Search results for " Mutation"

showing 10 items of 1212 documents

PDXK mutations cause polyneuropathy responsive to pyridoxal 5′‐phosphate supplementation

2019

OBJECTIVE: To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy. METHODS: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of variants on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on recombinant protein, patient-derived fibroblasts, plasma, and erythrocytes. Response to supplementation was measured with clinical validated rating sc…

0301 basic medicineMale[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyLOCAL TRANSLATIONMedizinmedicine.disease_causeDISEASEchemistry.chemical_compound0302 clinical medicinepolineuropathyCinètica enzimàticaGene Regulatory NetworksPyridoxal phosphateChildPyridoxal KinaseAdenosine triphosphate (ATP)Research ArticlesAged 80 and overMutationGene Regulatory NetworkPLASMAAutosomal recessive axonal polyneuropathyDisease gene identificationPyridoxal kinase3. Good healthSettore MED/26 - NEUROLOGIANeuropaties perifèriquesTreatment OutcomePolyneuropathieNeurologyChild PreschoolPyridoxal PhosphateRELIABILITYVitamin B ComplexFemaleLife Sciences & BiomedicinePolyneuropathyHumanResearch ArticleAdultAdolescentPDXKClinical NeurologyCHARCOT-MARIE-TOOTHCHARCOT-MARIE-TOOTH CMT NEUROPATHY SCORE LOCAL TRANSLATION DISEASE RELIABILITY; MECHANISMS DISCOVERY FRAMEWORK KINASE PLASMAMECHANISMS03 medical and health sciencesPolyneuropathiesAtrophy[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]KINASEmedicineHumansCMT NEUROPATHY SCOREPDXK mutationsPyridoxalDietary SupplementAgedPeripheral neuropathiesScience & Technology[SCCO.NEUR]Cognitive science/NeuroscienceEnzyme kineticsNeurosciencesFRAMEWORKmedicine.diseaseMolecular biology030104 developmental biologychemistryDISCOVERYDietary SupplementsMutationNeurosciences & NeurologyNeurology (clinical)Adenosine triphosphate030217 neurology & neurosurgeryAnnals of Neurology
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Evolution of transmitted HIV-1 drug resistance and viral subtypes circulation in Italy from 2006 to 2016

2018

Objectives: The aim was to evaluate the evolution of transmitted HIV-1 drug resistance (TDR) prevalence in antiretroviral therapy (ART)-naïve patients from 2006 to 2016. Methods: HIV-1 sequences were retrieved from the Antiviral Response Cohort Analysis (ARCA) database and TDR was defined as detection of at least one mutation from the World Health Organization (WHO) surveillance list. Results: We included protease/reverse transcriptase sequences from 3573 patients; 455 had also integrase sequences. Overall, 68.1% of the patients were Italian, the median CD4 count was 348 cells/μL [interquartile range (IQR) 169–521 cells/μL], and the median viral load was 4.7 log 10 HIV-1 RNA copies/mL (IQR …

0301 basic medicineMaleantiretroviral therapy; HIV; recent HIV infection; resistance epidemiology; transmitted HIV drug resistance; Adult; Anti-HIV Agents; CD4 Lymphocyte Count; Female; HIV Infections; HIV-1; Humans; Italy; Male; Middle Aged; Mutation; Odds Ratio; Prevalence; Viral Proteins; Drug Resistance Viralantiretroviral therapy; HIV; recent HIV infection; resistance epidemiology; transmitted HIV drug resistance; Health Policy; Infectious Diseases; Pharmacology (medical)Drug ResistanceHIV InfectionsDrug resistanceGastroenterologyInterquartile rangeOdds RatioPrevalenceHIV InfectionPharmacology (medical)ViralbiologyHealth PolicyMiddle AgedIntegraseInfectious DiseasesItalyFemaleViral loadHumanresistance epidemiologyAdultmedicine.medical_specialtytransmitted HIV drug resistanceAnti-HIV AgentsHIV; antiretroviral therapy; recent HIV infection; resistance epidemiology; transmitted HIV drug resistance030106 microbiologyantiretroviral therapySettore MED/17 - MALATTIE INFETTIVEVirus03 medical and health sciencesrecent HIV infectionViral ProteinsInternal medicineDrug Resistance ViralmedicineViral ProteinHumansbusiness.industryAnti-HIV AgentHIVOdds ratioReverse transcriptaseConfidence intervalCD4 Lymphocyte CountMutationbiology.proteinHIV-1business
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Total colonic aganglionosis and cleft palate in a newborn with Janus-cysteine 618 mutation of RET proto-oncogene: a case report.

