Search results for "Minigene"

showing 10 items of 13 documents

Homozygous familial hypobetalipoproteinemia: two novel mutations in the splicing sites of apolipoprotein B gene and review of the literature.

2015

Objective: Familial hypobetalipoproteinemia (FHBL) is autosomal codominant disorder of lipoprotein metabolism characterized by low plasma levels of total cholesterol (TC), low-density lipoproteincholesterol (LDL-C) and apolipoprotein B (apoB) below the 5 th percentile of the distribution in the population. Patients with the clinical diagnosis of homozygous FHBL (Ho-FHBL) are extremely rare and few patients have been characterized at the molecular level. Here we report the medical history and the molecular characterization of one paediatric patient with clinical features of Ho-FHBL. Methods: A one month old infant with failure to thrive, severe hypocholesterolemia and acanthocytosis was clin…

ProbandAdultMaleAcanthocytosiSettore MED/09 - Medicina InternaApolipoprotein BPopulationDNA Mutational AnalysisBiologyHypobetalipoproteinemiasExonHumanseducationGeneGeneticseducation.field_of_studyHomozygoteIntronInfantCholesterol LDLAbetalipoproteinemiaIntronsAlternative SplicingHomozygous familial hypobetalipoproteinemiaCholesterolRNA splicingApolipoprotein B-100Mutationbiology.proteinlipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineApolipoprotein BMinigeneAtherosclerosis
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Muscleblind isoforms are functionally distinct and regulate α-actinin splicing

2007

Drosophila Muscleblind (Mbl) proteins control terminal muscle and neural differentiation, but their molecular function has not been experimentally addressed. Such an analysis is relevant as the human Muscleblind-like homologs (MBNL1-3) are implicated in the pathogenesis of the inherited muscular developmental and degenerative disease myotonic dystrophy. The Drosophila muscleblind gene expresses four protein coding splice forms (mblA to mblD) that are differentially expressed during the Drosophila life cycle, and which vary markedly in their ability to rescue the embryonic lethal phenotype of muscleblind mutant flies. Analysis of muscleblind mutant embryos reveals misregulated alternative sp…

Gene isoformCancer ResearchMolecular Sequence DataBiologyKidneyChlorocebus aethiopsAnimalsDrosophila ProteinsHumansProtein IsoformsActininMuscle Skeletal3' Untranslated RegionsMolecular BiologyGeneCells CulturedCell NucleusGeneticsBase SequenceAlternative splicingGene Expression Regulation DevelopmentalNuclear ProteinsRNA-Binding ProteinsRNAKidney metabolismCell BiologyAlternative SplicingDrosophila melanogasterCOS CellsMutationRNA splicingTrinucleotide Repeat ExpansionTrinucleotide repeat expansionDevelopmental BiologyMinigeneDifferentiation
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Extensive molecular analysis of patients bearing CFTR-related disorders.

2012

Cystic fibrosis transmembrane conductance regulator (CFTR)–related disorders (CFTR-RDs) may present with pancreatic sufficiency, normal sweat test results, and better outcome. The detection rate of mutations is lower in CFTR-RD than in classic CF: mutations may be located in genes encoding proteins that interact with CFTR or support channel activity. We tested the whole CFTR coding regions in 99 CFTR-RD patients, looking for gene mutations in solute carrier (SLC) 26A and in epithelial Na channel (ENaC) in 33 patients who had unidentified mutations. CFTR analysis revealed 28 mutations, some of which are rare. Of these mutations, RT-PCR demonstrated that the novel 1525-1delG impairs exon 10 s…

Epithelial sodium channelcongenital hereditary and neonatal diseases and abnormalitiesCystic fibrosis CFTR SLC26A SCNNCystic FibrosisAnion Transport ProteinsDNA Mutational Analysismolecular analysiCystic Fibrosis Transmembrane Conductance RegulatorGene mutationPathology and Forensic Medicinecongenital bilateral absence of vasa deferentesExonGene Frequencydisseminated bronchiectasiscongenital bilateral absence of vasa deferenteHumansTrypsinmolecular analysisEpithelial Sodium ChannelsGeneCells CulturedGenetic Association StudiesGeneticsbiologydisseminated bronchiectasiEpithelial Cellsrespiratory systemrecurrent pancreatitidigestive system diseasesCystic fibrosis transmembrane conductance regulatorrespiratory tract diseasesSolute carrier familyCFTR related disordersTrypsin Inhibitor Kazal PancreaticCase-Control StudiesRNA splicingMutationbiology.proteinMolecular MedicineCFTR related disorderSLC26 familyCarrier ProteinsNa channel ENaCMinigenerecurrent pancreatitis
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Functional analyses of a novel splice variant in the CHD7 gene, found by next generation sequencing, Confirm Its pathogenicity in a Spanish patient a…

