Search results for "MUTATION"

showing 10 items of 2830 documents

Mutations affecting MHC class II binding of the superantigen streptococcal erythrogenic toxin A.

1993

Streptococcal pyrogenic exotoxin A (SPEA) is an important pathogenicity factor of group A streptococci. It is a member of the family of 'superantigens' produced by Staphylococcus aureus and Streptococcus pyogenes, and its T lymphocyte stimulating activity is involved in the pathogenesis of certain diseases caused by pyogenic streptococci. In this study we have generated nine mutant SPEA molecules by substituting amino acids in the regions of homology between different streptococcal and staphylococcal superantigens. An additional mutant was created by deletion of the 10 N-terminal amino acids. The mutants were expressed as fusion proteins. Several mutations led to a loss of function due to a…

Streptococcus pyogenesT-LymphocytesImmunologyMutantMolecular Sequence DataExotoxinsBiologymedicine.disease_causeLymphocyte ActivationMicrobiologyMiceStructure-Activity Relationshipstomatognathic systemBacterial ProteinsSuperantigenmedicineImmunology and AllergyAnimalsHumansAmino Acid SequencePeptide sequencechemistry.chemical_classificationMice Inbred BALB CSuperantigensBase SequenceHistocompatibility Antigens Class IIMembrane ProteinsGeneral Medicinebiology.organism_classificationFusion proteinAmino acidchemistrySpeaStreptococcus pyogenesMutationExotoxinInternational immunology
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The Principle of Stasis: Why drift is not a Zero-Cause Law

2016

This paper analyses the structure of evolutionary theory as a quasi-Newtonian theory and the need to establish a Zero-Cause Law. Several authors have postulated that the special character of drift is because it is the default behaviour or Zero-Cause Law of evolutionary systems, where change and not stasis is the normal state of them. For these authors, drift would be a Zero-Cause Law, the default behaviour and therefore a constituent assumption impossible to change without changing the system. I defend that drift's causal and explanatory power prevents it from being considered as a Zero-Cause Law. Instead, I propose that the default behaviour of evolutionary systems is what I call the Princ…

Structure (mathematical logic)HistoryPhilosophy05 social sciences06 humanities and the artsGeneral MedicineBiological evolutionNormal state050905 science studies0603 philosophy ethics and religionBiological EvolutionModels BiologicalZero (linguistics)History and Philosophy of ScienceLaw060302 philosophyMutation (genetic algorithm)Quantitative Biology::Populations and EvolutionEvolutionary systems0509 other social sciencesExplanatory powerEvolutionary theoryStudies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences
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Comparing fMRI inter-subject correlations between groups using permutation tests

2018

AbstractInter-subject correlation (ISC) based analysis is a conceptually simple approach to analyze functional magnetic resonance imaging (fMRI) data acquired under naturalistic stimuli such as a movie. We describe and validate the statistical approaches for comparing ISCs between two groups of subjects implemented in the ISC toolbox, which is an open source software package for ISC-based analysis of fMRI data. The approaches are based on permutation tests. We validated the approaches using five different data sets from the ICBM functional reference battery tasks. First, we created five null datasets (one for each task) by dividing the subjects into two matched groups and assumed that no gr…

Studentized rangemedicine.diagnostic_testComputer sciencebusiness.industryPoolingPattern recognitioncomputer.software_genre01 natural sciences010104 statistics & probability03 medical and health sciencesPermutation0302 clinical medicineVoxelmedicineArtificial intelligence0101 mathematicsFunctional magnetic resonance imagingbusinesscomputer030217 neurology & neurosurgery
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Regulation of cell cycle transcription factor Swi5 by karyopherin Msn5

2012

AbstractInactivation of S. cerevisiae β-karyopherin Msn5 causes hypersensitivity to the overexpression of mitotic cyclin Clb2 and aggravates growth defects of many mutant strains in mitotic exit, suggesting a connection between Msn5 and mitotic exit. We determined that Msn5 controlled subcellular localization of the mitotic exit transcription factor Swi5, since it was required for Swi5 nuclear export. Msn5 physically interacted with the N-terminal end of Swi5. Inactivation of Msn5 caused a severe reduction in cellular levels of Swi5 protein. This effect occurred by a post-transcriptional mechanism, since SWI5 mRNA levels were not affected. The reduced amount of Swi5 in msn5 mutant cells was…