2020

Abstract Background Hirschsprung disease, the most important congenital colonic dysmotility in children results from neural crest migration, differentiation, proliferation, or apoptosis defects where the rearranged during transfection (RET)-Protooncogene pathway has a central role. Although palatal and retinal anomalies in the context of chromosomopathies and some mono−/oligogenic syndromes are reported associated with Hirschsprung disease the role of inactivating RET mutations in these cases is not clarified. Case presentation We report on a dysmorphic newborn with cleft palate and palatal synechia, who showed intestinal obstruction after 24 h of life. Transient ileostomy and surgical biop…

0301 basic medicineMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyCongenital digestive system abnormalitieNeurocristopathyCase ReportContext (language use)RET proto-oncogenemedicine.disease_causeProto-Oncogene MasCongenital digestive system abnormalities03 medical and health sciences0302 clinical medicineGermline mutationCase-reportmedicineCarcinomaHumansCysteineHirschsprung DiseaseTotal colonic aganglionosisLoss functionGerm-Line MutationJanus KinasesNeurocristopathyMutationbusiness.industryProto-Oncogene Proteins c-retlcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseCleft Palate030104 developmental biologyItaly030220 oncology & carcinogenesisREarranged during TransfectionbusinessItalian journal of pediatrics
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Sequential cleavage of the proteins encoded by HNOT/ALG3, the human counterpart of the Drosophila NOT and yeast ALG3 gene, results in products acting…

2017

This study provides first insights into the biosynthesis, structure, biochemistry and complex processing of the proteins encoded by hNOT/ALG3, the human counterpart of the Drosophila Neighbour of TID (NOT) and the yeast asparagine linked glycosylation 3 gene (ALG3), which encodes a mannosyltransferase. Unambiguous evidence that both the fly and human proteins act as mannosyltransferases has not been provided yet. Previously, we showed that hNOT/ALG3 encodes two alternatively spliced main transcripts, hNOT-1/ALG3-1 and hNOT-4/ALG3-4, and their 15 truncated derivatives that lack diverse sets of exons and/or carry point mutations that result in premature termination codons. Here we show that t…

0301 basic medicineMannosyltransferaseGlycosylationSaccharomyces cerevisiae ProteinsGlycosylationProtein ConformationRNA SplicingSaccharomyces cerevisiaeBiologyMannosyltransferases03 medical and health scienceschemistry.chemical_compoundExonNuclear Receptor Subfamily 4 Group A Member 2GeneticsAnimalsHumansAmino Acid SequenceAsparagineMolecular BiologyGeneGenetics (clinical)Cellular compartmentPoint mutationComputational BiologyMembrane ProteinsExonsGeneral MedicineCell biologyAlternative Splicing030104 developmental biologychemistryCodon NonsenseDrosophilaCytokinesisHuman Molecular Genetics
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Comprehensive evaluation of coding region point mutations in microsatellite-unstable colorectal cancer

2018

Microsatellite instability (MSI) leads to accumulation of an excessive number of mutations in the genome, mostly small insertions and deletions. MSI colorectal cancers (CRCs), however, also contain more point mutations than microsatellite-stable (MSS) tumors, yet they have not been as comprehensively studied. To identify candidate driver genes affected by point mutations in MSI CRC, we ranked genes based on mutation significance while correcting for replication timing and gene expression utilizing an algorithm, MutSigCV. Somatic point mutation data from the exome kit-targeted area from 24 exome-sequenced sporadic MSI CRCs and respective normals, and 12 whole-genome-sequenced sporadic MSI CR…

