Search results for " Mutation"

showing 10 items of 1212 documents

Late infantile neuronal ceroid lipofuscinosis: Quantitative description of the clinical course in patients withCLN2 mutations

2002

We examined 26 individuals with clinical and electron microscopic signs of late infantile neuronal ceroid lipofuscinosis (LINCL). In 22 cases, we found both pathogenic alleles. Sixteen patients exclusively carried either one or a combination of the two common mutations R208X and IVS5-1G > C. In the remaining cases, four missense mutations could be detected, of which R127Q, N286S, and T353P represent novel, previously not described alleles. A clinical performance score was developed by rating motor, visual, and verbal functions and the incidence of cerebral seizures in 3-month intervals during the course of the disease. A Total Disability Score was derived by summing up the single scores for…

Pediatricsmedicine.medical_specialtyDNA Mutational AnalysisCerliponase alfaDiseaseNeurological disorderAminopeptidasesSeverity of Illness IndexNeuronal Ceroid-LipofuscinosesSeizuresEndopeptidasesSeverity of illnessmedicineMissense mutationDipeptidyl-Peptidases and Tripeptidyl-PeptidasesVision OcularGenetics (clinical)Tripeptidyl-Peptidase 1business.industryDNAmedicine.diseaseTripeptidyl peptidase INeuronal Ceroid Lipofuscinosis Type 2MutationNeuronal ceroid lipofuscinosisSerine ProteasesbusinessPsychomotor PerformancePeptide HydrolasesAmerican Journal of Medical Genetics
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Trouble always comes in threes: three mutations for three auto inflammatory genes in a child and in his father

2014

The coexistence of mutations in more than one gene, linked to Autoinflammatory Diesases, can confuse and make difficult the diagnosis and management of these patients, especially in childhood, when the clinical history is still brief.

Pediatricsmedicine.medical_specialtyauto inflammatory geneBioinformaticsSettore MED/38 - Pediatria Generale E SpecialisticaRheumatologyClinical historyInternal medicinemedicineImmunology and AllergyPediatrics Perinatology and Child HealthGeneInflammatory genesHeterozygous mutationgene mutationsbusiness.industryMultiple sclerosisfood and beveragesmedicine.diseaseRheumatologyPharyngitisCanakinumabPediatrics Perinatology and Child HealthPoster Presentationmedicine.symptombusinessmedicine.drug
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Nonsense-mediated decay mechanism is a possible modifying factor of clinical outcome in nonsense cd39 beta thalassemia genotype

2012

Nonsense-mediated mRNA decay (NMD) is a surveillance system to prevent the synthesis of non-functional proteins. In β-thalassemia, NMD may have a role in clinical outcome. An example of premature translation stop codons appearing for the first time is the β-globin cd39 mutation; when homozygous, this results in a severe phenotype. The aim of this study was to determine whether the homozygous nonsense cd39 may have a milder phenotype in comparison with IVS1,nt110/cd39 genotype. Genotypes have been identified from a cohort of 568 patients affected by β-thalassemia. These genotypes were compared with those found in 577 affected fetuses detected among 2292 prenatal diagnoses. The…

Pediatricsmedicine.medical_specialtymedia_common.quotation_subjectNonsense-mediated decayNonsenseBeta thalassemiaBiologynonsense-mediated mRNA decay; beta-thalassemia; clinical outcame; beta-globin gene mutationsmedicine.diseaseGastroenterologynonsense-mediated mRNA decay beta-thalassemia beta-globin gene mutationsnonsense-mediated mRNA decay beta-thalassemia clinical outcame beta-globin gene mutations.Internal medicineGenotypemedicineDiseases of the blood and blood-forming organsRC633-647.5media_commonThalassemia Reports
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Nonsense codons suppression. An acute toxicity study of three optimized TRIDs in murine model, safety and tolerability evaluation.

2022

Stop mutations cause 11% of the genetic diseases, due to the introduction of a premature termination codon (PTC) in the mRNA, followed by the production of a truncated protein. A promising therapeutic approach is the suppression therapy by Translational Readthrough Inducing Drugs (TRIDs), restoring the expression of the protein. Recently, three new TRIDs (NV848, NV914, NV930) have been proposed, and validated by several in vitro assays, for the rescue of the CFTR protein, involved in Cystic Fibrosis disease. In this work, an acute toxicological study for the three TRIDs was conducted in vivo on mice, according to the OECD No.420 guidelines. Animals were divided into groups and treated with …

PharmacologyNonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorGeneral MedicineOxadiazoleMiceDisease Models AnimalPremature termination codon (PTC)Pharmaceutical PreparationsCodon NonsenseProtein BiosynthesisAnimalsToxicity studyTranslational readthrough inducing drugs(TRIDs)Biomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Molecular Basis Of Mild Hyperphenylalaninaemia In Turkey

2000

Öz bulunamadı.

