Search results for "Splicing"

showing 10 items of 235 documents

Conserved alternative splicing in the 5'-untranslated region of the muscle-specific enolase gene. Primary structure of mRNAs, expression and influenc…

1995

We report here the isolation and characterization of cDNAs covering the 5'-end region of mouse and rat mRNAs that encode the beta or muscle-specific isoform of the glycolytic enzyme enolase. As previously determined for humans, two classes of beta-enolase transcripts with distinct sequences in their 5'-untranslated regions are present in both mouse and rat muscles. A mechanism of alternative splicing, conserved from mouse to man, generates the two forms of mRNA. Secondary-structure predictions indicated that, in all cases, a more stable secondary structure could exist in the 5' end of the message with the longer leader. In vitro transcripts containing defined human or mouse 5'-untranslated …

Untranslated regionGene isoformFive prime untranslated regionMolecular Sequence DataBiologyBiochemistryMicePolysomeComplementary DNAAnimalsHumansRNA MessengerMuscle SkeletalGeneConserved SequenceMessenger RNABase SequenceMolecular StructureAlternative splicingMolecular biologyRatsAlternative SplicingPhosphopyruvate HydrataseProtein BiosynthesisRabbitsSequence AlignmentEuropean journal of biochemistry
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The KH-type splicing regulatory protein (KSRP) regulates type III interferon expression post-transcriptionally.

2019

Abstract Type III interferons (IFNs) are the latest members of the IFN family. They play an important role in immune defense mechanisms, especially in antiviral responses at mucosal sites. Moreover, they control inflammatory reactions by modulating neutrophil and dendritic cell functions. Therefore, it is important to identify cellular mechanisms involved in the control of type III IFN expression. All IFN family members contain AU-rich elements (AREs) in the 3′-untranslated regions (3′-UTR) of their mRNAs that determine mRNA half-life and consequently the expressional level of these cytokines. mRNA stability is controlled by different proteins binding to these AREs leading to either stabili…

Untranslated regionImmunoprecipitationRNA SplicingBiochemistry03 medical and health sciencesMice0302 clinical medicineInterferonCell Line TumormedicineAnimalsHumansHeterogeneous Nuclear Ribonucleoprotein D0Heterogeneous-Nuclear Ribonucleoprotein DMolecular Biology3' Untranslated Regions030304 developmental biologyRegulation of gene expressionMice Knockout0303 health sciencesMessenger RNABinding SitesChemistryRNA-Binding ProteinsCell BiologyDendritic cellCell biology030220 oncology & carcinogenesisRNA splicingTrans-ActivatorsInterferonsFunction (biology)medicine.drugThe Biochemical journal
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Design of novel small molecule base-pair recognizers of toxic CUG RNA transcripts characteristics of DM1.

2020

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Untranslated regioncongenital hereditary and neonatal diseases and abnormalitiesBase pairMyotonic dystrophyBiophysicsComputational biologyBase recognitionBiologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineStructural BiologyRNA targetingGeneticsMBNL1030304 developmental biologyComputingMethodologies_COMPUTERGRAPHICS0303 health sciencesDrug discoveryAlternative splicingRNABiological activityNon-coding RNAComputer Science Applicationschemistry030220 oncology & carcinogenesisMolecular modellingTP248.13-248.65Small moleculeBiotechnologyResearch ArticleComputational and structural biotechnology journal
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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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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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Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
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Alternative splicing regulation by Muscleblind proteins: from development to disease.

2011

Regulated use of exons in pre-mRNAs, a process known as alternative splicing, strongly contributes to proteome diversity. Alternative splicing is finely regulated by factors that bind specific sequences within the precursor mRNAs. Members of the Muscleblind (Mbl) family of splicing factors control critical exon use changes during the development of specific tissues, particularly heart and skeletal muscle. Muscleblind homologs are only found in metazoans from Nematoda to mammals. Splicing targets and recognition mechanisms are also conserved through evolution. In this recognition, Muscleblind CCCH-type zinc finger domains bind to intronic motifs in pre-mRNA targets in which the protein can e…

Zinc fingerGeneticsAlternative splicingExonic splicing enhancerRNA-Binding ProteinsRNA-binding proteinBiologyGeneral Biochemistry Genetics and Molecular BiologyCell biologyExonchemistry.chemical_compoundAlternative SplicingchemistryGene Expression RegulationMultigene FamilyProteomeRNA splicingMBNL1AnimalsHumansMyotonic DystrophyRNAGeneral Agricultural and Biological SciencesProtein BindingBiological reviews of the Cambridge Philosophical Society
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Preclinical characterization of antagomiR-218 as a potential treatment for myotonic dystrophy

