Search results for "mutation."

showing 10 items of 2808 documents

Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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Cannabinoid receptor 1 deficiency in a mouse model of Alzheimer's disease leads to enhanced cognitive impairment despite of a reduction in amyloid de…

2012

Alzheimer's disease (AD) is characterized by amyloid-beta deposition in amyloid plaques, neurofibrillary tangles, inflammation, neuronal loss, and cognitive deficits. Cannabinoids display neuromodulatory and neuroprotective effects and affect memory acquisition. Here, we studied the impact of cannabinoid receptor type 1 (CB1) deficiency on the development of AD pathology by breeding amyloid precursor protein (APP) Swedish mutant mice (APP23), an AD animal model, with CB1-deficient mice. In addition to the lower body weight of APP23/CB1(-/-) mice, most of these mice died at an age before typical AD-associated changes become apparent. The surviving mice showed a reduced amount of APP and its …

Agingmedicine.medical_specialtyPathologyCannabinoid receptormedicine.medical_treatmentMutantMice TransgenicInflammationDiseaseNeuroprotectionAmyloid beta-Protein PrecursorMiceReceptor Cannabinoid CB1Alzheimer DiseaseCell Line TumorInternal medicinemental disordersmedicineAmyloid precursor proteinAnimalsHumansMaze LearningCognitive impairmentAmyloid beta-Peptidesbiologybusiness.industryGeneral NeuroscienceBody WeightAge FactorsBrainPeptide FragmentsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinlipids (amino acids peptides and proteins)MicrogliaNeurology (clinical)CannabinoidGeriatrics and Gerontologymedicine.symptomCognition DisordersbusinessDevelopmental BiologyNeurobiology of Aging
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Na+ ions binding to the bradykinin B2 receptor suppress agonist-independent receptor activation.

1996

Control of the balance between receptor activation and inactivation is a prerequisite for seven transmembrane domain (7TM) receptor function. We asked for a mechanism to stabilize the inactive receptor conformation which prevents agonist-independent receptor activation. Na+ ions have reciprocal effects on agonist versus antagonist interaction with various 7TM receptors. To investigate the Na+ dependence of receptor activation we chose the bradykinin B2 receptor as a prototypic 7TM receptor. Decrease of the intracellular Na+ content from 40 mM to 10 mM of COS-1 cells transiently expressing rat B2 receptors activated the B2 receptor in the absence of agonist as shown by a 3-fold increase in t…

AgonistIntracellular FluidIntrinsic activityReceptor Bradykinin B2medicine.drug_classInositol PhosphatesBradykininIn Vitro TechniquesBradykininLigandsBiochemistryCell Linechemistry.chemical_compoundmedicineAnimalsHumansPoint MutationBradykinin receptorPhosphorylationReceptorG protein-coupled receptorReceptors BradykininSodiumRatschemistryCOS CellsBiophysicsMutagenesis Site-DirectedAlpha-4 beta-2 nicotinic receptorIntracellularBiochemistry
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Altered atypical coupling of γ-aminobutyrate type A receptor agonist and convulsant binding sites in subunit-deficient mouse lines

2001

We searched for subunit correlations for GABA(A) receptor-associated atypically GABA-insensitive [35S]TBPS binding. The homomeric beta3 subunit receptors could be excluded, as GABA-insensitive [35S]TBPS binding was present in beta3-/- mice. Localization of GABA-insensitive [35S]TBPS binding correlated best with those of delta, alpha4 and alpha6 subunit mRNAs. The amounts of GABA-insensitive [35S]TBPS binding components were increased in delta-/- mice, but dramatically reduced in alpha6-/- mice, suggesting a role for alpha6 but excluding delta subunits.

Agonistmedicine.medical_specialtymedicine.drug_classProtein subunitMolecular Sequence DataConvulsantsBiologySulfur Radioisotopesmedicine.disease_causeMiceRadioligand AssayCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsHomomericRNA MessengerBinding siteReceptorGABA AgonistsMolecular BiologyBrain ChemistryMice KnockoutMutationBinding SitesGABAA receptorBridged Bicyclo Compounds HeterocyclicReceptors GABA-AMolecular biologyEndocrinologynervous systemConvulsantMolecular Brain Research
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Finitary shadows of compact subgroups of $$S(\omega )$$

2020

AbstractLet LF be the lattice of all subgroups of the group $$SF(\omega )$$SF(ω) of all finitary permutations of the set of natural numbers. We consider subgroups of $$SF(\omega )$$SF(ω) of the form $$C\cap SF(\omega )$$C∩SF(ω), where C is a compact subgroup of the group of all permutations. In particular, we study their distribution among elements of LF. We measure this using natural relations of orthogonality and almost containedness. We also study complexity of the corresponding families of compact subgroups of $$S(\omega )$$S(ω).

