Search results for "mutation."

showing 10 items of 2808 documents

Isolation and characterization of Saccharomyces cerevisiae mutants resistant to aculeacin A

1991

Aculeacin A is a lipopeptide that inhibits beta-glucan synthesis in yeasts. A number of Saccharomyces cerevisiae mutants resistant to this antibiotic were isolated, and four loci (ACR1, ACR2, ACR3, and ACR4) whose products are involved in the sensitivity to aculeacin A of yeast cells were defined. Mutants containing mutations in the four loci were also resistant to echinocandin B, another member of this lipopeptide family of antibiotics. In contrast, acr1, acr3, and acr4 mutants were resistant to papulacandin B (an antibiotic containing a disaccharide linked to two fatty acid chains that also inhibits beta-glucan synthesis), but acr2 mutants were susceptible to this antibiotic. This result …

Antifungal AgentsLlevat de cervesaGenotypeMutantSaccharomyces cerevisiaePapulacandin BSaccharomyces cerevisiaemedicine.disease_causePeptides CyclicMicrobiologyFungal ProteinsEchinocandinschemistry.chemical_compoundCell WallEchinocandin BmedicinePharmacology (medical)PharmacologyFungal proteinMutationbiologyMutagenicity TestsMembrane ProteinsLipopeptideAminoglicòsidbiology.organism_classificationYeastAnti-Bacterial AgentsAminoglucòsidsAminoglycosidesInfectious DiseaseschemistryBiochemistryGlucosyltransferasesMutationSchizosaccharomyces pombe ProteinsPeptidesResearch Article
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Dosage-dependent roles of the Cwt1 transcription factor for cell wall architecture, morphogenesis, drug sensitivity and virulence in Candida albicans.

2009

The Cwt1 transcription factor is involved in cell wall architecture of the human fungal pathogen Candida albicans. We demonstrate here that deficiency of Cwt1 leads to decreased β1,6-glucan in the cell wall, while mannoproteins are increased in the cell wall of exponentially growing cells and are released into the medium of stationary phase cells. Hyphal morphogenesis of cwt1 mutants is reduced on the surfaces of some inducing media. Unexpectedly, the CWT1/cwt1 heterozygous strains shows some stronger in vitro phenotypes compared to the homozygous mutant. The heterozygous but not the homozygous strain is also strongly impaired for its virulence in a mouse model of systemic infection. We sug…

Antifungal AgentsMutantMorphogenesisGene DosageHyphaeVirulenceBioengineeringApplied Microbiology and BiotechnologyBiochemistryMicrobiologyCell wallFungal ProteinsMiceCell WallDrug Resistance FungalGene Expression Regulation FungalCandida albicansGeneticsMorphogenesisAnimalsHumansCandida albicansDNA FungalTranscription factorOligonucleotide Array Sequence AnalysisMembrane GlycoproteinsbiologyVirulenceHomozygoteCandidiasisbiology.organism_classificationPhenotypeCorpus albicansMutationBiotechnologyTranscription FactorsYeast (Chichester, England)
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Missense mutations in the fas gene resulting in autoimmune lymphoproliferative syndrome: A molecular and immunological analysis

1997

AbstractProgrammed cell death (or apoptosis) is a physiological process essential to the normal development and homeostatic maintenance of the immune system. The Fas/Apo-1 receptor plays a crucial role in the regulation of apoptosis, as demonstrated by lymphoproliferation in MRL-lpr/lpr mice and by the recently described autoimmune lymphoproliferative syndrome (ALPS) in humans, both of which are due to mutations in the Fas gene. We describe a novel family with ALPS in which three affected siblings carry two distinct missense mutations on both the Fas gene alleles and show lack of Fas-induced apoptosis. The children share common clinical features including splenomegaly and lymphadenopathy, b…

Antigens Differentiation T-LymphocyteMaleAdolescentT-LymphocytesCD3ImmunologyLymphoproliferative disordersBiologyLymphocyte ActivationAutoimmune DiseaseBiochemistryFas ligandImmunophenotypingImmune systemPedigree; Antigens Differentiation T-Lymphocyte; Solubility; Apoptosis; Autoimmune Diseases; Humans; Antigens CD95; Child; Lymphocytes; Child Preschool; Lymphocyte Activation; Syndrome; Lymphoproliferative Disorders; Adolescent; Mutation; Immunophenotyping; Male; Biological Markers; T-LymphocytesmedicineChildAutoimmune diseaseApoptosiSyndromeCell BiologyHematologymedicine.diseaseFas receptorPedigreeAntigens CD95SolubilityApoptosisChild PreschoolLymphoproliferative DisorderAutoimmune lymphoproliferative syndromeMutationBiological MarkerImmunologybiology.proteinLymphocyteHuman
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Role of the virulence plasmid pR99 and the metalloprotease Vvp in resistance of Vibrio vulnificus serovar E to eel innate immunity