2018

Mutations in CHD7 have been shown to be a major cause of CHARGE syndrome, which presents many symptoms and features common to other syndromes making its diagnosis difficult. Next generation sequencing (NGS) of a panel of intellectual disability related genes was performed in an adult patient without molecular diagnosis. A splice donor variant in CHD7 (c.5665 + 1G > T) was identified. To study its potential pathogenicity, exons and flanking intronic sequences were amplified from patient DNA and cloned into the pSAD® splicing vector. HeLa cells were transfected with this construct and a wild-type minigene and functional analysis were performed. The construct with the c.5665 + 1G > T variant p…

0301 basic medicinelcsh:QH426-470BiologyDNA sequencingCHD703 medical and health sciencesExonalternative splicing0302 clinical medicineNext generation sequencingGeneticsspliceminigeneGeneGenetics (clinical)Geneticsnext generation sequencingCHARGE syndromeAlternative splicingIntron3. Good healthlcsh:Genetics030104 developmental biology030220 oncology & carcinogenesisRNA splicingMolecular MedicineMinigeneAlternative splicing
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Development of aDrosophila melanogasterspliceosensor system forin vivohigh-throughput screening in myotonic dystrophy type 1

2014

AbstractAlternative splicing of pre-mRNAs is an important mechanism that regulates cellular function in higher eukaryotes. A growing number of human genetic diseases involve splicing defects that are directly connected to their pathology. In myotonic dystrophy type 1 (DM1), several clinical manifestations have been proposed to be the consequence of tissue-specific missplicing of numerous genes. These events are triggered by an RNA gain-of-function and resultant deregulation of specific RNA-binding factors, such as the nuclear sequestration of muscleblind-like family factors (MBNL1-MBNL3). Thus, the identification of chemical modulators of splicing events could lead to the development of the…

Myotonic dystrophyNeuroscience (miscellaneous)lcsh:MedicineMedicine (miscellaneous)BiologySplicingMyotonic dystrophyGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundMinigeneImmunology and Microbiology (miscellaneous)lcsh:PathologymedicineAnimalsMBNL1Resource ArticleGeneGeneticsDrug discoverylcsh:RAlternative splicingmedicine.diseasebiology.organism_classificationHigh-Throughput Screening AssaysAlternative SplicingDrosophila melanogasterchemistryIn vivo screeningRNA splicingDrosophila melanogasterLuciferaselcsh:RB1-214MinigeneDisease Models & Mechanisms
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Study of USH1 Splicing Variants through Minigenes and Transcript Analysis from Nasal Epithelial Cells

2012

Usher syndrome type I (USH1) is an autosomal recessive disorder characterized by congenital profound deafness, vestibular areflexia and prepubertal retinitis pigmentosa. The first purpose of this study was to determine the pathologic nature of eighteen USH1 putative splicing variants found in our series and their effect in the splicing process by minigene assays. These variants were selected according to bioinformatic analysis. The second aim was to analyze the USH1 transcripts, obtained from nasal epithelial cells samples of our patients, in order to corroborate the observed effect of mutations by minigenes in patient’s tissues. The last objective was to evaluate the nasal ciliary beat fre…

Usher syndromelcsh:Medicinemedicine.disease_causeGene SplicingMolecular cell biologyAutosomal Recessivelcsh:ScienceGeneticsMutationMultidisciplinaryCadherinsMyosin VIIaRNA splicingSensory PerceptionUsher SyndromesResearch ArticleRNA SplicingCadherin Related ProteinsBiologyMyosinsNoseGenetic MutationRetinitis pigmentosamedicineGeneticsotorhinolaryngologic diseasesHumansCiliaBiologyMessenger RNAlcsh:RIntronMutation TypesComputational BiologyGenetic VariationEpithelial CellsHuman Geneticsmedicine.diseaseMolecular biologyRNA processingMutagenesisCase-Control StudiesMutationGenetics of Diseaselcsh:QGene expressionSensory DeprivationPCDH15MinigeneCloningNeuroscience
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Novel mutations of CETP gene in Italian subjects with hyeralphalipoproteinemia