Algebra and Number TheoryCompact groups of permutationsDistribution (number theory)Group (mathematics)010102 general mathematicsLattice (group)Almost containednessNatural number0102 computer and information sciences01 natural sciencesOmegaMeasure (mathematics)CombinatoricsOrthogonality010201 computation theory & mathematicsOrthogonality of finitary subgroupsFinitary0101 mathematicsMartin’s axiom.MathematicsAlgebra universalis
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L'eau et les territoires sahariens en Algérie, Mutations et enjeux

2007

International audience; Les rapports complexes et multiformes que les territoires entretiennent avec la question hydraulique prennent au Sahara une dimension toute particulière. Les mutations territoriales du XXe siècle qui l'ont caractérisé – urbanisation, accroissement démographique, intégration territorial... – ont remis en cause le fragile équilibre qui s'était institué depuis des siècles entre l'homme et son environnement. Ces mutations complexes ont engendré de nombreuses interrogations quant à la gestion actuelle et future de la question hydraulique au sein des territoires sahariens. Nous nous proposons ici de mettre en lumière quelques éléments permettant d'appréhender cette questio…

AlgérieMutations territorialesRessources hydrauliquesGestion territoriale[SHS.GEO] Humanities and Social Sciences/Geography[SHS.GEO]Humanities and Social Sciences/GeographySahara[ SHS.GEO ] Humanities and Social Sciences/Geography
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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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Interaction between filaggrin mutations and neonatal cat exposure in atopic dermatitis

2020

Atopic dermatitis (AD) is a prevalent inflammatory skin disease. Loss-of-function mutations in filaggrin gene (FLG) represent the strongest genetic risk factors for AD, being strongly associated with early disease onset and persistence into adulthood.1 The epidermis of individuals with mutations in FLG is fundamentally different from normal skin being characterized by increased penetration of allergens.2 Recent birth cohort studies showed a significant interaction between cat ownership at birth and mutations in FLG (R501X, 2282del4) on the development of early-onset AD.3 This finding was replicated for the 2282del4 FLG mutation in a Dutch cohort study, and extended to further associate with…

AllergyAllergyImmunologyFilaggrin ProteinsDermatitis Atopic03 medical and health sciences0302 clinical medicineCAT EXPOSUREIntermediate Filament ProteinsmedicineImmunology and AllergyAnimalsHumansGenetic Predisposition to Disease030304 developmental biologyRISK0303 health sciencesScience & TechnologyCATSbusiness.industryInfant NewbornAtopic dermatitismedicine.disease030228 respiratory system1107 ImmunologyMutation (genetic algorithm)ImmunologyMutationCatsbusinessLife Sciences & BiomedicineFilaggrinAllergy
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Antiretroviral genotypic resistance in plasma RNA and whole blood DNA in HIV-1 infected patients failing HAART

2008

The extent to which HIV-1 proviral DNA mutations cause clinically relevant antiretroviral resistance is still controversial. Paired plasma HIV-1 RNA and whole blood DNA were compared in patients failing HAART to investigate if the additional knowledge of archived mutations could improve the selection of potentially active drugs. Seventy-three HIV-1-infected patients with first/second HAART failure were studied before starting a new regimen based on RNA genotyping. Follow-up data after a 12-week therapy were available. DNA genotyping was retrospectively performed on stored whole blood samples and mutational profiles were compared to those from RNA. The mean number of IAS pol mutations was si…

Anti-HIV AgentsDNA Mutational AnalysisMolecular Sequence DataProviral DNAHIV InfectionsHAART failuremedicine.disease_causeDNA Mutational Analysichemistry.chemical_compoundHIV ProteaseProvirusesAntiretroviral Therapy Highly ActiveVirologyDrug Resistance ViralDNA Mutational AnalysismedicineHumansMulticenter Studies as TopicHIV InfectionTreatment FailureGenotypingRandomized Controlled Trials as TopicCOLD-PCRMutationPlasma RNAbiologyProviruseSequence Analysis RNAAnti-HIV AgentRNASequence Analysis DNAbiology.organism_classificationVirologyHIV Reverse TranscriptaseReverse transcriptaseAntiretroviral genotypic resistanceInfectious DiseaseschemistryDNA ViralMutationLentivirusImmunologyHIV-1RNA ViralDNAantiretroviral genotypic resistance; haart failure; hiv-1; plasma rna; proviral dnaHumanJournal of Medical Virology
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Glycoprotein molecules in the walls of Schizosaccharomyces pombe wild-type cells and a morphologically altered mutant resistant to papulacandin B

1990

SUMMARY: Schizosaccharomyces pombe cell walls contain two major glycoprotein species, I and II, with molecular masses of 2 x 106 and 5 x 105 Da respectively, as determined by gel filtration chromatography and PAGE. The ratio of sugar to protein is higher in species I than in species II. Much of the sugar in both glycoproteins (about 85% in wild-type cells) is O-linked to the peptide moiety. The morphological sph1 mutant is resistant to papulacandin B, and its cell wall contains less glycoprotein II (but not less glycoprotein I) than the parental wild-type strain, although glycoprotein II is still synthesized and released into the growth medium. Papulacandin B largely reverses the morphologi…

Antifungal AgentsHydrolasesMutantCarbohydratesDrug ResistancePapulacandin BBiologyCell morphologyMicrobiologyCell wallchemistry.chemical_compoundCell WallAcetylglucosaminidaseSchizosaccharomycesGlycoproteinsGel electrophoresischemistry.chemical_classificationWild typebiology.organism_classificationAnti-Bacterial AgentsCulture MediaMolecular WeightAminoglycosidesMannosyl-Glycoprotein Endo-beta-N-AcetylglucosaminidaseSolubilityBiochemistrychemistryMutationSchizosaccharomyces pombeChromatography GelGlycoproteinJournal of General Microbiology
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