Search results for "MUTATION"

showing 10 items of 2830 documents

Combined B, T and NK Cell Deficiency Accelerates Atherosclerosis in BALB/c Mice.

2016

This study focused on the unique properties of both the Ldlr knockout defect (closely mimicking the human situation) and the BALB/c (C) inbred mouse strain (Th-2 slanted immune response). We generated two immunodeficient strains with severe combined B- and T-cell immunodeficiency with or without a complete lack of natural killer cells to revisit the role of adaptive immune responses on atherogenesis. C-Ldlr-/- Rag1-/- mice, which show severe combined B- and T-cell immunodeficiency and C-Ldlr-/- Rag1-/- Il2rg-/- mice, which combine the T- and B-cell defect with a complete lack of natural killer cells and inactivation of multiple cytokine signalling pathways were fed an atherogenic Western ty…

0301 basic medicineT-Lymphocyteslcsh:MedicineNK cellsAdaptive ImmunityBiochemistryVascular MedicineMicechemistry.chemical_compoundCellular typesReceptorlcsh:ScienceImmunodeficiencyMice KnockoutB-LymphocytesMice Inbred BALB CMultidisciplinarybiologyT CellsImmune cellsAcquired immune systemLipidsPlaque AtheroscleroticKiller Cells NaturalCholesterolPhenotypeWhite blood cellsFemalelipids (amino acids peptides and proteins)Research ArticleCell biologyBlood cellsLipoproteinsImmunologyResearch and Analysis MethodsBALB/cImmune Deficiency03 medical and health sciencesImmune systemmedicineAnimalsImmunohistochemistry TechniquesTriglyceridesMedicine and health sciencesBiology and life sciencesCholesterolMacrophageslcsh:RImmunologic Deficiency SyndromesWild typeProteinsAtherosclerosisbiology.organism_classificationmedicine.diseaseMolecular biologyHistochemistry and Cytochemistry Techniques030104 developmental biologyAnimal cellsReceptors LDLchemistryImmune SystemMutationImmunologyLDL receptorImmunologic TechniquesClinical Immunologylcsh:QClinical MedicinePLoS ONE
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Acute depletion of telomerase components DKC1 and NOP10 induces oxidative stress and disrupts ribosomal biogenesis via NPM1 and activation of the P53…

2020

Mutations in DKC1, NOP10, and TINF2 genes, coding for proteins in telomerase and shelterin complexes, are responsible for diverse diseases known as telomeropathies and ribosomopathies, including dyskeratosis congenita (DC, ORPHA 1775). These genes contribute to the DC phenotype through mechanisms that are not completely understood. We previously demonstrated in models of DC that oxidative stress is an early and independent event that occurs prior to telomere shortening. To clarify the mechanisms that induce oxidative stress, we silenced genes DKC1, NOP10, and TINF2 with siRNA technology. With RNA array hybridisation, we found several altered pathways for each siRNA model. Afterwards, we ide…

0301 basic medicineTelomeraseTelomere-Binding ProteinsCell Cycle ProteinsShelterin ComplexCell LineAdherens junction03 medical and health sciences0302 clinical medicineRibonucleoproteins Small NucleolarmedicineRNA Small InterferingMolecular BiologyTelomeraseTelomere ShorteningRibonucleoproteinChemistryRNANuclear ProteinsCell BiologyTelomereShelterinmedicine.diseaseCell biologyTelomereOxidative Stress030104 developmental biology030220 oncology & carcinogenesisMutationTumor Suppressor Protein p53NucleophosminRibosomesDyskeratosis congenitaBiogenesisBiochimica et biophysica acta. Molecular cell research
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Rett Syndrome Mutant Neural Cells Lacks MeCP2 Immunoreactive Bands.

