Search results for "DAS"

showing 10 items of 4164 documents

Differential expression of SUC genes: A question of bases

1994

Non-coding nucleotide sequences located 5' upstream of the transcriptional start site play an essential role in gene expression as they contain binding sites for transcription and regulatory factors. The yeast SUC gene family is a useful model to study the influence that nucleotide exchanges within the promoter regions have on their expression, since (i) these genes, regulated by glucose repression, are differentially transcribed (invertase activity produced by distinct SUC genes may show variations of about 10-fold); and (ii) promoter sequences of SUC3, SUC4, SUC5 and SUC7 are more than 99% homologous, showing only six base exchanges among all of them. Comparison of these nucleotide exchan…

GeneticsGlycoside Hydrolasesbeta-FructofuranosidaseGenes FungalSaccharomyces cerevisiaeNucleic acid sequenceGenetic VariationSaccharomyces cerevisiaeBiologybiology.organism_classificationMicrobiologyInfectious DiseasesPlasmidTranscription (biology)Gene Expression Regulation FungalMultigene FamilyGene expressionGene familyBinding sitePromoter Regions GeneticGeneFEMS Microbiology Reviews
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The clinical spectrum of alpha-L-iduronidase deficiency.

1985

We present five patients with alpha-L-iduronidase deficiency who do not have the typical Hurler or Scheie phenotypes; they are compared to 28 similarly atypical cases from the literature. Phenotypic differences are pointed out and intrafamilial similarities stressed. Among the various possible explanations for this situation, the existence of genetic compounds seems acceptable for some of the cases, but others seem to be caused by different mutations. The elucidation of these alternative possibilities from recent biochemical research is discussed.

GeneticsMaleAutosomal recessive inheritanceα l iduronidaseAdolescentGlycoside HydrolasesMucopolysaccharidosisMucopolysaccharidosis IInfantBiologyMucopolysaccharidosesmedicine.diseasePhenotypeIduronidasePhenotypeChild PreschoolmedicineHumansFemaleChildGenetics (clinical)American journal of medical genetics
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Detection of three rare (G377S, T134P and 1451delAC), and two novel mutations (G195W and Rec[1263del55;1342G>C] in Spanish Gaucher disease patients

1999

To study glucocerebrosidase mutations causing Gaucher disease, we have screened 30 apparently unrelated patients for the presence of 7 previous described mutations. N370S (1226A>G) was the most common mutation (43%), followed by L444P (1448T>C) (23%). To identify the other unknown mutations, we screened regions of the glucocerebrosidase gene (GBA), by SSCP and sequencing. These analyses allowed identification of one novel G195W (700G>T), and two rare T134P (517A>C) and G377S (1246G>A) missense mutations. Mutation T134P (517A>C) was present in a type I patient, while G195W (700G>T), was encountered in two patients (types I, and III). The prevalence of mutation G377S (1246G>A), previously und…

GeneticsMutationPseudogeneSingle-strand conformation polymorphismBiologymedicine.disease_causeGeneticsmedicineHomologous chromosomeMissense mutationAlleleGlucocerebrosidaseGeneGenetics (clinical)Human Mutation
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TMPRSS4 is a type II transmembrane serine protease involved in cancer and viral infections.

2012

Abstract Proteolytic enzymes are involved in almost all biological processes reflecting their importance in health and disease. The human genome contains nearly 600 protease-encoding genes forming more than 2% of the total human proteome. The serine proteases, with about 180 members, built the oldest and second largest family of human proteases. Ten years ago, a novel serine protease family named the type II transmembrane family (TTSP) was identified. This minireview summarizes the up-to-date knowledge about the still growing TTSPs, particularly focusing on the pathophysiological functions of the family member type II transmembrane serine protease (TMPRSS) 4. Recent studies provided importa…

GeneticsSerine proteaseTMPRSS6ProteasesClinical BiochemistrySerine EndopeptidasesProteolytic enzymesMembrane ProteinsBiologyBiochemistryTransmembrane proteinSerineBiochemistryVirus DiseasesNeoplasmsbiology.proteinHuman proteome projectAnimalsHumansMolecular BiologyMASP1Biological chemistry
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The Association between a MAOB Variable Number Tandem Repeat Polymorphism and Cocaine and Opiate Addictions in Polyconsumers

2021

Genetic analysis of the association between alcohol, cocaine, and opiate addiction and variable number tandem repeat (VNTR) polymorphisms in monoamine oxidase B (MAOB) and serotonergic 5-hydroxytryptamine (serotonin) receptor 1B and 2C (HTR1B 21 and HTR2C) pathway genes was performed in a sample of 302 polyconsumers. Our genetic association analysis revealed a significant association between a 184 base pair (bp) VNTR polymorphism in the MAOB gene and addiction to cocaine and opiates. This work highlights new genetic marker associations in cocaine and opiate polyconsumer addictions. These data help to clarify and quantify the complex role of genetics in addictive disorders, as well as their …

Geneticsbusiness.industryGeneral NeuroscienceAddictionmedia_common.quotation_subjectGenetic counselingMAOBcocaineopioidsNeurosciences. Biological psychiatry. NeuropsychiatrySerotonergicArticlepolymorphismVariable number tandem repeatGenetic markerPharmacogenomicsmental disordersMedicinegeneticsMonoamine oxidase BOpiatepolydrug usebusinessRC321-571media_common
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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Functional and genetic characterization of the non-lysosomal glucosylceramidase 2 as a modifier for Gaucher disease.

