Search results for " genetica"

showing 10 items of 659 documents

CHCH10 mutations in an Italian cohort of familial and sporadic amyotrophic lateral sclerosis patients

2015

Mutations in CHCHD10 have recently been described as a cause of frontotemporal dementia (FTD) comorbid with amyotrophic lateral sclerosis (ALS). The aim of this study was to assess the frequency and clinical characteristics of CHCHD10 mutations in Italian patients diagnosed with familial (n= 64) and apparently sporadic ALS (n= 224). Three apparently sporadic patients were found to carry c.100C>T (p.Pro34Ser) heterozygous variant in the exon 2 of CHCHD10. This mutation had been previously described in 2 unrelated French patients with FTD-ALS. However, our patients had a typical ALS, without evidence of FTD, cerebellar or extrapyramidal signs, or sensorineural deficits. We confirm that CHC…

MaleAgingPediatricsmedicine.medical_specialtyPathologyAmyotrophic lateral sclerosis; CHCHD10; Familial; Sporadic; Aged; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Frontotemporal Dementia; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Mitochondrial Proteins; Genetic Association Studies; MutationGenetic Association StudieDiseaseSettore MED/03 - GENETICA MEDICAmedicine.disease_causeCohort StudiesMitochondrial ProteinsExonFamilialmental disordersmedicineHumansMitochondrial ProteinDementiaGenetic Predisposition to DiseaseAmyotrophic lateral sclerosisAmyotrophic lateral sclerosis; CHCHD10; Familial; Sporadic; Aged; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Frontotemporal Dementia; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Mitochondrial Proteins; Genetic Association Studies; Mutation; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyGenetic Association StudiesAmyotrophic lateral sclerosiAgedMutationNeuroscience (all)business.industryGeneral NeuroscienceMiddle AgedAmyotrophic lateral sclerosisSporadicmedicine.disease3. Good healthAmyotrophic lateral sclerosis; CHCHD10; Familial; SporadicCHCHD10ItalyFrontotemporal DementiaMutationCohortFemaleNeurology (clinical)Cohort StudieGeriatrics and GerontologybusinessHumanDevelopmental BiologyFrontotemporal dementiaCohort studyNeurobiology of Aging
researchProduct

FUS MUTATIONS IN SPORADIC AMYOTROPHIC LATERAL SCLEROSIS: CLINICAL AND GENETIC ANALYSIS

2012

Fused in sarcoma (FUS) or translocation in liposarcoma (TLS), a DNA/RNA-binding protein, causes a dominant autosomal inherited form of amyotrophic lateral sclerosis (ALS), ALS 6. Its main role in neurodegeneration is highlighted by the presence of cytoplasmic accumulation of its mutant protein form in ALS patients. To further define the frequency and spectrum of FUS gene mutations, we have performed a molecular screening of a cohort of 327 Italian patients from Southern Italy with sporadic ALS (SALS). We identified 4 patients carrying 3 different missense mutations and several polymorphisms. Two different substitutions occurring in the same amino acidic position have been observed in 2 pati…

MaleAgingPopulationDNA Mutational AnalysisBiologyGene mutationmedicine.disease_causeGenetic analysisFUS geneMutant proteinALS; FUS gene; mutation; sporadicmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmyotrophic lateral sclerosiseducationAgedGeneticsAged 80 and overNeurologic ExaminationMutationeducation.field_of_studyGeneral NeuroscienceNeurodegenerationAmyotrophic Lateral SclerosisExonsMiddle AgedALS; FUS gene; Mutation; Sporadicmedicine.diseaseMagnetic Resonance ImagingSettore BIO/18 - GeneticasporadicMutationRNA-Binding Protein FUSFemaleSettore MED/26 - NeurologiaNeurology (clinical)ALSGeriatrics and GerontologyDevelopmental Biology
researchProduct

C9ORF72 hexanucleotide repeat expansions in the Italian sporadic ALS population.

