Search results for "splice"

showing 10 items of 53 documents

Linking C5 deficiency to an exonic splicing enhancer mutation

2005

Abstract As an important component of the innate immune system, complement provides the initial response to prevent infections by pathogenic microorganisms. Patients with dysfunction of C5 display a propensity for severe recurrent infections. In this study, we present a patient with C5 deficiency demonstrated by immunochemical and functional analyses. Direct sequencing of all C5 exons displayed no mutation of obvious functional significance, except for an A to G transition in exon 10 predicting an exchange from lysine to arginine. This sequence alteration was present in only one allele of family members with a reduced serum C5 concentration and in both alleles of the patient with almost com…

MaleSequence analysisDNA Mutational AnalysisImmunologyExonic splicing enhancerBiologymedicine.disease_causeExonmedicineHumansImmunology and AllergyGeneFamily HealthGeneticsMutationSplice site mutationComplement C5ExonsSequence Analysis DNAC5 DeficiencyMolecular biologyAlternative SplicingPhenotypeChild PreschoolMutationRNA splicingThe Journal of Immunology
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Four new cases of congenital secondary hypothyroidism due to a splice site mutation in the thyrotropin-beta gene: Phenotypic variability and founder …

2004

WOS: 000223072400081 PubMed ID: 15292359 Isolated TSH deficiency is a rare cause of congenital hypothyroidism. We here report four children from two consanguineous Turkish families with isolated TSH deficiency. Affected children who were screened at newborn age had an unremarkable TSH result and a low serum TSH level at diagnosis. Age at diagnosis and clinical phenotype were variable. All affected children carried an identical homozygous splice site mutation (IVS2 + 5 Gdouble right arrowA) in the TSHbeta gene. This mutation leads to skipping of exon 2 and a loss of the translational start codon without ability to produce a TSH-like protein. However, using specific monoclonal antibodies, we …

Malemedicine.medical_specialtyendocrine systemGuanineendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryThyrotropinLocus (genetics)Thyrotropin beta SubunitBiologyBiochemistryExonEndocrinologyHypothyroidismInternal medicinemedicineCongenital HypothyroidismHumansChildGeneGenotypingGeneticsSplice site mutationAdenineBiochemistry (medical)HaplotypeHomozygoteInfant NewbornInfantmedicine.diseaseFounder EffectIntronsCongenital hypothyroidismPedigreeEndocrinologyPhenotypeHaplotypesChild PreschoolMutationFemalehormones hormone substitutes and hormone antagonistsFounder effect
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Oligonucleotide probes detect splicing variants insituinDrosophilaembryos

1992

We describe a method for the in situ detection of specific splicing variants. The method is based on the use of antisense oligonucleotides designed to span splice junctions labelled with digoxigenin by terminal transferase tailing. We find that the spatial patterns of Ubx splicing variants Ia and IIa are similar in early embryos, but differ in late embryos. Variant IVa is only detected in the CNS (ps6) at stages 16 and 17. We also present evidence indicating that the first splicing event is cotranscriptional.

Messenger RNAanimal structuresBase SequenceTranscription GeneticOligonucleotideMolecular Sequence DataAlternative splicingExonic splicing enhancerOligonucleotides AntisenseBiologyMolecular biologyAlternative Splicingchemistry.chemical_compoundchemistryRNA splicingGeneticsAnimalsDigoxigeninDrosophilaspliceOligonucleotide ProbesDigoxigeninIn Situ HybridizationUltrabithoraxNucleic Acids Research
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Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