2007

Vibrio vulnificus biotype 2 serovar E (VSE) is a bacterial pathogen that produces a haemorrhagic septicaemia called vibriosis in eels. Its ability to grow in blood is conferred by a recently described virulence plasmid [Lee CT, Amaro C, Wu KM, Valiente E, Chang YF, Tsai SF, et al. A common virulence plasmid in biotype 2 Vibrio vulnificus and its dissemination aided by a conjugal plasmid. Journal of Bacteriology, submitted for publication.]. In this study, we analyzed the role of this plasmid together with the role played by the metalloprotease (Vvp) in the interaction between bacteria and eel innate immunity. To this end, we compared and statistically analyzed the differences in resistance …

Antimicrobial peptidesVirulenceMicrobial Sensitivity TestsVibrio vulnificusAquatic ScienceMicrobiologyPlasmidAnti-Infective AgentsBacterial ProteinsPhagocytosisBacteriologyAnimalsEnvironmental ChemistryImmunity MucosalVibrio vulnificusPathogenAntigens BacterialPhagocytesInnate immune systembiologyComplement Fixation TestsTransferrinMetalloendopeptidasesGeneral MedicineAnguillabiology.organism_classificationAntibodies BacterialVirologyImmunity InnateAntigens SurfaceMutationAlternative complement pathwayMuramidaseAntimicrobial Cationic PeptidesPlasmidsFish & Shellfish Immunology
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Nitic oxide promotes strong cytotoxicity of phenolic compounds against escherichia coli. The influence of antioxidant defenses

2003

[EN] The induction of mutagenic and cytotoxic effects by simple phenolics, including catechol (CAT), 3,4dihydroxyphenylacetic acid (DOPAC), hydroquinone (HQ), and 2,5-dihydroxyphenylacetic (homogentisic) acid (HGA), appears to occur through an oxidative mechanism based on the ability of these compounds to undergo autoxidation, leading to quinone formation with the production of reactive oxygen species. This is supported by the detection of such adverse effects in plate assays using Escherichia coli tester strains deficient in the OxyR function, but not in OxyR(+) strains. The OxyR protein is a redox-sensitive regulator of genes encoding antioxidant enzymes including catalase and alkyl hydro…

AntioxidantUltraviolet Raysmedicine.medical_treatmentCatecholsOxidative toxicityFree radicalsOxidative phosphorylationNitric OxideBiochemistryAntioxidantschemistry.chemical_compoundCaffeic AcidsQUIMICA ORGANICASuperoxidesPhysiology (medical)medicineEscherichia coliBIOQUIMICA Y BIOLOGIA MOLECULARHydrogen peroxidechemistry.chemical_classificationMelaninsReactive oxygen speciesbiologyHydroquinoneAutoxidationDose-Response Relationship DrugPhenolEscherichia coli ProteinsNitric oxideHydrogen PeroxideCatalaseFlow CytometryQuinoneHydroquinonesDNA-Binding ProteinsOxygenRepressor ProteinschemistryBiochemistryCatalaseMutationbiology.proteinQuinoneOxyROxidation-ReductionDNA DamageMutagensTranscription Factors
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Ursolic acid ameliorates stress and reactive oxygen species in C. elegans knockout mutants by the dopamine Dop1 and Dop3 receptors.

2020

Abstract Background Depression and stress-related disorders are leading causes of death worldwide. Standard treatments elevating serotonin or noradrenaline levels are not sufficiently effective and cause adverse side effects. A connection between dopamine pathways and stress-related disorders has been suggested. Compounds derived from herbal medicine could be a promising alternative. We examined the neuroprotective effects of ursolic acid (UA) by focusing on dopamine signalling. Methods Trolox equivalent capacity assay was used to determine the antioxidant activities of UA in vitro. C. elegans N2 wildtype and dopamine receptor-knockout mutants (dop-1-deficient RB665 and dop-3-deficient LX70…

Antioxidantmedicine.medical_treatmentDopamineLongevityPharmaceutical SciencePharmacologyNeuroprotectionAntioxidants03 medical and health scienceschemistry.chemical_compoundGene Knockout Techniques0302 clinical medicineDopamineStress PhysiologicalDrug DiscoverymedicineAnimalsHumansReceptorCaenorhabditis elegansCaenorhabditis elegans Proteins030304 developmental biologyPharmacologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesChemistryReceptors Dopamine D2Receptors Dopamine D1Receptors Dopamine D3TriterpenesMolecular Docking SimulationComplementary and alternative medicineDopamine receptor030220 oncology & carcinogenesisMutationMolecular MedicineSerotoninTroloxReactive Oxygen Speciesmedicine.drugSignal TransductionPhytomedicine : international journal of phytotherapy and phytopharmacology
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The triterpenoid ursolic acid ameliorates stress in Caenorhabditis elegans by affecting the depression-associated genes skn-1 and prdx2.

