Search results for "Suppressor"

showing 10 items of 532 documents

Efecto de supresión y mediación en el contexto de la intervención psicosocial: Diferencias, similitudes y ejemplos

2013

ResumenEl presente trabajo compara el efecto mediador y el supresor de una tercera variable. Ambos efectos parcelan la varianza de la variable dependiente (Y). La mediación es la reducción, tras introducir una tercera variable (Z) en el modelo, de la proporción de varianza explicada directamente por la variable independiente (X) en la variable criterio (Y) y la supresión es el incremento de la proporción de varianza explicada directamente por la independiente en la variable criterio, al incluir la tercera variable en el modelo. Se analizan las características y diferencias de cada efecto y se examina en qué situaciones se produce uno u otro. Cada situación, compuesta de tres variables corre…

Mediation (statistics)VariablesSocial Psychologymedia_common.quotation_subjectWelfare economicsContext (language use)Investigación psicosocialExplained variationSuppressor effectThird variablesVariable (computer science)Terceras variablesPsychosocial researchIntervención psicosocialDevelopmental and Educational PsychologyPsychosocial interventionSocial psychologyMediaciónSupresiónApplied PsychologyMathematicsmedia_commonMediator effectPsychosocial Intervention
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Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine

2006

Methylating drugs such as temozolomide (TMZ) are widely used in the treatment of brain tumours (malignant gliomas). The mechanism of TMZ-induced glioma cell death is unknown. Here, we show that malignant glioma cells undergo apoptosis following treatment with the methylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and TMZ. Cell death determined by colony formation and apoptosis following methylation is greatly stimulated by p53. Transfection experiments with O(6)-methylguanine-DNA methyltransferase (MGMT) and depletion of MGMT by O(6)-benzylguanine showed that, in gliomas, the apoptotic signal originates from O(6)-methylguanine (O(6)MeG) and that repair of O(6)MeG by MGMT prevent…

MethylnitronitrosoguanidineCancer ResearchProgrammed cell deathFas Ligand ProteinGuanineDNA repairFas-Associated Death Domain ProteinBlotting WesternApoptosisBiologymedicine.disease_causeO(6)-Methylguanine-DNA MethyltransferaseGliomaTemozolomideTumor Cells CulturedGeneticsmedicineHumansDNA Breaks Double-StrandedRNA Small InterferingAntineoplastic Agents AlkylatingneoplasmsMolecular BiologyTumor Stem Cell AssayCell ProliferationTemozolomideBrain NeoplasmsCell CycleGliomaCell cycleFlow CytometryFas receptormedicine.diseaseDacarbazineProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesCancer researchTumor Suppressor Protein p53CarcinogenesisDNA Damagemedicine.drugOncogene
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Apoptosis induced by MNNG in human TK6 lymphoblastoid cells is p53 and Fas/CD95/Apo-1 related.

2003

Agents inducing O(6)-methylguanine (O(6)MeG) in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), are not only highly mutagenic and carcinogenic but also cytotoxic because of the induction of apoptosis. In CHO fibroblasts, apoptosis triggered by O(6)MeG requires cell proliferation and MutSalpha-dependent mismatch repair and is related to the induction of DNA double-strand breaks (DSBs). Furthermore, it is mediated by Bcl-2 degradation and does not require p53 for which the cells were mutated [Cancer Res. 60 (2000) 5815]. Here we studied cytotoxicity and apoptosis induced by MNNG in a pair of human lymphoblastoid cells expressing wild-type p53 (TK6) and mutant p53 (WTK1) and show tha…

MethylnitronitrosoguanidineCell SurvivalHealth Toxicology and MutagenesisApoptosisCHO CellsBiologyCell LineBcl-2-associated X proteinCricetinaeProto-Oncogene ProteinsGeneticsCytotoxic T cellAnimalsHumansfas Receptorbcl-2-Associated X ProteinMitogen-Activated Protein Kinase 1Cell growthLymphoblastFas receptorMolecular biologyKineticsCell killingProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisbiology.proteinTumor Suppressor Protein p53DNA DamageMutation research
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O6-methylguanine DNA methyltransferase and p53 status predict temozolomide sensitivity in human malignant glioma cells

2006

Temozolomide (TMZ) is a methylating agent which prolongs survival when administered during and after radiotherapy in the first-line treatment of glioblastoma and which also has significant activity in recurrent disease. O6-methylguanine DNA methyltransferase (MGMT) is a DNA repair enzyme attributed a role in cancer cell resistance to O6-alkylating agent-based chemotherapy. Using a panel of 12 human glioma cell lines, we here defined the sensitivity to TMZ in acute cytotoxicity and clonogenic survival assays in relation to MGMT, mismatch repair and p53 status and its modulation by dexamethasone, irradiation and BCL-X(L). We found that the levels of MGMT expression were a major predictor of T…