2012

It has been recently reported that a large proportion of patients with familial amyotrophic lateral sclerosis (familial ALS) and frontotemporal dementia (FTD) are associated with a hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72. We have assessed 1,757 Italian sporadic ALS cases, 133 from Sardinia, 101 from Sicily, and 1,523 from mainland Italy. Sixty (3.7%) of 1,624 mainland Italians and Sicilians and 9 (6.8%) of the 133 Sardinian sporadic ALS cases carried the pathogenic repeat expansion. None of the 619 regionally-matched control samples (1,238 chromosomes) carried the expansion. Twenty-five cases (36.2%) had behavioral FTD in addition to ALS. FTD or unspecified d…

MaleAgingSurvivalPedigree chartSettore MED/03 - GENETICA MEDICARepetitive Sequences0302 clinical medicineC9orf72Polymorphism (computer science)Risk FactorsPrevalenceAmyotrophic lateral sclerosisGenetics0303 health scienceseducation.field_of_studyGeneral NeuroscienceSingle NucleotideMiddle Aged3. Good healthSettore MED/26 - NEUROLOGIAItalyFemaleSettore MED/26 - NeurologiaFrontotemporal dementiaFrontotemporal dementiaGenetic MarkersPopulationC9ORF72BiologyPolymorphism Single NucleotideArticle03 medical and health sciencesmedicineHumansGenetic Predisposition to DiseasePolymorphismeducationamyotrophic lateral sclerosis; C9orf672; frontotemporal dementia; survivalAmyotrophic lateral sclerosi030304 developmental biologyRepetitive Sequences Nucleic AcidAmyotrophic lateral sclerosis; C9ORF72; sporadicC9orf72 ProteinNucleic AcidAmyotrophic lateral sclerosis C9ORF72 Frontotemporal dementia SurvivalGenetic VariationProteinsmedicine.diseaseAmyotrophic lateral sclerosisC9orf672C9orf72 ProteinAmyotrophic lateral sclerosis; C9ORF72; Frontotemporal dementia; Survival;Settore BIO/18 - GeneticasporadicNeurology (clinical)Geriatrics and GerontologyALSTrinucleotide repeat expansion030217 neurology & neurosurgeryDevelopmental Biology
researchProduct

HFE p.H63D polymorphism does not influence ALS phenotype and survival.

2015

It has been recently reported that the p.His63Asp polymorphism of the HFE gene accelerates disease progression both in the SOD1 transgenic mouse and in amyotrophic lateral sclerosis (ALS) patients. We have evaluated the effect of HFE p.His63Asp polymorphism on the phenotype in 1351 Italian ALS patients (232 of Sardinian ancestry). Patients were genotyped for the HFE p.His63Asp polymorphism (CC, GC, and GG). All patients were also assessed for C9ORF72, TARDBP, SOD1, and FUS mutations. Of the 1351 ALS patients, 363 (29.2%) were heterozygous (GC) for the p.His63Asp polymorphism and 30 (2.2%) were homozygous for the minor allele (GG). Patients with CC, GC, and GG polymorphisms did not significa…

MaleAgingSurvivalSettore MED/03 - GENETICA MEDICAMiceSuperoxide Dismutase-1C9orf72HFE polymorphismAmyotrophic lateral sclerosisAmyotrophic lateral sclerosis; HFE polymorphisms; Phenotype; SOD1; Survival; Aged; Alleles; Amyotrophic Lateral Sclerosis; Animals; Disease Progression; Female; Hemochromatosis Protein; Histocompatibility Antigens Class I; Humans; Italy; Male; Membrane Proteins; Mice; Middle Aged; Polymorphism Genetic; Superoxide Dismutase; Superoxide Dismutase-1; Survival Rate; Genetic Association Studies; PhenotypeHFE polymorphismsMembrane ProteinAlleleAmyotrophic lateral sclerosis; HFE polymorphisms; Phenotype; SOD1; Survival; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyGeneral NeuroscienceSOD1Middle AgedPhenotypeSurvival RatePhenotypeItalyAmyotrophic lateral sclerosis; HFE polymorphisms; SOD1; phenotype; survivalDisease ProgressionFemaleHumanmedicine.medical_specialtySOD1Amyotrophic lateral sclerosis; HFE polymorphisms; Phenotype; SOD1; Survival;Genetic Association StudieBiologyTARDBPArticleGeneticInternal medicinemedicineAnimalsHumansAllelePolymorphismHemochromatosis ProteinSurvival rateAmyotrophic lateral sclerosiAllelesGenetic Association StudiesAgedNeuroscience (all)Polymorphism GeneticAnimalSuperoxide DismutaseAmyotrophic Lateral SclerosisHistocompatibility Antigens Class Inutritional and metabolic diseasesMembrane Proteinsmedicine.diseaseMinor allele frequencyEndocrinologyImmunologyNeurology (clinical)Geriatrics and GerontologyDevelopmental BiologyNeurobiology of aging
researchProduct

Altered lipid metabolism in a Drosophila model of Friedreich's ataxia

2010

13 páginas, 5 figuras.-- et al.