2016

Dysfunctions of MeCP2 protein lead to various neurological disorders such as Rett syndrome and Autism. The exact functions of MeCP2 protein is still far from clear. At a molecular level, there exist contradictory data. MeCP2 protein is considered a single immunoreactive band around 75 kDa by western-blot analysis but several reports have revealed the existence of multiple MeCP2 immunoreactive bands above and below the level where MeCP2 is expected. MeCP2 immunoreactive bands have been interpreted in different ways. Some researchers suggest that multiple MeCP2 immunoreactive bands are unidentified proteins that cross-react with the MeCP2 antibody or degradation product of MeCP2, while others…

0301 basic medicineThreonineHeredityMethyl-CpG-Binding Protein 2Genetic LinkageMutantFluorescent Antibody TechniqueSocial Scienceslcsh:MedicinePC12 CellsBiochemistryEpitopeImmunoenzyme TechniquesCell FusionNeuroblastomaFluorescence MicroscopyAnimal CellsMedicine and Health SciencesPsychologyPost-Translational ModificationPhosphorylationAmino Acidslcsh:ScienceCells CulturedCross ReactivityNeuronsStainingMicroscopyMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionOrganic CompoundsCell StainingLight MicroscopyTransfectionChemistryX-Linked TraitsSex LinkagePhysical SciencesCellular TypesResearch ArticleCell signalingCell Physiologycongenital hereditary and neonatal diseases and abnormalitiesBlotting WesternImmunologyRett syndromeBiologyReal-Time Polymerase Chain ReactionResearch and Analysis MethodsMECP203 medical and health sciencesNeurologiaAntigenHydroxyl Amino Acidsmental disordersmedicineRett SyndromeGeneticsAnimalsHumansRNA MessengerClinical GeneticsHEK 293 cellsOrganic Chemistrylcsh:RChemical CompoundsBiology and Life SciencesProteinsCell Biologymedicine.diseaseMolecular biologyRatsnervous system diseases030104 developmental biologyHEK293 CellsSpecimen Preparation and TreatmentCellular NeuroscienceMutationDevelopmental PsychologyMalaltieslcsh:QNeuroscience
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Long-term genomic coevolution of host-parasite interaction in the natural environment

2017

Antagonistic coevolution of parasite infectivity and host resistance may alter the biological functionality of species, yet these dynamics in nature are still poorly understood. Here we show the molecular details of a long-term phage–bacterium arms race in the environment. Bacteria (Flavobacterium columnare) are generally resistant to phages from the past and susceptible to phages isolated in years after bacterial isolation. Bacterial resistance selects for increased phage infectivity and host range, which is also associated with expansion of phage genome size. We identified two CRISPR loci in the bacterial host: a type II-C locus and a type VI-B locus. While maintaining a core set of conse…

0301 basic medicineTime Factorsmedicine.medical_treatmentvirusesGeneral Physics and AstronomyGenomeCRISPR SpacersbakteeritBacteriophageEnvironmental MicrobiologyCRISPRBacteriophagesClustered Regularly Interspaced Short Palindromic RepeatsANTAGONISTIC COEVOLUTIONADAPTATIONbacteriaInfectivityGenetics0303 health scienceseducation.field_of_studyMultidisciplinaryQgenomiikkaBACTERIOPHAGE RESISTANCE MECHANISMSresistance (medicine)bacteriophagesPhage therapyScienceAntagonistic Coevolution030106 microbiologyPopulationevoluutioVirulencePHAGELocus (genetics)Genome ViralBiologyFlavobacteriumArticlebakteriofagitGeneral Biochemistry Genetics and Molecular BiologyHost-Parasite InteractionsEvolution Molecular03 medical and health sciencesCRISPR-CAS SYSTEMSFISHevolutionmedicinegenomicseducationGenome size1172 Environmental sciences030304 developmental biology030306 microbiologyGeneral Chemistrybiology.organism_classificationEVOLUTIONresistenssiPATHOGEN FLAVOBACTERIUM-COLUMNARE030104 developmental biologyMutationCRISPR LociVIRULENCEIMMUNE-SYSTEMGenome BacterialNature Communications
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Hypoxia-Induced miR-675-5p Supports β-Catenin Nuclear Localization by Regulating GSK3-β  Activity in Colorectal Cancer Cell Lines

2020

The reduction of oxygen partial pressure in growing tumors triggers numerous survival strategies driven by the transcription factor complex HIF1 (Hypoxia Inducible Factor-1). Recent evidence revealed that HIF1 promotes rapid and effective phenotypic changes through the induction of non-coding RNAs, whose contribution has not yet been fully described. Here we investigated the role of the hypoxia-induced, long non-coding RNA H19 (lncH19) and its intragenic miRNA (miR-675-5p) into HIF1-Wnt crosstalk. During hypoxic stimulation, colorectal cancer cell lines up-regulated the levels of both the lncH19 and its intragenic miR-675-5p. Loss of expression experiments revealed that miR-675-5p inhibitio…