2009

Abstract Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that catalyses the transfer of cholesteryl esters from HDL to the other plasma lipoproteins. Genetic deficiency of CETP is one of the known causes of elevation of plasma HDL-C (primary hyperalphalipoproteinemia, HALP). We sequenced CETP gene in a group of 24 Italian subjects with primary HALP (HDL-C>80 mg/dl) suspected to have CETP deficiency. Two unrelated subjects both coming from the same geographical district, were found to be heterozygous for a nucleotide substitution in exon 6 (c.544C>T) and another subject was found to be heterozygous for a C>T transition in exon 9 (c.802C>T). Both mutations introduce a prema…

MaleHyperlipoproteinemiasMessengerDNA Mutational Analysismedicine.disease_causeExonFamilial hyperalphalipoproteinemiaChlorocebus aethiopsCETP activity; CETP gene mutations; Familial hyperalphalipoproteinemia; HDL size; Adolescent; Adult; Aged; Animals; Biomarkers; COS Cells; Cercopithecus aethiops; Cholesterol Ester Transfer Proteins; Cholesterol HDL; DNA Mutational Analysis; European Continental Ancestry Group; Female; Humans; Hyperlipoproteinemias; Italy; Male; Middle Aged; Phenotype; RNA Messenger; Transfection; Up-Regulation; Young Adult; Mutation; Cardiology and Cardiovascular MedicineGeneticsMutationTransition (genetics)biologyCETP activityMiddle AgedUp-RegulationCholesterolPhenotypeItalyCOS CellsRNA splicingFemaleFamilial hyperalphalipoproteinemia; CETP gene mutations; CETP activity; HDL sizelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultHDLAdolescentEuropean Continental Ancestry GroupSocio-culturaleHDL sizeTransfectionWhite PeopleCercopithecus aethiopsYoung AdultCETP gene mutationsCholesterylester transfer proteinmedicineAnimalsHumansRNA MessengerGeneAgedCholesterol HDLIntroncetpCholesterol Ester Transfer Proteinscarbohydrates (lipids)biology.proteinRNAmutationBiomarkersMinigene
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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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Haploinsufficiency of ARFGEF1 is associated with developmental delay, intellectual disability, and epilepsy with variable expressivity

2021

PURPOSE: ADP ribosylation factor guanine nucleotide exchange factors (ARFGEFs) are a family of proteins implicated in cellular trafficking between the Golgi apparatus and the plasma membrane through vesicle formation. Among them is ARFGEF1/BIG1, a protein involved in axon elongation, neurite development, and polarization processes. ARFGEF1 has been previously suggested as a candidate gene for different types of epilepsies, although its implication in human disease has not been well characterized.METHODS: International data sharing, in silico predictions, and in vitro assays with minigene study, western blot analyses, and RNA sequencing.RESULTS: We identified 13 individuals with heterozygous…

0301 basic medicineGeneticsCandidate geneHeterozygoteEpilepsyADP ribosylation factorIn silicoHeterozygote advantageHaploinsufficiency030105 genetics & heredityBiologymedicine.disease03 medical and health sciencesEpilepsy030104 developmental biologyIntellectual DisabilitymedicineGuanine Nucleotide Exchange FactorsHumansGuanine nucleotide exchange factorHaploinsufficiencyGenetics (clinical)MinigeneGenetics in Medicine
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Mutational screening of the USH2A gene in Spanish USH patients reveals 23 novel pathogenic mutations

2011

Abstract Background Usher Syndrome type II (USH2) is an autosomal recessive disorder, characterized by moderate to severe hearing impairment and retinitis pigmentosa (RP). Among the three genes implicated, mutations in the USH2A gene account for 74-90% of the USH2 cases. Methods To identify the genetic cause of the disease and determine the frequency of USH2A mutations in a cohort of 88 unrelated USH Spanish patients, we carried out a mutation screening of the 72 coding exons of this gene by direct sequencing. Moreover, we performed functional minigene studies for those changes that were predicted to affect splicing. Results As a result, a total of 144 DNA sequence variants were identified.…

AdultMaleSequence VariantsAdolescentGenotypegenetic structuresUsher syndromeDNA Mutational AnalysisMutation Missenselcsh:MedicineBiologymedicine.disease_causeExonYoung AdultUSH2ARetinitis pigmentosaGenotypemedicineotorhinolaryngologic diseasesHumansGenetics(clinical)Pharmacology (medical)<it>USH2A</it>GeneAllele frequencyGenetics (clinical)GeneticsMedicine(all)MutationExtracellular Matrix ProteinsResearchlcsh:RGeneral MedicineExonsMiddle Agedmedicine.diseaseeye diseasesPhenotypeSpainMutationFemalesense organsUsher SyndromeUsher SyndromesMutationsMinigeneOrphanet Journal of Rare Diseases
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