Search results for "MUTATION"

showing 10 items of 2830 documents

A co-registration investigation of inter-word spacing and parafoveal preview: Eye movements and fixation-related potentials

2019

Participants’ eye movements (EMs) and EEG signal were simultaneously recorded to examine foveal and parafoveal processing during sentence reading. All the words in the sentence were manipulated for inter-word spacing (intact spaces vs. spaces replaced by a random letter) and parafoveal preview (identical preview vs. random letter string preview). We observed disruption for unspaced text and invalid preview conditions in both EMs and fixation-related potentials (FRPs). Unspaced and invalid preview conditions received longer reading times than spaced and valid preview conditions. In addition, the FRP data showed that unspaced previews disrupted reading in earlier time windows of analysis, com…

MaleTime FactorsEye MovementsPhysiologyVisual SystemVisionComputer scienceSpeech recognitionSensory PhysiologyVisual PhysiologySocial ScienceslukeminensilmänliikkeetOcular physiology0302 clinical medicineFovealMedicine and Health SciencesPsychologyAttentionMacula LuteaEEGNeurolinguisticsClinical NeurophysiologyBrain MappingMultidisciplinaryQ05 social sciencesRElectroencephalographyHealthy VolunteersSensory SystemsSemanticsElectrophysiologyBioassays and Physiological AnalysisPattern Recognition VisualBrain ElectrophysiologyPhysical SciencestekstinymmärtäminenMedicineFemaleSensory PerceptionAnatomyResearch ArticleAdultAdolescentImaging TechniquesPermutationScienceNeurophysiologyCo registrationNeuroimagingFixation OcularResearch and Analysis Methods050105 experimental psychologyYoung Adult03 medical and health sciencesHumans0501 psychology and cognitive sciencesScalpDiscrete MathematicsElectrophysiological TechniquesCognitive PsychologyBiology and Life SciencesEye movementLinguisticsReadingSentence ProcessingCombinatoricsFixation (visual)katseenseurantaCognitive ScienceClinical MedicineHeadMathematics030217 neurology & neurosurgeryNeurosciencePLOS ONE
researchProduct

The time course of recombinant production in Streptomyces coelicolor.

1971

SUMMARYThe process leading to gene recombination can be interrupted in the filamentous bacteriaStreptomyces coelicolorby growing mixed cultures on cellophane disks lying on complete medium. The mycelium is harvested, broken, diluted and the broken hyphae plated at different time intervals. By this means some markers can be excluded from heteroclones or from recombinant progeny in early samples. The recombinant pattern clearly changes with time, with an increase of markers contributed to the recombinant progeny. In crosses between male (NF) and female (UF) strains, the maleness is the first donor trait to appear in the cells of the recipient parent. The fertility factor does not produce a tr…

MaleTime FactorsHyphaBiologyGenetic recombinationlaw.inventionlawGeneticsMyceliumCrosses GeneticInfertility MaleRecombination GeneticSpores BacterialFertility factor (bacteria)fungiStreptomyces coelicolorChromosomeChromosome MappingGeneral MedicineChromosomes Bacterialbiology.organism_classificationMolecular biologyStreptomycesSporePhenotypeConjugation GeneticMutationRecombinant DNAGenetical research
researchProduct

Increased Activity of Coagulation Factor XII (Hageman Factor) Causes Hereditary Angioedema Type III

2006

International audience; Hereditary angioedema (HAE) is characterized clinically by recurrent acute skin swelling, abdominal pain, and potentially life-threatening laryngeal edema. Three forms of HAE have been described. The classic forms, HAE types I and II, occur as a consequence of mutations in the C1-inhibitor gene. In contrast to HAE types I and II, HAE type III has been observed exclusively in women, where it appears to be correlated with conditions of high estrogen levels--for example, pregnancy or the use of oral contraceptives. A recent report proposed two missense mutations (c.1032C-->A and c.1032C-->G) in F12, the gene encoding human coagulation factor XII (FXII, or Hageman factor…