2017

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) partici…

MiD51 mitochondrial dynamics proteins of 51 kDaΔΨm mitochondrial membrane potential0301 basic medicineMitochondrial fission factorClinical BiochemistryMitochondrial DegradationMFN2Review ArticleTXNIP thioredoxin interacting proteinMitochondrial DynamicsBiochemistryAdenosine TriphosphateGRP78 78 kDa glucose-regulated proteinMFF mitochondrial fission factorMFN2 mitofusin 2TRX2 thioredoxin 2Redox biologylcsh:QH301-705.5NF-κB nuclear factor kappa Blcsh:R5-920MitophagyType 2 diabetesDRP1 dynamin-related protein 1FIS1 fission protein 1BNIP3 BCL2/adenovirus E1B 19 kDa interacting protein 3MitochondriaOPA1 optic atrophy 1SIRT1/3 sirtuin 1/3Biochemistrymitochondrial fusionTGF-β1 transforming growth factor-β1Mitochondrial fissionOMM outer mitochondrial membranelcsh:Medicine (General)MiD49 mitochondrial dynamics proteins of 49Nox 4 NADPH oxidase-4IMM inner mitochondrial membraneFIS1ATF6 activating transcription factor 6PINK1mTOR mammalian target of rapamycinCHOP C/EBP homologous proteinBiologymdivi-1 mitochondrial division inhibitor-1Mitochondrial Proteins03 medical and health sciencesROS reactive oxygen speciessXBP1 spliced X-box binding protein 1UCP-1 uncoupling protein-1MFN1 mitofusin 1SOD superoxide dismutaseLC3 1 A/1B-light chain 3HumansPINK1 (PTEN)-induced putative kinase 1S3 15-OxospiramilactoneOrganic ChemistrymtDNA mitochondrial DNAAMPK AMP-activated protein kinase030104 developmental biologyDiabetes Mellitus Type 2Mitochondrial biogenesislcsh:Biology (General)Oxidative stressp38 MAPK p38 mitogen-activated protein kinasep62/SQSTM1 ubiquitin and sequestosome-1Reactive Oxygen SpeciesRedox Biology
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All-atom simulations disentangle the functional dynamics underlying gene maturation in the intron lariat spliceosome

2018

The spliceosome (SPL) is a majestic macromolecular machinery composed of five small nuclear RNAs and hundreds of proteins. SPL removes noncoding introns from precursor messenger RNAs (pre-mRNAs) and ligates coding exons, giving rise to functional mRNAs. Building on the first SPL structure solved at near–atomic-level resolution, here we elucidate the functional dynamics of the intron lariat spliceosome (ILS) complex through multi-microsecond-long molecular-dynamics simulations of ∼1,000,000 atoms models. The ILS essential dynamics unveils (i) the leading role of the Spp42 protein, which heads the gene maturation by tuning the motions of distinct SPL components, and (ii) the critical particip…

Models Molecular0301 basic medicineProtein ConformationSplicingExonMolecular dynamicsRNA; gene maturation; molecular dynamics; spliceosome; splicingModelsRNA Small NuclearRNA PrecursorsMagnesiumPrincipal Component AnalysisMultidisciplinaryChemistrySpliceosomeFungalPhysical SciencesRNA splicingSpliceosomeRNA Splicing1.1 Normal biological development and functioningStatic ElectricityComputational biologyMolecular dynamicsMolecular Dynamics Simulation03 medical and health sciencesMotionsplicingU5 Small NuclearSmall NuclearGeneticUnderpinning researchSchizosaccharomycesGeneticsComputer SimulationGeneRibonucleoprotein U5 Small NuclearModels Geneticgene maturationIntronRNAMolecularRNA FungalRibonucleoproteinIntronsmolecular dynamicsRepressor Proteins030104 developmental biologyGene maturationHelixSpliceosomesRNANucleic Acid ConformationSchizosaccharomyces pombe ProteinsGeneric health relevancespliceosome
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Can multiscale simulations unravel the function of metallo-enzymes to improve knowledge-based drug discovery?