MaleAtaxiaCell SurvivalLipid Metabolism Disordersmedicine.disease_causeNervous SystemAnimals Genetically ModifiedLipid peroxidationchemistry.chemical_compoundDownregulation and upregulationIron-Binding ProteinsLipid dropletGeneticsmedicineAnimalsDrosophila ProteinsHumansMolecular BiologyGenetics (clinical)Membrane GlycoproteinsbiologyCélulas glialesFatty AcidsLipid metabolismArticlesGeneral MedicineCell biologyDisease Models AnimalOxidative Stressmedicine.anatomical_structurechemistryBiochemistryFriedreich AtaxiaFrataxinbiology.proteinNeurogliaDrosophilaLipid Peroxidationmedicine.symptomCarrier ProteinsNeurogliaOxidative stress
researchProduct

A new p65 isoform that bind the glucocorticoid hormone and is expressed in inflammation liver diseases and COVID-19

2021

AbstractInflammation is a physiological process whose deregulation causes some diseases including cancer. Nuclear Factor kB (NF-kB) is a family of ubiquitous and inducible transcription factors, in which the p65/p50 heterodimer is the most abundant complex, that play critical roles mainly in inflammation. Glucocorticoid Receptor (GR) is a ligand-activated transcription factor and acts as an anti-inflammatory agent and immunosuppressant. Thus, NF-kB and GR are physiological antagonists in the inflammation process. Here we show that in mice and humans there is a spliced variant of p65, named p65 iso5, which binds the corticosteroid hormone dexamethasone amplifying the effect of the glucocorti…

MaleCOVID-19.Molecular biologyGene ExpressionDexamethasoneHepatitisMiceGlucocorticoid receptorAdrenal Cortex HormonesProtein IsoformsNF-kBMultidisciplinaryLiver DiseasesQLiver NeoplasmsRNF-kappa BMiddle AgedLiverMedicineFemalemedicine.symptomliver diseaseTranscriptionNFKB P65iso5 inflammationGlucocorticoidmedicine.drugAdultGene isoformCarcinoma HepatocellularScienceImmunologyInflammationBiologyGlucocorticoid ReceptorArticleReceptors GlucocorticoidmedicineAnimalsHumansGlucocorticoidsTranscription factorDexamethasoneInflammationSARS-CoV-2p65 isoformTranscription Factor RelAWild typeCOVID-19Mice Inbred C57BLAlternative SplicingSettore BIO/18 - GeneticaGene Expression RegulationLeukocytes MononuclearCancer researchHormone
researchProduct

Trans-Reactivation: A New Epigenetic Phenomenon Underlying Transcriptional Reactivation of Silenced Genes

2015

In order to study the role played by cellular RNA pools produced by homologous genomic loci in defining the transcriptional state of a silenced gene, we tested the effect of non-functional alleles of the white gene in the presence of a functional copy of white, silenced by heterochromatin. We found that non-functional alleles of white, unable to produce a coding transcript, could reactivate in trans the expression of a wild type copy of the same gene silenced by heterochromatin. This new epigenetic phenomenon of transcriptional trans-reactivation is heritable, relies on the presence of homologous RNA’s and is affected by mutations in genes involved in post-transcriptional gene silencing. Ou…

MaleCancer ResearchPEV white Trans-reactivation Epigenetics Gynogenesis ncRNAsRNA Untranslatedlcsh:QH426-470Transcription GeneticHeterochromatinSettore BIO/11 - Biologia MolecolareGenes InsectBiologySettore MED/13 - EndocrinologiaRNA interferenceSettore BIO/10 - BiochimicaHeterochromatinGene clusterGene expressionGeneticsGene silencingAnimalsDrosophila ProteinsEpigeneticsCompound Eye ArthropodEye ProteinsMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and SystematicsAllelesGeneticsEye ColorRNAlcsh:GeneticsSettore BIO/18 - GeneticaDrosophila melanogasterATP-Binding Cassette TransportersFemaleRNA InterferenceResearch ArticlePLoS Genetics
researchProduct