2021

Myotonic dystrophy type 1 (DM1) is a rare neuromuscular disease caused by expansion of unstable CTG repeats in a non-coding region of the DMPK gene. CUG expansions in mutant DMPK transcripts sequester MBNL1 proteins in ribonuclear foci. Depletion of this protein is a primary contributor to disease symptoms such as muscle weakness and atrophy and myotonia, yet upregulation of endogenous MBNL1 levels may compensate for this sequestration. Having previously demonstrated that antisense oligonucleotides against miR-218 boost MBNL1 expression and rescue phenotypes in disease models, here we provide preclinical characterization of an antagomiR-218 molecule using the HSALR mouse model and patient-d…

antisense oligonucleotidetissue distributionRM1-950BiologyMyotonic dystrophyTranscriptomechemistry.chemical_compoundalternative splicingtranscriptomicsAtrophyDrug DiscoverymicroRNAmedicineMBNL1AntagomirCTG repeat expansionstherapeutic gene modulationCTG repeat expansions MBNL1 protein alternative splicing antisense oligonucleotide microRNAs myotonic dystrophy therapeutic gene modulation tissue distribution transcriptomicsmyotonic dystrophyMyogenesisMyotoniamedicine.diseasemicroRNAschemistryCancer researchMolecular MedicineOriginal ArticleTherapeutics. PharmacologyMBNL1 protein
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No Difference in Penetrance between Truncating and Missense/Aberrant Splicing Pathogenic Variants in MLH1 and MSH2: A Prospective Lynch Syndrome Data…

2021

Background. Lynch syndrome is the most common genetic predisposition for hereditary cancer. Carriers of pathogenic changes in mismatch repair (MMR) genes have an increased risk of developing colorectal (CRC), endometrial, ovarian, urinary tract, prostate, and other cancers, depending on which gene is malfunctioning. In Lynch syndrome, differences in cancer incidence (penetrance) according to the gene involved have led to the stratification of cancer surveillance. By contrast, any differences in penetrance determined by the type of pathogenic variant remain unknown. Objective. To determine cumulative incidences of cancer in carriers of truncating and missense or aberrant splicing pathogenic …

cancer incidence0302 clinical medicineMalalties hereditàriesMissense mutation8Q23.3CàncerCancerGenetics0303 health sciencesmedicine.diagnostic_testFactors de risc en les malaltiesMISMATCH REPAIR GENESRMLH1General MedicinePenetranceLynch syndrome3. Good healthsyöpägeenit030220 oncology & carcinogenesisMedicinesyöpätauditilmaantuvuusGenetic diseasescongenital hereditary and neonatal diseases and abnormalitiesmissense11Q23.1Risk factors in diseasesCANCER-RISKMLH1Articleaberrant splicing03 medical and health sciencesAGEmedicineGenetic predispositionddc:610<i>MSH2</i>Lynchin oireyhtymäpenetrance030304 developmental biologyGenetic testingMLH1; MSH2; penetrance; cancer incidence; truncating; missense; aberrant splicing; Lynch syndromeperinnölliset tauditbusiness.industryMUTATIONSHMSH2Cancernutritional and metabolic diseasesmedicine.diseasedigestive system diseasesMSH2Lynch syndromeMSH23121 General medicine internal medicine and other clinical medicine<i>MLH1</i>businesstruncating
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Intragenic G-quadruplex structure formed in the human CD133 and its biological and translational relevance.

2016

Cancer stem cells (CSCs) have been identified in several solid malignancies and are now emerging as a plausible target for drug discovery. Beside the questionable existence of CSCs specific markers, the expression of CD133 was reported to be responsible for conferring CSC aggressiveness. Here, we identified two G-rich sequences localized within the introns 3 and 7 of the CD133 gene able to form G-quadruplex (G4) structures, bound and stabilized by small molecules. We further showed that treatment of patient-derived colon CSCs with G4-interacting agents triggers alternative splicing that dramatically impairs the expression of CD133. Interestingly, this is strongly associated with a loss of C…

cancer stem cells0301 basic medicineDNA damageSettore BIO/11 - Biologia MolecolareTumor initiationBiologyG-quadruplex03 medical and health sciencesCancer stem cellAntigens CDCell Line TumorG-QuadruplexeGeneticsHumansNeoplasm InvasivenessAC133 AntigenGeneGlycoproteinsCell ProliferationSettore MED/04 - Patologia GeneraleNeoplasm InvasiveneG-quadruplexProtein BiosynthesiDrug discoveryGene regulation Chromatin and EpigeneticsAlternative splicingIntroncd133Molecular biologyG-QuadruplexesGene Expression Regulation Neoplastic030104 developmental biologyCell Transformation NeoplasticDrug Resistance NeoplasmProtein BiosynthesisPeptideNeoplastic Stem CellsCancer researchNeoplastic Stem CellSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioGlycoproteinPeptidesHuman
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