2019

Metallo-enzymes are a large class of biomolecules promoting specialized chemical reactions. Quantum-classical quantum mechanics/molecular mechanics molecular dynamics, describing the metal site at quantum mechanics level, while accounting for the rest of system at molecular mechanics level, has an accessible time-scale limited by its computational cost. Hence, it must be integrated with classical molecular dynamics and enhanced sampling simulations to disentangle the functions of metallo-enzymes. In this review, we provide an overview of these computational methods and their capabilities. In particular, we will focus on some systems such as CYP19A1 a Fe-dependent enzyme involved in estroge…

Models MolecularSpliceosomeQM/MM molecular dynamicsProtein ConformationComputer scienceMetallo enzymeComputational biology01 natural sciencesMolecular mechanicsribozymeStructure-Activity Relationship03 medical and health sciencesMolecular dynamicsMM molecular dynamicsAromataseCatalytic DomainDrug Discoverysteroid synthesisCYP19A1RNA CatalyticDensity Functional Theory030304 developmental biologyQMPharmacologychemistry.chemical_classificationDNA processing enzymes0303 health sciencesMetallo-proteinsbiologyDrug discoveryBiomoleculeRibozymeDNABiosynthetic PathwaysEnzymes0104 chemical sciences010404 medicinal & biomolecular chemistrychemistrySettore CHIM/03 - Chimica Generale E InorganicaMetalsbiology.proteinRNAThermodynamicsMolecular MedicinespliceosomeFunction (biology)Protein BindingFuture Medicinal Chemistry
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The nuclear autoantigen La/SS-associated antigen B: One gene, three functional mRNAs

1997

Transcription of the gene encoding for the nuclear autoantigen La resulted in three mRNA forms. A promoter switching combined with an alternative splicing pathway replaced exon 1 with either exon 1´ or exon 1´´. The exon 1´´ donor splice site was located 4 nts downstream of the exon 1´ donor splice site. All three La mRNA forms were expressed in all the tissues analysed including peripheral blood lymphocytes, liver, fetal spleen, cultured primary endothelial cells, and mouse LTA cell lines permanently transfected with the human La gene. Both the exons 1´ and 1´´ had unusual structures. They contained GC-rich regions and an oligo(U)-tail of 23 uridine residues. Moreover, they encoded for thr…

Molecular Sequence DataBiologyAutoantigensPolymerase Chain ReactionBiochemistryMiceExonExon trappingAnimalsHumansAmino Acid SequenceRNA MessengerMolecular BiologyGeneRibonucleoproteinAdenosine TriphosphatasesMessenger RNASplice site mutationBase SequenceAlternative splicingExonsSequence Analysis DNACell BiologyMolecular biologyOpen reading frameGenetic TechniquesRibonucleoproteinsResearch ArticleTranscription Factors
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Splice donor site mutation in the lysosomal neuraminidase gene causing exon skipping and complete loss of enzyme activity in a sialidosis patient.

2001

Sialidosis is a lysosomal storage disease caused by the deficiency of K K-N-acetylneuraminidase (NEU1; sialidase), the key enzyme for the intralysosomal catabolism of sialylated glycoconjugates. We have identified a homozygous transversion in the last intron (IVSE +1 Gs C) in neu1 of a sialidosis patient. Sequencing of the truncated cDNA revealed an alternatively spliced neu1 transcript which lacks the complete sequence of exon 5. Skipping of exon 5 leads to a frameshift and results in a premature termination codon. This is the first description of an intronic point mutation causing a complete deficiency of the lysosomal neuraminidase activity. fl 2001 Federation of Euro- pean Biochemical S…

Molecular Sequence DataBiophysicsNeuraminidaseBiochemistryFrameshift mutationNEU1ExonLysosomal neuraminidaseStructural BiologyMucolipidosesGeneticsLysosomal storage diseasemedicineHumansSialidosisAmino Acid SequenceMolecular BiologyGeneticsSialidosisSplice site mutationbiologySequence Homology Amino AcidReverse Transcriptase Polymerase Chain ReactionDonor splice siteCell BiologyExonsFibroblastsmedicine.diseaseMolecular biologyExon skippingMutationbiology.proteinRNA Splice SitesLysosomesNeuraminidaseExon skippingGene DeletionFEBS letters
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The Detection of Androgen Receptor Splice Variant 7 in Plasma-derived Exosomal RNA Strongly Predicts Resistance to Hormonal Therapy in Metastatic Pro…