0301 basic medicineTranscription factor complexKaplan-Meier Estimatelcsh:Chemistry0302 clinical medicineGSK-3poxiahylcsh:QH301-705.5long non-coding H19Spectroscopybeta CateninKinaseChemistryGeneral MedicineCell HypoxiaComputer Science ApplicationsCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColorectal NeoplasmsProtein BindingActive Transport Cell Nucleuscolorectal cancermiR-675TransfectionCatalysisArticleInorganic Chemistry03 medical and health sciencesCell Line TumormicroRNAGene silencingHumansPhysical and Theoretical ChemistryMolecular BiologyGlycogen Synthase Kinase 3 betahypoxiaOrganic ChemistryRNAComputational Biologyβ-cateninHCT116 CellsMicroRNAs030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Microscopy FluorescenceCateninMutationNuclear localization sequenceInternational Journal of Molecular Sciences
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Genome Mutational and Transcriptional Hotspots Are Traps for Duplicated Genes and Sources of Adaptations

2017

Gene duplication generatesnewgeneticmaterial,which has been shownto lead tomajor innovations in unicellular andmulticellular organisms.Awhole-genome duplication occurred in the ancestor of Saccharomyces yeast species but 92%of duplicates returned to single-copy genes shortly after duplication. The persisting duplicated genes in Saccharomyces led to the origin of major metabolic innovations, which have been the source of the unique biotechnological capabilities in the Baker's yeast Saccharomyces cerevisiae. What factors have determined the fate of duplicated genes remains unknown. Here,we report the first demonstration that the local genome mutation and transcription rates determine the fate…

0301 basic medicineTranscription GeneticGene duplicationAdaptation BiologicalSaccharomyces cerevisiaeEnvironmental stressPhenotypic plasticityBiologyGenomeEnvironmental stressMutational genome hotspots03 medical and health sciencesMutation RateStress PhysiologicalGene duplicationGeneticsPromoter Regions GeneticEcology Evolution Behavior and SystematicsGeneticsAdaptationsGenetic redundancyDuplicated genes030104 developmental biologyMutationGenetic redundancyExpression genome hotspotsResearch Article
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Characterisation of CDKL5 Transcript Isoforms in Human and Mouse.

2016

Mutations in the X-linked Cyclin-Dependent Kinase-Like 5 gene (CDKL5) cause early onset infantile spasms and subsequent severe developmental delay in affected children. Deleterious mutations have been reported to occur throughout the CDKL5 coding region. Several studies point to a complex CDKL5 gene structure in terms of exon usage and transcript expression. Improvements in molecular diagnosis and more extensive research into the neurobiology of CDKL5 and pathophysiology of CDKL5 disorders necessitate an updated analysis of the gene. In this study, we have analysed human and mouse CDKL5 transcript patterns both bioinformatically and experimentally. We have characterised the predominant brai…

0301 basic medicineUntranslated regionTranscription GeneticCDKL5lcsh:MedicineGene ExpressionArtificial Gene Amplification and ExtensionPolymerase Chain ReactionBiochemistryExonMice0302 clinical medicineCoding regionProtein Isoformslcsh:ScienceGeneticsRegulation of gene expressionMultidisciplinaryMammalian GenomicsHigh-Throughput Nucleotide SequencingExonsGenomicsNucleic acidsRNA isolationPhenotypeSpasms InfantileResearch ArticleGene isoformBiologyProtein Serine-Threonine KinasesPolyadenylationResearch and Analysis MethodsBiomolecular isolation03 medical and health sciencesGeneticsAnimalsHumansAdultsAmino Acid SequenceMolecular Biology TechniquesGeneMolecular BiologyAlternative splicinglcsh:RGene MappingInfant NewbornBiology and Life SciencesReverse Transcriptase-Polymerase Chain ReactionAlternative Splicing030104 developmental biologyGene Expression RegulationRNA processingAge GroupsAnimal GenomicsMutationPeople and PlacesExon MappingRNAlcsh:QPopulation Groupings030217 neurology & neurosurgeryPloS one
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Impact of the Usher syndrome on olfaction