Phenylalanine hydroxylaseGenotypeTurkeyPhenylalanineDNA Mutational AnalysisMEDLINEHyperphenylalaninemiaGene FrequencyPhenylketonuriasGenotypeDNA Mutational AnalysisGeneticsmedicineHumansChildAllele frequencyGenetics (clinical)Geneticsbiologybusiness.industryInfantPhenylalanine Hydroxylasemedicine.diseasePhenotypeHuman geneticsPhenotypeChild Preschoolbiology.proteinbusiness
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Exon deletions of the phenylalanine hydroxylase gene in Italian hyperphenylalaninemics

2009

A consistent finding of many studies describing the spectrum of mutant phenylalanine hydroxylase (PAH) alleles underlying hyperphenylalaninemia is the impossibility of achieving a 100% mutation ascertainment rate using conventional gene-scanning methods. These methods include denaturing gradient gel electrophoresis (DGGE), denaturing high performance liquid chromatography (DHPLC), and direct sequencing. In recent years, it has been shown that a significant proportion of undetermined alleles consist of large deletions overlapping one or more exons. These deletions have been difficult to detect in compound heterozygotes using gene-scanning methods due to a masking effect of the non-deleted al…

Phenylalanine hydroxylasePhenylketonuriasDNA Mutational AnalysisClinical Biochemistrygene dosageCompound heterozygosityBiochemistryGene dosageDenaturing high performance liquid chromatographyExonHyperphenylalaninemiaGene FrequencyPhenylketonuriasmedicineHumansMultiplex ligation-dependent probe amplificationMolecular BiologySequence DeletionGeneticsphenylalanine hydroxylase; phenylketonurias; ligase chain reaction; gene deletion; gene dosagebiologygene deletionReverse Transcriptase Polymerase Chain ReactionPhenylalanine HydroxylaseExonsmedicine.diseaseMolecular biologyItalyDisease Progressionbiology.proteinligase chain reactionMolecular MedicineOriginal ArticleExperimental and Molecular Medicine
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Maternal phenylketonuria in two Sicilian families identified by maternal blood phenylalanine level screening and identification of a new phenylalanin…

1999

not available

Phenylketonuria MaternalPhenylalanine hydroxylasephenylalanine 4 monooxygenasePhenylalanineGene mutationMaternal bloodNeonatal ScreeningPregnancyPhenylketonuriasMedicineHumansMaternal phenylketonuriaGenetic TestingPhenylalanine levelGeneticsbiologybusiness.industryInfant NewbornPhenylalanine HydroxylasePedigreeItalyPediatrics Perinatology and Child HealthMutationbiology.proteinIdentification (biology)FemalebusinessEuropean journal of pediatrics
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Single amino acids in the lumenal loop domain influence the stability of the major light-harvesting chlorophyll a/b complex.

2004

The major light-harvesting complex of photosystem II (LHCIIb) is one of the most abundant integral membrane proteins. It greatly enhances the efficiency of photosynthesis in green plants by binding a large number of accessory pigments that absorb light energy and conduct it toward the photosynthetic reaction centers. Most of these pigments are associated with the three transmembrane and one amphiphilic alpha helices of the protein. Less is known about the significance of the loop domains connecting the alpha helices for pigment binding. Therefore, we randomly exchanged single amino acids in the lumenal loop domain of the bacterially expressed apoprotein Lhcb1 and then reconstituted the muta…

Photosynthetic reaction centreProtein FoldingPhotosystem IIPigment bindingDNA Mutational AnalysisLight-Harvesting Protein ComplexesPeasPhotosystem II Protein ComplexBiologyBiochemistryTransmembrane proteinProtein Structure SecondaryProtein Structure TertiaryB vitaminsBiochemistryAmino Acid SubstitutionMutant proteinMutagenesis Site-DirectedPoint MutationAmino AcidsIntegral membrane proteinAccessory pigmentGene LibraryPlant ProteinsBiochemistry
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Globally defining the effects of mutations in a picornavirus capsid

2021

The capsids of non-enveloped viruses are highly multimeric and multifunctional protein assemblies that play key roles in viral biology and pathogenesis. Despite their importance, a comprehensive understanding of how mutations affect viral fitness across different structural and functional attributes of the capsid is lacking. To address this limitation, we globally define the effects of mutations across the capsid of a human picornavirus. Using this resource, we identify structural and sequence determinants that accurately predict mutational fitness effects, refine evolutionary analyses, and define the sequence specificity of key capsid-encoded motifs. Furthermore, capitalizing on the derive…

PicornavirusViral proteinQH301-705.5Sciencevirusesmedicine.medical_treatmentPicornaviridaeComputational biologymedicine.disease_causeGenomeGeneral Biochemistry Genetics and Molecular BiologyVirusImmune systemcapsidmedicineSingle amino acidBiology (General)GeneTropismHost proteinGeneticsEvolutionary BiologyMicrobiology and Infectious DiseaseMutationmutational fitness effectsProteaseGeneral Immunology and MicrobiologybiologyGeneral NeuroscienceQRviral proteaseGeneral Medicinebiochemical phenomena metabolism and nutritionbiology.organism_classificationViruspicornavirusViral proteaseCapsidMutationMedicineCapsid ProteinsHuman genomeDeep mutational scanningResearch ArticleHuman
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Effectiveness of screening for known mutations in Sicilian patients with "probable" familial hypercholesterolemia.

2002

Background and Aim: More than 750 mutations in the low-density lipoprotein (LDL) receptor gene are currently known to cause familial hypercholesterolemia (FH), but the array of mutations varies considerably in different populations. The definition of essentially all the LDL receptor gene mutations in a population is therefore a prerequisite for the implementation of nation-wide genetic testing for FH. Methods and Results: In this study, a screening strategy based on PCR-enzymatic digestion and PCR-allele specific hybridisation procedures was used to evaluate the frequency distributions of 11 known mutations in a cohort of 214 unrelated subjects meeting the diagnostic criteria of "probable" …

Point mutationNutrition and DieteticsSettore MED/09 - Medicina InternaEndocrinology Diabetes and MetabolismMedicine (miscellaneous)ExonsPolymerase Chain ReactionFHCohort StudiesHyperlipoproteinemia Type IIGene FrequencyReceptors LDLMutationScreeningHumansGenetic TestingCardiology and Cardiovascular MedicineSicilyFood Science
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