the regulatory T cells associated with LZ…

AllergyT cellApoptosisBiologyCD8-Positive T-LymphocytesDermatitis Contactlaw.inventionImmune toleranceMicelawmedicineHypersensitivityImmune ToleranceAnimalsReceptors Tumor Necrosis Factor Type IIReceptorMice KnockoutEffectorTumor Necrosis Factor-alphaGeneral MedicineDendritic CellsAllergensmedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologySuppressorTumor necrosis factor alphaThe Journal of clinical investigation
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Depletion of Alloreactive Donor T Lymphocytes by CD95-Mediated Activation-Induced Cell Death Retains Antileukemic, Antiviral, and Immunoregulatory T …

2007

In allogeneic hematopoietic stem cell transplantation (AHSCT) graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) effect are closely but not invariably linked. Thus, harnessing donor lymphocyte mediated GVL immunity and separating it from GVHD is of particular interest. Based on results obtained in murine models we have explored the CD95-mediated activation-induced cell death (AICD) strategy to selectively deplete alloreactivity in human donor T lymphocytes in vitro. Following stimulation of CD3(+) T cells isolated from HLA-A* 0201-positive donors with HLA or minor histocompatibility antigen mismatched hematopoietic or nonhematopoietic cells in the presence of agonistic anti-CD…

AllodepletionLymphocyteApoptosisGraft vs Leukemia EffectHuman leukocyte antigenBiologyEpitopeLymphocyte DepletionImmune systemCell Line TumorMinor histocompatibility antigenmedicineCytotoxic T cellHumansTransplantation Homologousfas ReceptorTransplantationHematopoietic Stem Cell TransplantationFOXP3Hematologymedicine.anatomical_structureLymphocyte TransfusionImmunologyT cell depletionLymphocyte graft engineeringCD8Biology of Blood and Marrow Transplantation
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Selective erasure of a fear memory

2009

International audience; Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element-binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning b…

AmnesiaApoptosisMice TransgenicCREBAmygdalaMice03 medical and health sciences0302 clinical medicineMemoryConditioning PsychologicalmedicineAnimalsMemory disorderCyclic AMP Response Element-Binding ProteinNeuronal memory allocation030304 developmental biologyMemory consolidation0303 health sciencesMultidisciplinarybiologyCREBMemoriaFearmedicine.diseaseAmygdalamedicine.anatomical_structurenervous systemMental Recallbiology.proteinMemory traceMemory consolidation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AmnesiaNeuronPavlovian conditioningmedicine.symptomNeuroscience030217 neurology & neurosurgeryScience
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Induction of apoptosis in human retinoblastoma cells by topoisomerase inhibitors

1998

PURPOSE:To examine the apoptotic effect induced in human retinoblastoma Y79 cells by camptothecin, etoposide, and amsacrine, to examine the effect of these drugs on the expression of many apoptosis-related modulators, and to test the antiapoptotic effect exerted by insulin-like growth factor-I (IGF-I). METHODS:Morphologic features of apoptosis were demonstrated using acridine orange- ethidium bromide staining and electron microscopy. DNA fragmentation was determined by means of an in situ cell detection procedure (TdT-dUTP terminal nick-end labeling [TUNEL]) or by electrophoresis on agarose gels and was quantified by enzyme-linked immunosorbent assay. The expression of apoptosis-related mod…

AmsacrineCyclin-Dependent Kinase Inhibitor p21topoisomeraseCell SurvivalRetinal NeoplasmsRetinoblastomaApoptosisDNA NeoplasmInsulin-Like Growth Factor Binding Protein 3DNA Topoisomerases Type IProto-Oncogene Proteins c-bcl-2CyclinsProto-Oncogene ProteinsDactinomycinTumor Cells CulturedHumansCamptothecinCycloheximideEnzyme InhibitorsTopoisomerase I InhibitorsTumor Suppressor Protein p53DNA DamageEtoposidebcl-2-Associated X Protein
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Apoptotic effects of different drugs on cultured retinoblastoma Y79 cells

1998

This paper deals with the apoptotic effect exerted in human retinoblastoma Y79 cells by a number of compounds. A remarkable effect was observed after treatment with DNA-damaging agents, such as camptothecin, etoposide, cisplatin and carboplatin; camptothecin was found to be the most efficacious. Treatment with these compounds induced the appearance of morphological features of apoptosis in the cells together with the distinct fragmentation of DNA, as shown by agarose gel electrophoresis. These effects were also accompanied by a remarkable increase in the level of p53. Many other compounds, which are not DNA-damaging agents, induced the morphological features of apoptosis but none of them we…

AmsacrinePaclitaxelDNA damageAntineoplastic AgentsApoptosisSuraminDNA ladderingBiologyretinoblastomaCarboplatinchemistry.chemical_compoundTumor Cells CulturedmedicineHumansFragmentation (cell biology)EtoposideCisplatinSodium butyrateGeneral MedicineAntineoplastic Agents PhytogenicMolecular biologyButyrateschemistryApoptosisAgarose gel electrophoresisImmunologyButyric AcidCamptothecinCisplatinDrug Screening Assays AntitumorCamptothecinDNA Damagemedicine.drug
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The sea urchin embryo: a model to study Alzheimer's beta amyloid induced toxicity.

2009

Abstract Alzheimer’s disease (AD) is the most common form of dementia. The cause of AD is closely related to the accumulation of amyloid beta peptide in the neuritic plaques. The use of animal model systems represents a good strategy to elucidate the molecular mechanism behind the development of this pathology. Here we use the Paracentrotus lividus embryo to identify molecules and pathways that can be involved in the degenerative process. As a first step, we identified the presence of an antigen related to the human APP, called Pl APP. This antigen, after gastrula stage, is processed producing a polypeptide of about 10 kDa. By immunohistochemistry we localized the Pl APP antigen in some ser…

AmyloidAmyloid betaBiophysicsApoptosisBiochemistryNervous SystemParacentrotus lividusAlzheimer Diseasebiology.animalAnimalsHumansSenile plaquesAntigensMolecular BiologySea urchinCaspaseTUNEL assayAmyloid beta-Peptidesbiologybiology.organism_classificationPeptide FragmentsRecombinant ProteinsCell biologyBiochemistryApoptosisCaspasesModels Animalbiology.proteinParacentrotusParacentrotus lividusAmyloid-betaOligomers Fibrillar aggregatesApoptosisAnimal modelArchives of biochemistry and biophysics
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Concanavalin A aggregation and toxicity on cell cultures

2009

A number of neurodegenerative diseases are known to involve protein aggregation. Common mechanisms and structural properties of amyloids are thought to be involved in aggregation-related cytotoxicity. In this context we propose an experimental study on Concanavalin A (Con A) aggregation and use it as a model to study the relationship between cell toxicity and aggregation processes. Depending on solution conditions, Con A aggregation has been monitored by static and dynamic light scattering, Thioflavin T emission, and FTIR absorption. The morphology of different aggregate species was verified by means of Atomic Force Microscopy and Confocal Microscopy. During the aggregation pathway the nati…

AmyloidCell SurvivalBiophysicsApoptosisContext (language use)Protein aggregationMicroscopy Atomic ForceFibrilBiochemistryAnalytical Chemistrychemistry.chemical_compoundProtein structureCell Line TumorSpectroscopy Fourier Transform InfraredConcanavalin AExtracellularHumansProtein Structure QuaternaryCytotoxicityMolecular BiologyNeuronsbiologyChemistryBiochemistryConcanavalin Abiology.proteinThioflavinProtein aggregation Amyloids Citotoxicity Oligomers
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