2015

Usher syndrome is a genetically and clinically heterogeneous disease in humans, characterized by sensorineural hearing loss, retinitis pigmentosa and vestibular dysfunction. This disease is caused by mutations in genes encoding proteins that form complex networks in different cellular compartments. Currently, it remains unclear whether the Usher proteins also form networks within the olfactory epithelium (OE). Here, we describe Usher gene expression at the mRNA and protein level in the OE of mice and showed interactions between these proteins and olfactory signaling proteins. Additionally, we analyzed the odor sensitivity of different Usher syndrome mouse models using electro-olfactogram re…

0301 basic medicineUsher syndromeCell Cycle ProteinsMice TransgenicNerve Tissue ProteinsOlfactionMyosinsBiologyCell LineMice03 medical and health sciencesOlfactory MucosaGene expressionRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCiliaMolecular BiologyGeneGenetics (clinical)GeneticsExtracellular Matrix ProteinsMessenger RNAGene Expression ProfilingEpithelial CellsGeneral MedicineCadherinsmedicine.diseaseeye diseasesSmellCytoskeletal ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression RegulationMyosin VIIaMutationOdorantsSignal transductionCarrier ProteinsUsher SyndromesOlfactory epitheliumSignal TransductionHuman Molecular Genetics
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Next‐generation sequencing reveals the mutational landscape of clinically diagnosed Usher syndrome: copy number variations, phenocopies, a predominan…

2017

Background Combined retinal degeneration and sensorineural hearing impairment is mostly due to autosomal recessive Usher syndrome (USH1: congenital deafness, early retinitis pigmentosa (RP); USH2: progressive hearing impairment, RP). Methods Sanger sequencing and NGS of 112 genes (Usher syndrome, nonsyndromic deafness, overlapping conditions), MLPA, and array-CGH were conducted in 138 patients clinically diagnosed with Usher syndrome. Results A molecular diagnosis was achieved in 97% of both USH1 and USH2 patients, with biallelic mutations in 97% (USH1) and 90% (USH2), respectively. Quantitative readout reliably detected CNVs (confirmed by MLPA or array-CGH), qualifying targeted NGS as one …

0301 basic medicineUsher syndromeNonsense mutationnext‐generation sequencingBiologyGene mutationBioinformatics03 medical and health sciencessymbols.namesakeRetinitis pigmentosaGeneticsmedicineotorhinolaryngologic diseasesMultiplex ligation-dependent probe amplificationNonsyndromic deafnessMolecular BiologyGenetics (clinical)Sanger sequencingGeneticsHeimler syndromeCopy number variationPoint mutationOriginal Articlesmedicine.diseaseeye diseases030104 developmental biologysymbolsphenocopiestranslational read‐throughOriginal ArticleUsher syndromeMolecular Genetics & Genomic Medicine
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Multicenter validation study for the certification of a CFTR gene scanning method using next generation sequencing technology.

2018

AbstractBackground:Many European laboratories offer molecular genetic analysis of theCFTRgene using a wide range of methods to identify mutations causative of cystic fibrosis (CF) and CFTR-related disorders (CFTR-RDs). Next-generation sequencing (NGS) strategies are widely used in diagnostic practice, and CE marking is now required for most in vitro diagnostic (IVD) tests in Europe. The aim of this multicenter study, which involved three European laboratories specialized in CF molecular analysis, was to evaluate the performance of Multiplicom’s CFTR MASTR Dx kit to obtain CE-IVD certification.Methods:A total of 164 samples, previously analyzed with well-established “reference” methods for t…

0301 basic medicineValidation studycongenital hereditary and neonatal diseases and abnormalitiesCertification[SDV]Life Sciences [q-bio]Clinical BiochemistrySequencing dataCFTR molecular diagnosiCystic Fibrosis Transmembrane Conductance RegulatorComputational biology030105 genetics & heredityBiologyCFTR molecular diagnosisDNA sequencingIn vitro diagnosticCftr genecystic fibrosis03 medical and health sciencesHumanscystic fibrosiCE-IVD certificationBiochemistry (medical)Reproducibility of ResultsIllumina miseqSequence Analysis DNAGeneral MedicineMolecular analysisEurope030104 developmental biologyMulticenter studycomparative sequencing analysicomparative sequencing analysisMutationnext-generation sequencingMultiplex Polymerase Chain Reaction
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