Swi5Saccharomyces cerevisiae ProteinsGenes FungalActive Transport Cell NucleusMitosisCell Cycle ProteinsSaccharomyces cerevisiaeKaryopherinsProtein degradationBiologyNuclear export signalMolecular BiologyMitosisTranscription factorKaryopherinMsn5Cell Nucleuschemistry.chemical_classificationProtein StabilityCell CycleCell BiologyCell cycleβ-karyopherinMolecular biologyCell biologyProtein TransportchemistryMitotic exitMutationNuclear transportProtein BindingSubcellular FractionsTranscription FactorsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Molecular study of porcine transmissible gastroenteritis virus after serial animal passages revealed point mutations in S protein

2010

Porcine respiratory coronavirus is related genetically to porcine transmissible gastroenteritis virus with a large deletion in S protein. The respiratory virus is a mutated form that may be a consequence of the gastroen- teritis virus's evolution. Intensive passages of the virus in its natural host may enhance the appearance of mutations and therefore may contribute to any attenuated form of the virus. The objective of this study was to characterize the porcine transmissible gastroenteritis virus TMK22 strain after passages in piglets from 1992 until 2007. A typical experimental infection, molecular characterization, and serological analysis were also carried out to further char- acterize a…

SwineSequence analysisvirusesMolecular Sequence DataRT-PCRBiologymedicine.disease_causeArticleVirusViral Envelope ProteinsImmunityVirologyGeneticsmedicineAnimalsPoint MutationDNA sequencingAmino Acid SequenceExperimental infectionPorcine diseaseMolecular BiologyPeptide sequenceCells CulturedCoronavirusMembrane GlycoproteinsGastroenteritis Transmissible of SwineSequence Analysis RNAPoint mutationTransmissible gastroenteritis virusGeneral MedicineVirologyGastroenteritisSpike Glycoprotein CoronavirusRNA ViralRespiratory virusPorcine Respiratory CoronavirusVirus Genes
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HNRNPR Variants that Impair Homeobox Gene Expression Drive Developmental Disorders in Humans

2019

The heterogeneous nuclear ribonucleoprotein (HNRNP) genes code for a set of RNA-binding proteins that function primarily in the spliceosome C complex. Pathogenic variants in these genes can drive neurodegeneration, through a mechanism involving excessive stress-granule formation, or developmental defects, through mechanisms that are not known. Here, we report four unrelated individuals who have truncating or missense variants in the same C-terminal region of hnRNPR and who have multisystem developmental defects including abnormalities of the brain and skeleton, dysmorphic facies, brachydactyly, seizures, and hypoplastic external genitalia. We further identified in the literature a fifth ind…

TBX1MaleSpliceosomeHeterogeneous nuclear ribonucleoproteinDevelopmental DisabilitiesRNA SplicingBiologyHeterogeneous-Nuclear Ribonucleoproteins/geneticsHeterogeneous-Nuclear RibonucleoproteinsArticleWhole Exome Sequencing03 medical and health sciences0302 clinical medicineExome SequencingGeneticsHumansGenes Homeobox/geneticsPreschoolHox geneChildGeneTranscription factorGenetics (clinical)RNA Splicing/genetics030304 developmental biologyGeneticsFibroblasts/metabolism0303 health sciencesHomeobox/geneticsGenes HomeoboxInfantFibroblastsOxidative StressPhenotypeGenesDevelopmental Disabilities/etiologyGene Expression RegulationChild PreschoolRNA splicingMutationHomeoboxFemale030217 neurology & neurosurgery
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The Saccharomyces cerevisiae flavodoxin-like proteins Ycp4 and Rfs1 play a role in stress response and in the regulation of genes related to metaboli…

2011

SPI1 is a gene whose expression responds to many environmental stimuli, including entry into stationary phase. We have performed a screening to identify genes that activate SPI1 promoter when overexpressed. The phosphatidylinositol- 4-phosphate 5-kinase gene MSS4 was identified as a positive activator of SPI1. Another SPI1 transcriptional regulator isolated was the flavodoxin-like gene YCP4. YCP4 and its homolog RFS1 regulate the expression of many genes during the late stages of growth. The double deletion mutant in YCP4 and its homolog RFS1 has an impact on gene expression related to metabolism by increasing the expression of genes involved in hexose transport and glycolysis, and decreasi…