0301 basic medicineMedicine (General)Candidate geneclinical evaluationgenetic identificationgenetic analysisQH426-470medicine.disease_causeChromatin Epigenetics Genomics & Functional Genomicswhole exome sequencingddc:590mutator genesingle nucleotide polymorphismddc:576.5Gene Regulatory NetworksExomeExome sequencingCancercancer cellGeneticsMutation1184 Genetics developmental biology physiology3. Good healthgenetic codesyöpägeenitpriority journalMolecular Medicinewild typepoint mutationSystems MedicineColorectal Neoplasmscongenital hereditary and neonatal diseases and abnormalitiesddc:025.063/5703122 Cancerscancer geneticsSingle-nucleotide polymorphismcolorectal cancerBiologygene frequencyta3111mikrosatelliititcolony formationR105W geneArticle03 medical and health sciencesR5-920Gene interactionReportGeneticsmedicineHumanscontrolled studyhumanneoplasmspaksusuolisyöpäPoint mutationgene interactionhuman celltumor-related geneMicrosatellite instabilityMolecular Sequence AnnotationSequence Analysis DNAmedicine.diseaseta3122digestive system diseaseshuman tissueSTK38L gene030104 developmental biologyvalidation processgene expressionSMARCB1 genemicrosatellite instability3111 Biomedicinegene replicationReports
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Staphylococcal cassette chromosome mec typing and mecA sequencing in methicillin-resistant staphylococci from Algeria: a highly diversified element w…

2016

Genetic mechanisms of methicillin resistance are still relevant in staphylococci. The aims of this study are to assess the possible exchanges of staphylococcal cassette chromosome mec (SCCmec) among isolates of methicillin-resistant staphylococci (MRS) and to check for known or new mutations in mecA DNA. A total of 35 MRS non-repetitive isolates were recovered, including 20 Staphylococcus haemolyticus, 7 Staphylococcus aureus, 4 Staphylococcus sciuri, 2 Staphylococcus saprophyticus and 1 isolate each of Staphylococcus xylosus and Staphylococcus lentus. Only 16 of the 35 strains were assigned to known SCCmec types: 7 SCCmec VII, 6 SCCmec IV and 3 SCCmec III, with possible horizontal transfer…

0301 basic medicineMicrobiology (medical)Methicillin-Resistant Staphylococcus aureusSettore MED/07 - Microbiologia E Microbiologia ClinicaStaphylococcus030106 microbiologyMicrobial Sensitivity TestsBiologymedicine.disease_causebeta-LactamsMicrobiologyBacterial geneticsMicrobiology03 medical and health sciencesBacterial ProteinsmedicineMissense mutationHumansPenicillin-Binding ProteinsTypingmecAGeneticsMutationSCCmecChromosomeGeneral Medicinerespiratory systembiochemical phenomena metabolism and nutritionChromosomes BacterialStaphylococcal Infectionsbacterial infections and mycosesStaphylococcus aureusStaphylococcus aureus; Methicillin Resistance; mecAAlgeriaHorizontal gene transferMutationStaphylococcus aureuMethicillin ResistanceJournal of medical microbiology
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Highly heterogeneous mutation rates in the hepatitis C virus genome.

2016

Spontaneous mutations are the ultimate source of genetic variation and have a prominent role in evolution. RNA viruses such as hepatitis C virus (HCV) have extremely high mutation rates, but these rates have been inferred from a minute fraction of genome sites, limiting our view of how RNA viruses create diversity. Here, by applying high-fidelity ultradeep sequencing to a modified replicon system, we scored >15,000 spontaneous mutations, encompassing more than 90% of the HCV genome. This revealed >1,000-fold differences in mutability across genome sites, with extreme variations even between adjacent nucleotides. We identify base composition, the presence of high- and low-mutation clusters a…

0301 basic medicineMicrobiology (medical)Mutation rateGenotypeHepatitis C virusImmunologyGenome ViralHepacivirusBiologymedicine.disease_causeVirus ReplicationApplied Microbiology and BiotechnologyMicrobiologyGenome03 medical and health sciencesMutation RateMolecular evolutionGenetic variationGeneticsmedicineHumansTransversionGenetics030102 biochemistry & molecular biologyNucleotidesGenetic VariationHigh-Throughput Nucleotide SequencingCell BiologyResistance mutationHepatitis C030104 developmental biologyViral replicationRNA ViralRepliconNature microbiology
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C2orf69 mutations disrupt mitochondrial function and cause a multisystem human disorder with recurring autoinflammation