The first case of myoclonic epilepsy in a child with a de novo 22q11.2 microduplication

2011

Chromosome 22, particularly the q11.2 sub-band, has long been recognized as responsible for multiple congenital anomaly disorders. In particular, its susceptibility to subtle microdeletions or, more rarely, microduplications has been attributed to the presence of several low-copy repeats spanning the region as mediators of nonallelic homologous recombination that result in 22q11.2 rearrangements. While recent data suggest that the frequency of 22q11.2 microduplications could be approximately half of all deletions, now only 50 unrelated cases have been reported thus far. However, it is reasonable to suppose that microduplications of 22q11.2 may be largely undetected as a result of a less-dis…

MaleChromosomes Human Pair 22Non-allelic homologous recombinationEpilepsies MyoclonicMultiple congenital anomalyBiologyRAB36 genemyoclonic epilepsySettore MED/38 - Pediatria Generale E SpecialisticaChromosome DuplicationGene duplicationClinical heterogeneityGeneticsmedicineHumansChildIn Situ Hybridization FluorescenceGenetics (clinical)GeneticsComparative Genomic HybridizationFaciesmedicine.diseaseMild learning difficultiesdevelopmental delayPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolMyoclonic epilepsynonallelic homologous recombinationChromosome 2222q11.2 microduplicationComparative genomic hybridizationAmerican Journal of Medical Genetics Part A
researchProduct

The visual orientation memory of Drosophila requires Foraging (PKG) upstream of Ignorant (RSK2) in ring neurons of the central complex

2012

Orientation and navigation in a complex environment requires path planning and recall to exert goal-driven behavior. Walking Drosophila flies possess a visual orientation memory for attractive targets which is localized in the central complex of the adult brain. Here we show that this type of working memory requires the cGMP-dependent protein kinase encoded by the foraging gene in just one type of ellipsoid-body ring neurons. Moreover, genetic and epistatic interaction studies provide evidence that Foraging functions upstream of the Ignorant Ribosomal-S6 Kinase 2, thus revealing a novel neuronal signaling pathway necessary for this type of memory in Drosophila.

MaleCognitive NeuroscienceGreen Fluorescent ProteinsForagingBrief CommunicationRibosomal Protein S6 Kinases 90-kDaStatistics NonparametricAnimals Genetically ModifiedCellular and Molecular NeuroscienceMemoryOrientationCyclic GMP-Dependent Protein KinasesAnimalsDrosophila ProteinsProtein kinase ADrosophilaNeuronsRegulation of gene expressionMemory DisordersCommunicationBehavior AnimalbiologyRecallWorking memorybusiness.industryfungiBrainbiology.organism_classificationNeuropsychology and Physiological PsychologyGene Expression RegulationDrosophilaFemaleSignal transductionbusinessNeurosciencePhotic StimulationDrosophila ProteinSignal TransductionLearning & Memory
researchProduct

Ulnar ray defect in an infant with a 6q21;7q31.2 translocation: Further evidence for the existence of a limb defect gene in 6q21

1995

Ectrodactyly is a developmental defect of the distal limbs characterized by marked clinical variability and genetic heterogeneity, also reflected in the observation of different chromosome abnormalities non randomly associated with longitudinal postaxial limb deficiencies. The one most frequently found in patients with split hand-split foot (SHSF) involves chromosome band 7q22. Recently, structural anomalies of chromosome 6q21 have been reported in 2 unrelated patients with SHSF, suggesting that this region may also contain genes responsible for limb development [Braverman et al., 1993. Am J Hum Genet, suppl 53: 410; Viljoen and Smart, 1993. Clin Dysmorph 2: 274-277]. We report on a third p…

MaleEctrodactylyEctromeliaUlnaChromosomal translocationGene mutationBiologySettore MED/03 - GENETICA MEDICATranslocation GeneticmedicineHumansLimb developmentGenetics (clinical)Chromosome 7 (human)Genetic heterogeneityInfant NewbornChromosomeAnatomymedicine.diseaseChromosome BandingChromosome BandSPLITKaryotypingChromosomes Human Pair 6Hand Deformities CongenitalChromosomes Human Pair 7Gene DeletionAmerican Journal of Medical Genetics
researchProduct