Search results for "Trinucleotide repeat"

showing 10 items of 46 documents

The

2016

ABSTRACT Members of the Junctophilin (JPH) protein family have emerged as key actors in all excitable cells, with crucial implications for human pathophysiology. In mammals, this family consists of four members (JPH1-JPH4) that are differentially expressed throughout excitable cells. The analysis of knockout mice lacking JPH subtypes has demonstrated their essential contribution to physiological functions in skeletal and cardiac muscles and in neurons. Moreover, mutations in the human JPH2 gene are associated with hypertrophic and dilated cardiomyopathies; mutations in JPH3 are responsible for the neurodegenerative Huntington's disease-like-2 (HDL2), whereas JPH1 acts as a genetic modifier …

NotchGenotypeCardiomyopathyGenes InsectAnimals Genetically ModifiedAnimalsDrosophila ProteinsAllelesMammalsNeuronsHuntingtin ProteinReceptors NotchMusclesMyocardiumMembrane ProteinsReproducibility of ResultsDrosHuntington's diseaseDisease Models AnimalDrosophila melanogasterPhenotypeGene Knockdown TechniquesMutationNerve DegenerationPhotoreceptor Cells InvertebrateRNA InterferenceJunctophilinDrosophilaTrinucleotide Repeat ExpansionSignal TransductionResearch ArticleDisease modelsmechanisms
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Ataxin-1 and ataxin-2 intermediate-length PolyQ expansions in amyotrophic lateral sclerosis.

2012

ABSTRACT Objective: Recent evidence suggests that intermediate-length polyglutamine (PolyQ) expansions in the ataxin-2 ( ATXN-2 ) gene are a risk factor for amyotrophic lateral sclerosis (ALS). This work was undertaken with the aim to investigate the frequency of ataxin-1 ( ATXN-1 ) and ATXN-2 PolyQ expansions in a cohort of patients with sporadic ALS (sALS) and patients with familial ALS (fALS) from southern Italy. Methods: We assessed the PolyQ lengths of ATXN-1 and ATXN-2 in 405 patients with sALS, 13 patients with fALS, and 296 unrelated controls without history of neurodegenerative disorders. Results: We found significantly higher intermediate PolyQ expansions ≥32 for ATXN-1 alleles an…

OncologyAdultMalemedicine.medical_specialtyGenotypeALS; ATXN-1; ATXN-2Ataxin 1Nerve Tissue ProteinsRisk FactorsInternal medicinemedicineHumansIn patientGenetic Predisposition to DiseaseAmyotrophic lateral sclerosisAlleleRisk factorAge of OnsetATXN-2ATXN-1AllelesAtaxin-1AgedAged 80 and overbiologybusiness.industryAmyotrophic Lateral SclerosisAge FactorsNuclear ProteinsMiddle Agedmedicine.diseaseIncreased riskPOLYGLUTAMINE EXPANSIONS; HEXANUCLEOTIDE REPEAT; ALS; TYPE-1; NEURODEGENERATION; PHENOTYPE; GENETICS; PROTEIN; C9ORF72; RISKAtaxinsItalyAtaxinCohortbiology.proteinFemaleSettore MED/26 - NeurologiaNeurology (clinical)ALSbusinessPeptidesTrinucleotide Repeat Expansion
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Drosophila Muscleblind Is Involved in troponin T Alternative Splicing and Apoptosis

2008

Background: Muscleblind-like proteins (MBNL) have been involved in a developmental switch in the use of defined cassette exons. Such transition fails in the CTG repeat expansion disease myotonic dystrophy due, in part, to sequestration of MBNL proteins by CUG repeat RNA. Four protein isoforms (MblA-D) are coded by the unique Drosophila muscleblind gene. Methodology/Principal Findings: We used evolutionary, genetic and cell culture approaches to study muscleblind (mbl) function in flies. The evolutionary study showed that the MblC protein isoform was readily conserved from nematods to Drosophila, which suggests that it performs the most ancestral muscleblind functions. Overexpression of MblC…

Protein isoformGenetics and Genomics/Animal GeneticsScienceAmino Acid MotifsRNA-binding proteinApoptosisBiology03 medical and health sciencesExon0302 clinical medicineTroponin TAnimalsDrosophila ProteinsGenetics and Genomics/Genetics of Disease030304 developmental biologyGenetics0303 health sciencesMultidisciplinaryQAlternative splicingRRNA-Binding ProteinsAlternative SplicingGenetics and Genomics/Disease ModelsRNA splicingMedicineDrosophilaTNNT3Trinucleotide Repeat Expansion030217 neurology & neurosurgeryDrosophila ProteinGenèticaMinigeneResearch Article
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Myotonic dystrophy associated expanded CUG repeat muscleblind positive ribonuclear foci are not toxic to Drosophila