MaleTime FactorsKinins030204 cardiovascular system & hematologyMESH: Founder Effect[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityLinkage Disequilibrium0302 clinical medicineMissense mutationHereditary Angioedema Type IIIGenetics(clinical)MESH: Models GeneticGenetics (clinical)MESH: Heterozygote0303 health sciencesFactor XII[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyFounder EffectMarkov ChainsPedigree3. Good healthMESH: Linkage DisequilibriumFactor XIIHereditary angioedemaFemalemedicine.symptomMESH: Factor XIIHeterozygotemedicine.medical_specialtyMESH: MutationMESH: PedigreeMESH: Bayes TheoremCoagulation Factor XIIBiology03 medical and health sciencesMESH: Markov ChainsReportInternal medicinemedicineGeneticsHumansMESH: AngioedemaAngioedema030304 developmental biologyMESH: HumansModels GeneticAngioedemaHaplotypeMESH: Time FactorsBayes TheoremHeterozygote advantageMESH: Haplotypesmedicine.diseaseMESH: KininsMESH: MaleEndocrinologyHaplotypesMutationImmunologyMESH: Microsatellite RepeatsMESH: FemaleMicrosatellite RepeatsThe American Journal of Human Genetics
researchProduct

ALS-Related Mutant FUS Protein Is Mislocalized to Cytoplasm and Is Recruited into Stress Granules of Fibroblasts from Asymptomatic FUS P525L Mutation…

2017

Background: Amyotrophic lateral sclerosis (ALS) shows a strong genetic basis, with SOD1, FUS, TARDBP, and C9ORF72 being the genes most frequently involved. This has allowed identification of asymptomatic mutation carriers, which may be of help in understanding the molecular changes preceding disease onset. Objectives: We studied the cellular expression of FUS protein and the effect of heat-shock-and dithiothreitol-induced stress in fibroblasts from FUS P525L mutation carriers, healthy controls, and patients with sporadic ALS. Methods: Western blots and immunocytochemistry were performed to study the subcellular localization of FUS protein. Control and stressed cells were double stained with…

MaleTime FactorsProlineTime FactorNeural ConductionHuman fibroblastCytoplasmic GranulesFollow-Up StudieFUS P525L carrierCytoplasmic FUS expressionLeucineTubulinStress granuleAmyotrophic lateral sclerosis · FUS P525L carriers · Cytoplasmic FUS expression · Stress granules · Human fibroblastsHumansCell NucleuAmyotrophic lateral sclerosiCells CulturedSkinCell NucleusAmyotrophic Lateral SclerosisFibroblastsProtein TransportSubcellular FractionMutationFibroblastRNA-Binding Protein FUSFemaleCytoplasmic GranuleFollow-Up StudiesSubcellular FractionsHuman
researchProduct

Autoimmune polyendocrine syndrome type 1: an Italian survey on 158 patients

2021

Abstract Background Autoimmune Polyglandular Syndrome type 1 (APS-1) is a rare recessive inherited disease, caused by AutoImmune Regulator (AIRE) gene mutations and characterized by three major manifestations: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism (CH) and Addison’s disease (AD). Methods Autoimmune conditions and associated autoantibodies (Abs) were analyzed in 158 Italian patients (103 females and 55 males; F/M 1.9/1) at the onset and during a follow-up of 23.7 ± 15.1 years. AIRE mutations were determined. Results The prevalence of APS-1 was 2.6 cases/million (range 0.5–17 in different regions). At the onset 93% of patients presented with one or more component…