MethyltransferaseCell Survivalbcl-X ProteinBcl-xLTransfectionBiochemistryDNA methyltransferaseO(6)-Methylguanine-DNA MethyltransferaseCellular and Molecular NeuroscienceCell Line TumorGliomaTemozolomidemedicineHumansCytotoxicityAntineoplastic Agents AlkylatingneoplasmsTumor Stem Cell AssayTemozolomideCell DeathbiologyGliomamedicine.diseaseCarmustinedigestive system diseasesDacarbazineEnzyme ActivationGene Expression Regulation NeoplasticCancer cellbiology.proteinCancer researchDNA mismatch repairTumor Suppressor Protein p53medicine.drugJournal of Neurochemistry
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Genes, Ageing and Longevity in Humans: Problems, Advantages and Perspectives.

2006

Many epidemiological data indicate the presence of a strong familial component of longevity that is largely determined by genetics, and a number of possible associations between longevity and allelic variants of genes have been described. A breakthrough strategy to get insight into the genetics of longevity is the study of centenarians, the best example of successful ageing. We review the main results regarding nuclear genes as well as the mitochondrial genome, focusing on the investigations performed on Italian centenarians, compared to those from other countries. These studies produced interesting results on many putative "longevity genes". Nevertheless, many discrepancies are reported, l…

Mitochondrial DNAAgingProteasome Endopeptidase ComplexNuclear geneApolipoproteins geneticsInsulin-Like Growth Factor I geneticsmedia_common.quotation_subjectApolipoprotein E4LongevityBiologyGenetic polymorphisms ageing longevity centenarians association studies mitochondrial DNABiochemistryDNA MitochondrialInflammation geneticsApolipoprotein E4 geneticsCytokines geneticsAnimalsHumansAlleleInsulin-Like Growth Factor ILongevity geneticsGenemedia_commonGenetic associationGeneticsAged 80 and overInflammationPolymorphism GeneticAryldialkylphosphataseSuperoxide DismutaseLongevitySuperoxide Dismutase geneticsGeneral MedicineClusterin geneticsPoly(ADP-ribose) Polymerases geneticsAging geneticsApolipoproteinsClusterinTumor Suppressor Protein p53 geneticsGenesEvolutionary biologyTraitCytokinesGene poolPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53Aryldialkylphosphatase geneticsDNA Mitochondrial geneticsProteasome Endopeptidase Complex physiology
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Targeting Cavity-Creating p53 Cancer Mutations with Small-Molecule Stabilizers: the Y220X Paradigm

2020

We have previously shown that the thermolabile, cavity-creating p53 cancer mutant Y220C can be reactivated by small-molecule stabilizers. In our ongoing efforts to unearth druggable variants of the p53 mutome, we have now analyzed the effects of other cancer-associated mutations at codon 220 on the structure, stability, and dynamics of the p53 DNA-binding domain (DBD). We found that the oncogenic Y220H, Y220N, and Y220S mutations are also highly destabilizing, suggesting that they are largely unfolded under physiological conditions. A high-resolution crystal structure of the Y220S mutant DBD revealed a mutation-induced surface crevice similar to that of Y220C, whereas the corresponding pock…

Models Molecular0301 basic medicineMutantCarbazolesDruggabilityCancer therapyAntineoplastic Agents01 natural sciencesBiochemistryDNA-binding proteinStructure-Activity Relationship03 medical and health sciencesProtein DomainsHumansCancer mutationsThermolabileQD0415Protein Stability010405 organic chemistryChemistryArticlesGeneral MedicineSmall moleculeAffinities0104 chemical sciences030104 developmental biologyGene Expression RegulationMutationBiophysicsMolecular MedicineMutant ProteinsDrug Screening Assays AntitumorTumor Suppressor Protein p53CrystallizationProtein BindingQD0241ACS Chemical Biology
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Monoclonal antibody to a DNA-binding domain of p53 mimics charge structure of DNA: anti-idiotypes to the anti-p53 antibody are anti-DNA

2004

Antibodies to DNA are important markers of various autoimmune diseases and can be pathogenic; however, their generation is not understood. We previously reported that anti-DNA antibodies could be induced in mice by idiotypic immunization to PAb-421, an antibody to a DNA-binding domain of p53. We now report that two monoclonal antibodies of moderate affinity (K(D) asymptotically equal to 10(-7)), raised from PAb-421-immunized mice, specifically recognized both PAb-421 and DNA. These antibodies feature multiple arginine residues in the antigen-binding site, a unique characteristic of disease-associated anti-DNA antibodies; nevertheless, these anti-DNA antibodies show specific complementarity …