2021

BACKGROUND. Deciphering the function of the many genes previously classified as uncharacterized open reading frame (ORF) would complete our understanding of a cell’s function and its pathophysiology. METHODS. Whole-exome sequencing, yeast 2-hybrid and transcriptome analyses, and molecular characterization were performed in this study to uncover the function of the C2orf69 gene. RESULTS. We identified loss-of-function mutations in the uncharacterized C2orf69 gene in 8 individuals with brain abnormalities involving hypomyelination and microcephaly, liver dysfunction, and recurrent autoinflammation. C2orf69 contains an N-terminal signal peptide that is required and sufficient for mitochondrial…

0301 basic medicineMicrocephalyRespiratory chainBiologyMitochondrionCell LineMitochondrial ProteinsTranscriptomeMiceOpen Reading Frames03 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineLoss of Function MutationGlycogen branching enzymemedicineAnimalsHumansGeneMice KnockoutGeneticsMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Glycogen Debranching Enzyme SystemGeneral Medicinemedicine.diseaseMitochondriaOpen reading frameRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biology030220 oncology & carcinogenesisMicrocephalybiology.proteinClinical MedicineSignal transductionGlycogenJournal of Clinical Investigation
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Rescuing the CFTR protein function: Introducing 1,3,4-oxadiazoles as translational readthrough inducing drugs.

2018

Nonsense mutations in the CFTR gene prematurely terminate translation of the CFTR mRNA leading to the production of a truncated protein that lacks normal function causing a more severe form of the cystic fibrosis (CF) disease. About 10% of patients affected by CF show a nonsense mutation. A potential treatment of this alteration is to promote translational readthrough of premature termination codons (PTCs) by Translational Readthrough Inducing Drugs (TRIDs) such as PTC124. In this context we aimed to compare the activity of PTC124 with analogues differing in the heteroatoms position in the central heterocyclic core. By a validated protocol consisting of computational screening, synthesis an…

0301 basic medicineModels MolecularCell SurvivalNonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorSettore BIO/11 - Biologia MolecolareContext (language use)OxadiazoleSettore BIO/09 - FisiologiaCystic fibrosis03 medical and health sciencesStructure-Activity Relationship0302 clinical medicineDrug DiscoverymedicineHumansRNA MessengerGenetic disorderPharmacologyMessenger RNAOxadiazolesNonsense mutationDose-Response Relationship DrugMolecular StructureChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryTranslational readthroughPremature termination codonTranslation (biology)Settore CHIM/06 - Chimica OrganicaGeneral Medicinemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSmall moleculeCell biologySettore BIO/18 - Genetica030104 developmental biologyBiological targetCystic fibrosi030220 oncology & carcinogenesisHeLa CellsEuropean journal of medicinal chemistry
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Caffeine boosts Ataluren's readthrough activity

2019

Abstract The readthrough of nonsense mutations by small molecules like Ataluren is considered a novel therapeutic approach to overcome the gene defect in several genetic diseases as cystic fibrosis (CF). This pharmacological approach suppresses translation termination at premature termination codons (PTCs readthrough) thus restoring the expression of a functional protein. However, readthrough might be limited by the nonsense-mediated mRNA decay (NMD), a cell process that reduces the amount/level of PTCs containing mRNAs. Here we investigate the combined action of Ataluren and caffeine to enhance the readthrough of PTCs. IB3.1 CF cells with a nonsense mutation were treated with caffeine to a…

0301 basic medicineMolecular biologymedia_common.quotation_subjectCellNonsenseNonsense mutationMRNA DecaySettore BIO/11 - Biologia MolecolareBiochemistryCystic fibrosisArticleCystic fibrosisCFTR gene03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCaffeinemedicinelcsh:Social sciences (General)Settore BIO/06 - Anatomia Comparata E Citologialcsh:Science (General)media_commonMessenger RNAMultidisciplinaryNonsense mutationNonsense mutationsPTC readthroughAtaluren/PTC124Settore CHIM/06 - Chimica Organicamedicine.diseaseCell biologyAtalurenSettore BIO/18 - Genetica030104 developmental biologymedicine.anatomical_structurechemistryCystic fibrosilcsh:H1-99Caffeine030217 neurology & neurosurgerylcsh:Q1-390Heliyon
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