2013

Background: Gaucher disease (GD) is the most common inherited lysosomal storage disorder in humans, caused by mutations in the gene encoding the lysosomal enzyme glucocerebrosidase (GBA1). GD is clinically heterogeneous and although the type of GBA1 mutation plays a role in determining the type of GD, it does not explain the clinical variability seen among patients. Cumulative evidence from recent studies suggests that GBA2 could play a role in the pathogenesis of GD and potentially interacts with GBA1. Methods: We used a framework of functional and genetic approaches in order to further characterize a potential role of GBA2 in GD. Glucosylceramide (GlcCer) levels in spleen, liver and brain…

GenotypeDiseaseBiologymedicine.disease_causePolymorphism Single NucleotidePathogenesis03 medical and health sciencesMice0302 clinical medicineGenotypemedicineAnimalsGenetics(clinical)Pharmacology (medical)GeneGenetics (clinical)Cells Cultured030304 developmental biologyMedicine(all)Mice Knockout0303 health sciencesMutationGaucher DiseaseReverse Transcriptase Polymerase Chain ReactionResearchGeneral MedicineHematologyFibroblastsHuman genetics3. Good healthGlucosylceramidaseImmunologyGlucosylceramidaseGlucocerebrosidase030217 neurology & neurosurgery
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Acanthamoeba isolates belonging to T1, T2, T3, T4 and T7 genotypes from environmental freshwater samples in the Nile Delta region, Egypt.

2006

The free-living amoebae of the genus Acanthamoeba include non-pathogenic and pathogenic species and has been recently classified into 15 different genotypes, T1–T15. In this study, a survey was conducted in order to determine the presence and pathogenic potential of free-living amoebae of Acanthamoeba genus in freshwater sources associated with human activities in the Nile Delta region, Egypt. Identification of Acanthamoeba was based on the morphology of cyst and trophozoite forms and PCR amplification with a genus specific primer pair. The pathogenic potential of Acanthamoeba isolates was characterized using temperature and osmotolerance assays and PCR reactions with two primer pairs speci…

GenotypeVeterinary (miscellaneous)Molecular Sequence DataAcanthamoebaFresh WaterLoboseaPolymerase Chain ReactionMicrobiologylaw.inventionlawPhylogeneticsWater Supplyparasitic diseasesGenotypeAnimalsHumansPathogenRibosomal DNAPolymerase chain reactionPhylogenybiologyOsmolar ConcentrationSerine EndopeptidasesTemperatureSequence Analysis DNAbiology.organism_classificationAcanthamoebaInfectious DiseasesInsect ScienceProtozoaParasitologyEgyptPublic HealthActa tropica
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Genotyping of a nosocomial outbreak of pandemic influenza A/H1N1 2009

2011

Background: Epidemiological surveys have revealed outbreaks of pandemic influenza A (H1N1) 2009 in several different contexts. Molecular characterization of the influenza virus could help to provide a more accurate description of these outbreaks. Objective: To genotype pandemic influenza A (H1N1) 2009 isolates from an epidemiologically defined nosocomial outbreak. Study design: We sequenced the neuraminidase (NA) and hemagglutinin (HA) influenza A (H1N1) 2009 genes from ten HIV-positive patients involved in an epidemiologically defined outbreak in the Clinical Microbiology and Infectious Diseases (CMID) Department. Sequences were aligned to search for specific genetic features of the involv…

Genotyping TechniquesGenotypeMolecular Sequence DataNeuraminidaseHemagglutinin Glycoproteins Influenza VirusContext (language use)medicine.disease_causePandemic H1N1Disease OutbreaksViral ProteinsInfluenza A Virus H1N1 SubtypeVirologyPandemicHIV SeropositivityInfluenza HumanInfluenza A virusmedicineHumansViral ProteinSequencingHemagglutinin Glycoproteins Influenza ViruPandemicsGenotypingPhylogenyCross InfectionDisease OutbreakbiologyPandemicCoinfectionTransmissibilityOutbreakvirus diseasesOutbreakVirologyInfluenza A virus subtype H5N1Infectious DiseasesAmino Acid SubstitutionMutationbiology.proteinHuman mortality from H5N1Genotyping TechniqueNeuraminidaseHuman
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