TBX1Saccharomyces cerevisiae Proteins[SDV]Life Sciences [q-bio]Genes FungalFlavodoxinSaccharomyces cerevisiae[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyBiochemistryMicrobiology03 medical and health sciencesGene Expression Regulation FungalGene expressionGeneticsTranscriptional regulationPromoter Regions GeneticMolecular BiologyGeneHexose transportComputingMilieux_MISCELLANEOUS030304 developmental biologyOligonucleotide Array Sequence AnalysisGenetics0303 health sciencesSPI1Membrane GlycoproteinsActivator (genetics)Gene Expression Profiling030302 biochemistry & molecular biologyRNA FungalGeneral Medicine3. Good healthOxidative StressPhosphotransferases (Alcohol Group Acceptor)FermentationMutationTranslational elongation
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A novel S379A TARDBP mutation associated to late-onset sporadic ALS

2019

Since 2008, several groups have reported a lot of dominant mutations in TARDBP gene as a primary cause of Amyotrophic lateral sclerosis (ALS). Mutations in TARDBP gene are responsible for 4–5% of familial ALS (fALS) and nearly 1% of sporadic ALS (sALS). To date, over 50 dominant mutations were found in TDP-43 in both familial and sporadic ALS patients, most of which were missense mutations in the C-terminal glycine-rich region. Herein, we describe the clinical and genetic analysis of an Italian non-familial ALS patient with a late onset and a rapid disease progression, which led to the discovery of a novel TARDBP mutation. After neurological evaluation, molecular investigation highlighted t…

TDP-43DNA-Binding ProteinMutation MissenseLate onsetDermatologyBiologymedicine.disease_causeGenetic analysisTARDBP03 medical and health sciencesExon0302 clinical medicinemedicineHumansMissense mutation030212 general & internal medicineAmyotrophic lateral sclerosisAge of OnsetTARDBPGeneticsAged 80 and overMutationAmyotrophic Lateral SclerosisGeneral Medicinemedicine.diseaseDNA-Binding ProteinsPsychiatry and Mental healthMutationFemaleNeurology (clinical)Age of onsetALS030217 neurology & neurosurgeryAmyotrophic Lateral SclerosiHuman
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A Transition Zone Complex Regulates Mammalian Ciliogenesis and Ciliary Membrane Composition

2011

Mutations in genes encoding ciliary components cause ciliopathies, but how many of these mutations disrupt ciliary function is unclear. We investigated Tectonic1 (Tctn1), a regulator of mouse Hedgehog signaling, and found that it is essential for ciliogenesis in some, but not all, tissues. Cell types that do not require Tctn1 for ciliogenesis require it to localize select membrane-associated proteins to the cilium, including Arl13b, AC3, Smoothened and Pkd2. Tctn1 forms a complex with multiple ciliopathy proteins associated with Meckel (MKS) and Joubert (JBTS) syndromes, including Mks1, Tmem216, Tmem67, Cep290, B9d1, Tctn2, and Cc2d2a. Components of the Tectonic ciliopathy complex colocaliz…

TMEM67Inbred C57BLCiliopathiesMedical and Health SciencesMice0302 clinical medicineCerebellumMorphogenesisEye AbnormalitiesEncephalocelePediatricMice Knockout0303 health sciencesPolycystic Kidney DiseasesCiliumCiliary transition zoneBiological SciencesKidney Diseases CysticCell biologyOrgan SpecificityCiliary Motility DisordersKidney DiseasesRabbitsAbnormalitiesMultipleRetinitis PigmentosaCiliary Motility DisordersSignal TransductionKnockoutBiologyRetinaArticle03 medical and health sciencesCysticRare DiseasesCerebellar DiseasesCiliogenesisGeneticsMatrix-Assisted Laser Desorption-IonizationAnimalsHumansAbnormalities MultipleCiliaCiliary membrane030304 developmental biologySpectrometryCell MembraneMembrane ProteinsMassPeptide FragmentsMice Inbred C57BLSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMutationCiliary baseChickens030217 neurology & neurosurgeryDevelopmental BiologyNature genetics
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Hematopoietic stem cell quiescence and function are controlled by the CYLD–TRAF2–p38MAPK pathway

2015

Tesio at al. identify a novel pathway controlled by the tumor suppressor and deubiquitinase cylindromatosis (CYLD), which is involved in the regulation of hematopoietic stem cell quiescence and repopulation potential.

TRAF2Tumor suppressor geneMAP Kinase Signaling SystemImmunologyRegulatorBiologyp38 Mitogen-Activated Protein KinasesArticleMicemedicineAnimalsImmunology and AllergyMice KnockoutRegulation of gene expressionNF-kappa BHematopoietic stem cellCell BiologyHematopoietic Stem CellsTNF Receptor-Associated Factor 2PhenotypeDeubiquitinating Enzyme CYLDCell biologyCysteine EndopeptidasesHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutationStem cellJournal of Experimental Medicine
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