2005

Myotonic dystrophy type 1 is an autosomal dominant disorder associated with the expansion of a CTG repeat in the 3 0 untranslated region (UTR) of the DMPK gene. Recent data suggest that pathogenesis is predominantly mediated by a gain of function of the mutant transcript. In patients, these expanded CUG repeat-containing transcripts are sequestered into ribonuclear foci that also contain the muscleblind-like proteins. To provide further insights into muscleblind function and the pathogenesis of myotonic dystrophy, we generated Drosophila incorporating CTG repeats in the 3 0 -UTR of a reporter gene. As in patients, expanded CUG repeats form discrete ribonuclear foci in Drosophila muscle cell…

Untranslated regioncongenital hereditary and neonatal diseases and abnormalitiesRNA StabilityProtein Serine-Threonine KinasesBiologyMyotonic dystrophyMyotonin-Protein KinaseGeneticsmedicineAnimalsHumansMyotonic Dystrophy3' Untranslated RegionsMolecular BiologyGeneGenetics (clinical)GeneticsRNAGeneral MedicineNuclear matrixbiology.organism_classificationmedicine.diseaseCell biologyRNA silencingDrosophila melanogasterRNA splicingDrosophila melanogasterTrinucleotide Repeat ExpansionHuman Molecular Genetics
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Pentamidine rescues contractility and rhythmicity in a Drosophila model of myotonic dystrophy heart dysfunction

2015

Up to 80% of individuals with myotonic dystrophy type 1 (DM1) will develop cardiac abnormalities at some point during the progression of their disease, the most common of which is heart blockage of varying degrees. Such blockage is characterized by conduction defects and supraventricular and ventricular tachycardia, and carries a high risk of sudden cardiac death. Despite its importance, very few animal model studies have focused on the heart dysfunction in DM1. Here, we describe the characterization of the heart phenotype in a Drosophila model expressing pure expanded CUG repeats under the control of the cardiomyocyte-specific driver GMH5-Gal4. Morphologically, expression of 250 CUG repeat…

[SDV]Life Sciences [q-bio]Myotonic dystrophyMedicine (miscellaneous)lcsh:MedicineVentricular tachycardiaImmunology and Microbiology (miscellaneous)DiastoleHeart RateDrosophila ProteinsMyocytes CardiacGeneticsbiologyRNuclear ProteinsHeartPhenotype3. Good healthCell biology[SDV] Life Sciences [q-bio]Drosophila melanogasterPhenotypeDrosophilaDrosophila melanogasterDrosophila ProteinResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesSystoleLongevityNeuroscience (miscellaneous)In situ hybridizationMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyMuscleblindContractilitymedicinelcsh:PathologyAnimalsPentamidineHeart dysfunctionfungilcsh:RArrhythmias Cardiacbiology.organism_classificationmedicine.diseaseMyocardial ContractionSurvival AnalysisDisease Models AnimalTrinucleotide repeat expansionTrinucleotide Repeat Expansion
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C9ORF72 in a Large Series of Italian and Sardinian Familial and Sporadic ALS Patients (IN9-1.003)

2012

Objective: To assess the frequency and the phenotype of a large series of Italian sALS and fALS with C9ORF72 repeat expansions. Background Recently we found that large expansions of hexanucleotide repeats (GGGGCC) in the first intron of the C9ORF72 gene, located in the chromosome 9p21, are related to familial and sporadic ALS cases(Renton et al, 2011). Design/Methods: We assessed 126 index fALS (106 Italians, 20 of Sardinians) and 601 sALS (485 Italians, 116 Sardinians), negative for other ALS-related genes mutations. Patients were collected through the ITALSGEN consortium. Repeat primer PCR to screen the presence of the hexanucleotide expansion in the first intron of C9ORF72 have been perf…

business.industryLarge seriesPedigree chartmedicine.diseasePenetranceC9orf72NothingAnticipation (genetics)MedicineNeurology (clinical)businessTrinucleotide repeat expansionDemographyFrontotemporal dementiaNeurology
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Genetic and Chemical Modifiers Of A CUG Toxicity Model in Drosophila