MaleTranscription FactorEndocrinology Diabetes and MetabolismAutoimmune hepatitisGene mutationGastroenterologyChronic mucocutaneous candidiasisEndocrinologyAddison DiseaseAutoimmune Polyglandular Syndrome type 1 (APS-1)PrevalenceMedicineChronic mucocutaneous candidiasisPolyendocrinopathies AutoimmuneCandidiasis Chronic MucocutaneouAddison’s disease AIRE gene mutations Autoimmune Polyglandular Syndrome type 1 (APS-1) Autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED) Chronic hypoparathyroidism Chronic mucocutaneous candidiasis Interferon autoantibodiesCandidiasis Chronic MucocutaneousAIRE gene mutations; Addison’s disease; autoimmune polyglandular syndrome type 1 (APS-1); autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED); chronic hypoparathyroidism; chronic mucocutaneous candidiasis; interferon autoantibodiesAutoimmune regulatorAutoantibodieItalyInterferon autoantibodieAddison's diseaseInterferon Type IOriginal ArticleFemaleChronic hypoparathyroidismHumanAdultmedicine.medical_specialtyAutoimmune GastritisHypoparathyroidismAddison’s diseaseAIRE gene mutationsInternal medicineInterferon autoantibodiesHumansMortalityAutoantibodiesAddison’s disease; AIRE gene mutations; Autoimmune Polyglandular Syndrome type 1 (APS-1); Autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED); Chronic hypoparathyroidism; Chronic mucocutaneous candidiasis; Interferon autoantibodiesbusiness.industryChronic mucocutaneous candidiasiAIRE gene mutationAutoantibodymedicine.diseaseAutoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED)Interferon autoantibodies.Autoimmune polyendocrine syndrome type 1MutationbusinessTranscription Factors
researchProduct

Further Delineation of Duplications of ARX Locus Detected in Male Patients with Varying Degrees of Intellectual Disability

2022

The X-linked gene encoding aristaless-related homeobox (ARX) is a bi-functional transcription factor capable of activating or repressing gene transcription, whose mutations have been found in a wide spectrum of neurodevelopmental disorders (NDDs); these include cortical malformations, paediatric epilepsy, intellectual disability (ID) and autism. In addition to point mutations, duplications of the ARX locus have been detected in male patients with ID. These rearrangements include telencephalon ultraconserved enhancers, whose structural alterations can interfere with the control of ARX expression in the developing brain. Here, we review the structural features of 15 gain copy-number variants …

MaleTranscription FactorUltraconserved enhancersIntellectual disability3D structureCatalysisInorganic ChemistryMiceAnimalsHumansPhysical and Theoretical ChemistryChildMolecular BiologySpectroscopyHomeodomain ProteinsAnimalKDM5C-SYN1 axiOrganic ChemistryKDM5C-SYN1 axisGenes HomeoboxHomeodomain ProteinGeneral MedicineXp21.3 duplicationComputer Science ApplicationsUltraconserved enhancerSettore MED/03 - Genetica MedicaMutationARXHumanTranscription Factors
researchProduct

Lysosomal Signaling Licenses Embryonic Stem Cell Differentiation via Inactivation of Tfe3

2019

International audience; Self-renewal and differentiation of pluripotent murine embryonic stem cells (ESCs) is regulated by extrinsic signaling pathways. It is less clear whether cellular metabolism instructs developmental progression. In an unbiased genome-wide CRISPR/Cas9 screen, we identified components of a conserved amino-acid-sensing pathway as critical drivers of ESC differentiation. Functional analysis revealed that lysosome activity, the Ragulator protein complex, and the tumor-suppressor protein Folliculin enable the Rag GTPases C and D to bind and seclude the bHLH transcription factor Tfe3 in the cytoplasm. In contrast, ectopic nuclear Tfe3 represses specific developmental and met…

MaleTranscription GeneticGTPaseGTP PhosphohydrolasesPATHWAYMice0302 clinical medicineNeural Stem CellsCRISPRTUMOR-SUPPRESSORCell Self RenewalPhosphorylationSPECIFICATIONdevelopmental disorder0303 health sciencesGenomeBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell DifferentiationMouse Embryonic Stem CellsFlcndifferentiationCell biologymedicine.anatomical_structuremTORMolecular MedicineFemaleSignal transductionProtein BindingSignal TransductionRECRUITMENTBiology03 medical and health sciencesRag GTPasesLysosomeGeneticsmedicineAnimalsHumansPoint MutationNAIVE PLURIPOTENCYAMINO-ACID LEVELSTranscription factorAllelesPI3K/AKT/mTOR pathway030304 developmental biologyCOMPLEXFOLLICULINRagulatorCell Biologypluripotencyembryonic stem cellEmbryonic stem cellTfe3[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsCytoplasmLysosomes030217 neurology & neurosurgeryCell Stem Cell
researchProduct