Models Molecularmedicine.drug_classMolecular Sequence DataImmunologyOligonucleotidesMonoclonal antibodyMicechemistry.chemical_compoundImmunoglobulin IdiotypesmedicineAnimalsImmunology and AllergyA-DNAAmino Acid SequencebiologyOligonucleotideAntibodies MonoclonalDNAMolecular biologyPrimary and secondary antibodiesProtein Structure TertiarychemistryMonoclonalbiology.proteinTumor Suppressor Protein p53AntibodyDNAProtein BindingBinding domainEuropean Journal of Immunology
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Comparative genomic sequencing reveals a strikingly similar architecture of a conserved syntenic region on human chromosome 11p15.3 (including gene S…

2001

Comparative genomics is a superior way to identify phylogenetically conserved features like genes or regions involved in gene regulation. The comparison of extended orthologous chromosomal regions should also reveal other characteristic traits essential for chromosome or gene function. In the present study we have sequenced and compared a region of conserved synteny from human chromosome 11p15.3 and mouse chromosome 7. In human, this region is known to contain several genes involved in the development of various disorders like Beckwith-Wiedemann overgrowth syndrome and other tumor diseases. Furthermore, in the neighboring chromosome region 11p15.5 extensive imprinting of genes has been repo…

Molecular Sequence DataeducationGenomicsBiologyChromosomesContig MappingMiceGene OrderGeneticsAnimalsHumansCloning MolecularMolecular BiologyGeneConserved SequenceGenetics (clinical)Repetitive Sequences Nucleic AcidSyntenyRegulation of gene expressionChromosome 7 (human)Comparative genomicsGeneticsChromosomes Human Pair 11Tumor Suppressor ProteinsGenomic sequencingChromosomeSequence Analysis DNAGC Rich SequenceDNA-Binding ProteinsCytogenetic and Genome Research
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IL12A, MPHOSPH9/CDK2AP1 and RGS1 are novel multiple sclerosis susceptibility loci

2010

A recent meta-analysis identified seven single-nucleotide polymorphisms (SNPs) with suggestive evidence of association with multiple sclerosis (MS). We report an analysis of these polymorphisms in a replication study that includes 8,085 cases and 7,777 controls. A meta-analysis across the replication collections and a joint analysis with the discovery data set were performed. The possible functional consequences of the validated susceptibility loci were explored using RNA expression data. For all of the tested SNPs, the effect observed in the replication phase involved the same allele and the same direction of effect observed in the discovery phase. Three loci exceeded genome-wide significa…

Multiple SclerosisImmunologyGenome-wide association studyLocus (genetics)Single-nucleotide polymorphismBiologyPolymorphism Single NucleotideArticleInterleukin-12 Subunit p35Cell Line03 medical and health sciences0302 clinical medicineIL12AGeneticsmedicineHumansGenetic Predisposition to DiseaseAlleleGenetics (clinical)Cell Proliferation030304 developmental biologyGenetics0303 health sciencesTumor Suppressor ProteinsMultiple sclerosisCell cyclemedicine.disease3. Good healthCeliac DiseaseCase-Control StudiesImmunologyExpression quantitative trait lociLeukocytes MononuclearRGS Proteins030217 neurology & neurosurgeryGenes & Immunity
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Anti-p53-directed immunotherapy of malignant disease

2004

Mutation and aberrant expression of the p53 tumour suppressor protein are the most frequent molecular alterations in human malignancy. Peptides derived from the p53 protein and presented by major histocompatibility complex molecules for T-cell recognition could serve as universal tumour-associated antigens for cancer immunotherapy. Because p53 normally functions as a ubiquitously expressed self-protein, controlling cell-cycle progression and apoptosis, it also represents a paradigm target molecule for tumour-reactive yet self-antigen-specific T cells. Tailoring p53-based cancer immunotherapy thus requires both interference with p53-specific self-tolerance and induction of the entire reperto…

MutationT-Lymphocytesmedicine.medical_treatmentT-cell receptorGenetic TherapyImmunotherapyBiologymedicine.disease_causeMajor histocompatibility complexCell therapyGenes T-Cell ReceptorCancer immunotherapyAntigenNeoplasmsmedicineCancer researchbiology.proteinHumansMolecular MedicineImmunotherapyTumor Suppressor Protein p53ReceptorMolecular BiologyExpert Reviews in Molecular Medicine
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