2007

Non-coding CUG repeat expansions interfere with the activity of human Muscleblind-like (MBNL) proteins contributing to myotonic dystrophy 1 (DM1). To understand this toxic RNA gain-of-function mechanism we developed a Drosophila model expressing 60 pure and 480 interrupted CUG repeats in the context of a non-translatable RNA. These flies reproduced aspects of the DM1 pathology, most notably nuclear accumulation of CUG transcripts, muscle degeneration, splicing misregulation, and diminished Muscleblind function in vivo. Reduced Muscleblind activity was evident from the sensitivity of CUG-induced phenotypes to a decrease in muscleblind genetic dosage and rescue by MBNL1 expression, and furthe…

congenital hereditary and neonatal diseases and abnormalitiesGene Dosagelcsh:MedicineRNA-binding proteinBiologyEyechemistry.chemical_compoundTrinucleotide RepeatsAnimalsDrosophila ProteinsMyotonic DystrophyMBNL1lcsh:ScienceGeneGenetics and Genomics/Genetics of DiseaseGeneticsMessenger RNADNA Repeat ExpansionMultidisciplinaryAlternative splicinglcsh:RBrainNuclear ProteinsRNA-Binding ProteinsRNAPhenotypeCell biologyDisease Models AnimalGenetics and Genomics/Disease ModelschemistryRNA splicingDrosophilalcsh:QGenèticaResearch Article
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In vivo discovery of a peptide that prevents CUG-RNA hairpin formation and reverses RNA toxicity in myotonic dystrophy models

2011

6 pages, 5 figures. PMID:21730182[PubMed] PMCID: PMC3141925[Available on 2012/1/19]

congenital hereditary and neonatal diseases and abnormalitiesProtein ConformationRNA-binding proteinProtein Serine-Threonine KinasesBiologyMyotonic dystrophyMyotonin-Protein Kinasedrug discoveryMicechemistry.chemical_compoundnon-coding RNA diseasePeptide Librarymedicinal chemistryDrug DiscoveryGene expressionmedicineAnimalsMyotonic DystrophyMBNL1MultidisciplinaryMusclesdisease modelAlternative splicingRNA-Binding ProteinsRNADystrophyBiological Sciencesmedicine.diseaseRNA secondary structureMolecular biologyDNA-Binding ProteinschemistryRNA splicingDrosophilaTrinucleotide Repeat ExpansionOligopeptides
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Correction: Daunorubicin reduces MBNL1 sequestration caused by CUG-repeat expansion and rescues cardiac dysfunctions in a Drosophila model of myotoni…

2018

ABSTRACT Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant myotonin-protein kinase (DMPK) transcripts containing expanded CUG repeats. Pathogenic DMPK RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations in metabolism of various RNAs. Cardiac dysfunction represents the second most common cause of death in DM type 1 (DM1) patients. However, the contribution of MBNL sequestration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), the Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resem…

congenital hereditary and neonatal diseases and abnormalitiesRNA StabilityNeuroscience (miscellaneous)Medicine (miscellaneous)MuscleblindGeneral Biochemistry Genetics and Molecular BiologyImmunology and Microbiology (miscellaneous)AnimalsDrosophila ProteinsMyotonic DystrophyMyocytes CardiacRNA MessengerDaunorubicinCorrectionNuclear ProteinsReproducibility of ResultsHeartSurvival AnalysisAlternative SplicingDisease Models AnimalDrosophila melanogasterTrinucleotide repeat disorderDrosophilaTrinucleotide Repeat ExpansionResearch ArticleProtein BindingDisease Models & Mechanisms
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Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model

2015

ABSTRACT Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apopto…

lcsh:MedicineMedicine (miscellaneous)Genes InsectApoptosisDystrophyInhibitor of Apoptosis ProteinsAnimals Genetically ModifiedCTG repeat expansion0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsMyotonic DystrophyMyocyte0303 health sciencesTOR Serine-Threonine KinasesMyotonin-protein kinaseNuclear ProteinsMuscle atrophyUp-RegulationCell biologyMuscular AtrophyDrosophila melanogastermedicine.anatomical_structureFemalemedicine.symptomSignal TransductionResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathNeuroscience (miscellaneous)BiologyMyotonic dystrophyMyotonin-Protein KinaseMuscleblindGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAutophagylcsh:PathologymedicineAnimalsHumans030304 developmental biologylcsh:RAutophagyDystrophySkeletal musclemedicine.diseaseMolecular biologyDisease Models AnimalMuscle atrophyTrinucleotide Repeat Expansion030217 neurology & neurosurgeryDisease Models & Mechanisms
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