Search results for " splicing"

showing 10 items of 226 documents

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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Aceruloplasminemia: a case report

2008

Hereditary aceruloplasminemia is a rare autosomal recessive disease, firstly identified by Miyajima et al. in Japan in 1987 [1]. The disease is caused by the absence of an a2glycoprotein, the ceruloplasmin (Cp), a copper-containing ferroxidase, mainly synthesized in hepatocytes and widely expressed, including the central nervous system, which catalyses the oxidation of ferrous to ferric iron, a change required for release of iron to plasma transferrin [2]. It is hypothesized that in reticuloendothelial (RE) cells and hepatocytes Cp cooperates to export iron with the iron exporter protein ferroportin 1 (FPN1) [3]. As a consequence, Cp deficiency results in iron deposition in the liver, pancr…

chemistry.chemical_classificationmedicine.medical_specialtybiologybusiness.industryMetabolic disorderAlternative splicingGene mutationmedicine.diseaseExonEndocrinologychemistryTransferrinInternal medicineEmergency MedicineInternal Medicinebiology.proteinMedicineCeruloplasmin FerritinsbusinessCeruloplasminAceruloplasminemiaGeneInternal and Emergency Medicine
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Characterization of hOGG1 Promoter Structure, Expression During Cell Cycle and Overexpression in Mammalian Cells

2001

Oxygen radicals are produced in all cells either by the normal cellular metabolism or by the exposure to external mutagens. The reactive oxygen species (ROS) generated can induce DNA damage. Among the principal lesions found in DNA due to ROS is an oxidized form of guanine, 8-oxo-7,8-dihydroguanine (8-oxoG). The biological relevance of this lesion has been unveiled by the study of Escherichia colt and Saccharomyces cerevisiae genes involved in the neutralization of the mutagenic effects of 8-oxoG (Cabrera et al., 1988; Nghiem et al., 1988; Radicella et al., 1988; van der Kemp et al., 1996). These genes fpg and mutY for E. colt and OGG1 for yeast, code for DNA glycosylases. Inactivation of a…

chemistry.chemical_compoundbiologychemistryDNA glycosylaseDNA damageGene expressionSaccharomyces cerevisiaeAlternative splicingbiology.organism_classificationGeneMolecular biologyDNADNA-formamidopyrimidine glycosylase
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Role of epigenetic factors in the selection of the alternative splicing isoforms of human

2017

Mutation-driven activation of KRAS is crucial to cancer development. The human gene yields four mRNA splicing isoforms, 4A and 4B being translated to protein. Their different properties and oncogenic potential have been studied, but the mechanisms deciding the ratio 4A/4B are not known. To address this issue, the expression of the four KRAS isoforms was determined in 9 human colorectal cancer cell lines. HCT116 and SW48 were further selected because they present the highest difference in the ratio 4A/4B (twice as much in HCT116 than in SW48). Chromatin structure was analysed at the exon 4A, characteristic of isoform 4A, at its intronic borders and at the two flanking exons. The low nucleoso…

chromatin structurealternative splicingKRAS isoformsepigeneticscolorectal cancerResearch PaperOncotarget
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Circular RNAs in Sepsis: Biogenesis, Function, and Clinical Significance

2020

Sepsis is a life-threatening condition that occurs when the body responds to an infection that damages it is own tissues. The major problem in sepsis is rapid, vital status deterioration in patients, which can progress to septic shock with multiple organ failure if not properly treated. As there are no specific treatments, early diagnosis is mandatory to reduce high mortality. Despite more than 170 different biomarkers being postulated, early sepsis diagnosis and prognosis remain a challenge for clinicians. Recent findings propose that circular RNAs (circRNAs) may play a prominent role in regulating the patients’ immune system against different pathogens, including bacteria and viruses. Mou…

circular RNAs (circRNAs)ReviewBioinformaticssepsisSepsisalternative splicingImmune systemmedicineHumansDiagnostic biomarkerClinical significanceEpigeneticslcsh:QH301-705.5epigeneticsbusiness.industrySeptic shockRNA CircularGeneral Medicinemedicine.diseaselcsh:Biology (General)biomarkerBiomarker (medicine)transcriptionbusinessBiomarkersBiogenesisCells
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Effects of cold acclimation and dsRNA injections on Gs1l gene splicing in Drosophila montana

2017

Abstract Alternative splicing, in which one gene produce multiple transcripts, may influence how adaptive genes respond to specific environments. A newly produced transcriptome of Drosophila montana shows the Gs1-like (Gs1l) gene to express multiple splice variants and to be down regulated in cold acclimated flies with increased cold tolerance. Gs1l’s effect on cold tolerance was further tested by injecting cold acclimated and non-acclimated flies from two distantly located northern and southern fly populations with double stranded RNA (dsRNA) targeting Gs1l. While both populations had similar cold acclimation responses, dsRNA injections only effected the northern population. The nature of …

cold resistancemahlakärpäsetAcclimatizationlcsh:MedicineacclimationArticleInjectionskylmänkestävyysNucleotidasesAnimalsDrosophila ProteinsHumansProtein IsoformsDrosophilidaegeneslcsh:ScienceRNA Double-StrandedgeenitSequence Homology Amino Acidfungilcsh:RProteinsCold ClimateakklimatisaatioAlternative SplicingRNADrosophilalcsh:QScientific Reports
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A ceRNA analysis on LMNA gene focusing on the Hutchinson-Gilford progeria syndrome

2013

Background: Hutchinson-Gilford progeria syndrome is a rare dominant human disease of genetic origin. The average life expectancy is about 20 years, patients’ life quality is still very poor and no efficient therapy has yet been developed. It is caused by mutation of the LMNA gene, which results in accumulation in the nuclear membrane of a particular splicing form of Lamin-A called progerin. The mechanism by which progerin perturbs cellular homeostasis and leads to the symptoms is still under debate. Micro-RNAs are able to negatively regulate transcription by coupling with the 3’ UnTranslated Region of messenger RNAs. Several Micro-RNAs recognize the same 3’ UnTranslated Region and each Micr…

congenital hereditary and neonatal diseases and abnormalitiesCandidate geneCeRNA Hutchinson-Gilford Progeria LMNA Lamin-A 3’ UTR MiRNALMNACellular homeostasisHealth InformaticsLamin-ABiologySettore MED/13 - EndocrinologiaLMNAProgeriaCeRNAmedicineHutchinson-GilfordGeneticsProgeriaintegumentary systemCompeting endogenous RNAThree prime untranslated regionResearchnutritional and metabolic diseasesmedicine.diseaseProgerinSettore BIO/18 - GeneticaRNA splicing3’ UTRMiRNAJournal of Clinical Bioinformatics
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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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