2021

Abstract Introduction Depression is one of the leading causes of death worldwide. Lower antioxidant concentrations and increased oxidative stress levels contribute to the development of depression. Effective and tolerable medications are urgently needed. Nrf2 and PRDX2 are promising targets in the treatment of oxidative stress and, therefore, promising for the development of novel antidepressants. Ursolic acid (UA), a natural triterpenoid found in various plants is known to exert neuroprotective and antioxidant effects. Skn-1 (which corresponds to human Nrf2) and prdx2 deficient mutants of the nematode Caenorhabditis elegans are suitable models to study the effect of UA on these targets. Ad…

Antioxidantmedicine.medical_treatmentPharmaceutical SciencePharmacologymedicine.disease_causeProtective AgentsNeuroprotectionAntioxidants03 medical and health scienceschemistry.chemical_compound0302 clinical medicineUrsolic acidStress PhysiologicalDrug DiscoveryAdaptogenmedicineAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCaenorhabditis elegans030304 developmental biologyPharmacologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesbiologyDepressionPeroxiredoxinsbiology.organism_classificationAntidepressive AgentsTriterpenesDNA-Binding ProteinsMolecular Docking SimulationOxidative StressComplementary and alternative medicinechemistryGene Expression Regulation030220 oncology & carcinogenesisMutationMolecular MedicineReactive Oxygen SpeciesJugloneOxidative stressTranscription FactorsPhytomedicine : international journal of phytotherapy and phytopharmacology
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DctA- and Dcu-independent transport of succinate in Escherichia coli : contribution of diffusion and of alternative carriers

2001

Quintuple mutants of Escherichia coli deficient in the C4-dicarboxylate carriers of aerobic and anaerobic metabolism (DctA, DcuA, DcuB, DcuC, and the DcuC homolog DcuD, or the citrate/succinate antiporter CitT) showed only poor growth on succinate (or other C4-dicarboxylates) under oxic conditions. At acidic pH (pH 6) the mutants regained aerobic growth on succinate, but not on fumarate. Succinate uptake by the mutants could not be saturated at physiological succinate concentrations (≤5 mM), in contrast to the wild-type, which had a K m for succinate of 50 µM and a V max of 35 U/g dry weight at pH 6. At high substrate concentrations, the mutants showed transport activities (32 U/g dry weigh…

AntiporterMutantSuccinic AcidBiologymedicine.disease_causeBiochemistryMicrobiologyBacterial ProteinsFumaratesNitrilesEscherichia coliGeneticsmedicineMolecular BiologyEscherichia coliDicarboxylic Acid TransportersUncoupling AgentsEscherichia coli ProteinsBiological TransportGeneral MedicineMetabolismHydrogen-Ion ConcentrationFumarate reductasebiology.organism_classificationEnterobacteriaceaeBiochemistryMutationFermentationEffluxCarrier ProteinsArchives of Microbiology
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Association between HFE mutations and acute myocardial infarction: a study in patients from Northern and Southern Italy.

2003

There is interest in the role of iron in age-related diseases such as atherosclerosis. Tissue iron deposition could be harmful, because Fe(2+) can react with H(2)O(2) to form OH(-) radicals and Fe(2+) can react with O(2) to form reactive oxygen species. Free radicals react with cell membranes and cell organelles and could lead to the development of atherosclerosis by initiating lipid peroxidation. Hereditary hemochromatosis provides an opportunity for studying the effects of iron on cardiovascular disease. Some studies have shown that individuals who carried HFE mutations may be at greater risk of developing coronary heart disease than those without the mutations. In contrast, a large numbe…

Apolipoprotein EAdultMalePathologymedicine.medical_specialtySettore MED/09 - Medicina InternaGenotypePopulationApolipoprotein E4Mutation MissenseMyocardial InfarctionPhysiologyApolipoproteins EGene FrequencyGenotypeMedicineHumansAge FactorMyocardial infarctionAlleleeducationHemochromatosis ProteinMembrane ProteinMolecular BiologyAllele frequencyAgedAged 80 and overeducation.field_of_studybusiness.industryHistocompatibility Antigens Class ICase-control studyAge FactorsMembrane ProteinsCell BiologyHematologyMiddle Agedmedicine.diseaseItalyHereditary hemochromatosisCase-Control StudiesMolecular MedicineFemaleCase-Control StudiebusinessHumanBlood cells, moleculesdiseases
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Identification Of P.Leu167Del Apoe Gene Mutation By Next Generation Sequencing In A Large Hypercholesterolemic Family

2019

Apolipoprotein EGeneticsSettore MED/09 - Medicina InternaNEXT GENERATION SEQUENCING HYPERCHOLESTEROLEMIAMutation (genetic algorithm)APOE GENEIdentification (biology)BiologyCardiology and Cardiovascular MedicineMUTATIONDNA sequencingAtherosclerosis
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