Mandibular-pelvic-patellar syndrome (mpp) is a novel pitx1-related disorder due to alteration of pitx1 transactivation ability

2020

International audience; PITX1 is a homeobox transcription factor essential for hindlimb morphogenesis. Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a "lower limb" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We report two novel PITX1 missense variants, altering PITX1 transactivation ability, in three individuals from two unrelated families showing a distinct recognizable autosomal dominant syndrome, including first branchial arch, pelvic, patellar, and male genital abnormaliti…

MaleTranscriptional ActivationPathologymedicine.medical_specialtyHindlimb morphogenesis[SDV]Life Sciences [q-bio]Mutation MissensepelvisBiologyPierre-Robin03 medical and health sciencesTransactivationGeneticsmedicineMissense mutationAnimalsHumansPaired Box Transcription FactorsChildPITX1Genetics (clinical)030304 developmental biologyMice Knockoutcleft palate0303 health sciencesBone Diseases Developmental030305 genetics & heredityPreaxial polydactylyInfant NewbornLiebenberg syndromemedicine.disease3. Good healthgenitalpatella[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolHomeoboxEctopic expressionHaploinsufficiency
researchProduct

Gain of MYCN region in a Wilms tumor-derived xenotransplanted cell line.

2010

Wilms tumor is one of the most common pediatric malignant tumors of the kidney. Although the WT1 gene, located at 11p13, has been proven to be implicated in the development of Wilms tumor, other genes such as MYCN are also involved. The purpose of this study is to genetically characterize a Wilms tumor metastasis xenotransplanted in nude mice. Immunogenotype evolution of the xenografts material was monitored for 29 months using molecular techniques, fluorescent in situ hybridization and multiplex ligation-dependent probe amplification, in addition to immunohistochemistry in tissue microarrays. Genetic alterations present in the original tumor and retained in the xenotransplanted tumor were …

MaleTransplantation HeterologousMice NudeIn situ hybridizationBiologyN-Myc Proto-Oncogene ProteinWilms TumorPathology and Forensic MedicineMetastasisExonMiceINDEL MutationmedicineAnimalsHumansneoplasmsMolecular BiologyIn Situ Hybridization FluorescenceOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarrayNuclear ProteinsWilms' tumorCell BiologyNucleic acid amplification techniquemedicine.diseaseMolecular biologyImmunohistochemistryTransplantationChild PreschoolNucleic Acid Amplification TechniquesDiagnostic molecular pathology : the American journal of surgical pathology, part B
researchProduct

Anaplastic Wilms' tumour, a subtype displaying poor prognosis, harbours p53 gene mutations

1994

The genetics of Wilms' tumour (WT), a paediatric malignancy of the kidney, is complex. Inactivation of the tumour suppressor gene, WT1, is associated with tumour aetiology in approximately 10-15% of WTs. Chromosome 17p changes have been noted in cytogenetic studies of WTs, prompting us to screen 140 WTs for p53 mutations. When histopathology reports were available, p53 mutations were present in eight of eleven anaplastic WTs, a tumour subtype associated with poor prognosis. Amplification of MDM2, a gene whose product binds and sequesters p53, was excluded. Our results indicate that p53 alterations provide a molecular marker for anaplastic WTs.

MaleTumor suppressor geneDNA Mutational AnalysisMolecular Sequence DataGene mutationBiologyMalignancymedicine.disease_causePolymerase Chain ReactionWilms TumorProto-Oncogene ProteinsGeneticsmedicineHumansAmino Acid SequenceGeneAllelesMutationBase SequencefungiNuclear ProteinsCell DifferentiationProto-Oncogene Proteins c-mdm2Wilms' tumorGenes p53Prognosismedicine.diseaseKidney NeoplasmsNeoplasm ProteinsGene Expression Regulation Neoplasticbody regionsGenetic markerbiology.proteinCancer researchMdm2FemaleTumor Suppressor Protein p53Nature Genetics
researchProduct