2017

Abstract Background The androgen receptor splice variant 7 (AR-V7) is associated with resistance to hormonal therapy in castration-resistant prostate cancer (CRPC). Due to limitations of the methods available for AR-V7 analysis, the identification of a reliable detection method may facilitate the use of this biomarker in clinical practice. Objective To confirm AR-V7 as a predictor of resistance to hormonal therapy and develop a new approach to assess AR-V7 by highly sensitive digital droplet polymerase chain reaction (ddPCR) in plasma-derived exosomal RNA. Design, setting, and participants Plasma samples were collected from 36 CRPC patients before they began second-line hormonal treatment. …

Oncology0301 basic medicineMaleResistanceExosomeschemistry.chemical_compoundProstate cancer0302 clinical medicineProtein IsoformsNeoplasm MetastasisReceptorAged 80 and overProstate cancerMiddle AgedProstatic Neoplasms Castration-ResistantReceptors Androgen030220 oncology & carcinogenesisBenzamidesAdenocarcinomaBiomarker (medicine)Hormonal therapyAR-V7; Digital droplet PCR; Exosomes; Hormonal therapy; Pharmacogenetics; Prostate cancer; Resistance; UrologyAndrostenesHormonal therapymedicine.medical_specialtyAntineoplastic Agents Hormonalmedicine.drug_classUrologyCastration resistantAdenocarcinomaDisease-Free Survival03 medical and health sciencesSDG 3 - Good Health and Well-beingInternal medicineNitrilesPhenylthiohydantoinmedicineEnzalutamideHumansAgedDigital droplet PCRPlasma derivedbusiness.industryRNAAndrogen Receptor Splice Variant 7medicine.diseaseAndrogenEndocrinology030104 developmental biologychemistryPharmacogeneticsDrug Resistance NeoplasmCancer cellCancer researchRNAAR-V7businessPharmacogenetics
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Acquired BRAF inhibitor resistance: A multicenter meta-analysis of the spectrum and frequencies, clinical behaviour, and phenotypic associations of r…

2015

BackgroundAcquired resistance to BRAF inhibitors (BRAFi) is a near-universal phenomenon caused by numerous genetic and non-genetic alterations. In this study, we evaluated the spectrum, onset, pattern of progression, and subsequent clinical outcomes associated with specific mechanisms of resistance.MethodsWe compiled clinical and genetic data from 100 patients with 132 tissue samples obtained at progression on BRAFi therapy from 3 large, previously published studies of BRAFi resistance. These samples were subjected to whole-exome sequencing and/or polymerase chain reaction-based genetic testing.ResultsAmong 132 samples, putative resistance mechanisms were identified in 58%, including NRAS o…

OncologyNeuroblastoma RAS viral oncogene homologMaleCancer ResearchSkin NeoplasmsTime FactorsResistanceDNA Mutational AnalysisDrug ResistanceMedizinKaplan-Meier EstimateBioinformaticsmedicine.disease_causeRisk Factors2.1 Biological and endogenous factorsAetiologyVemurafenibMelanomaCancerMutationTumorDabrafenibMelanomaAcquiredMiddle AgedPhenotypeEuropePhenotypeTreatment OutcomeSpliceOncologyMeta-analysisPublic Health and Health ServicesDisease ProgressionFemalemedicine.drugSignal TransductionProto-Oncogene Proteins B-rafmedicine.medical_specialtyOncology and CarcinogenesisNRASAntineoplastic AgentsBiologyDisease-Free SurvivalArticleBRAFMEK1Clinical ResearchInternal medicineGeneticsmedicineBiomarkers TumorHumansGenetic Predisposition to DiseaseOncology & CarcinogenesisProtein Kinase InhibitorsProportional Hazards ModelsProportional hazards modelAustraliaDabrafenibmedicine.diseaseMAPKUnited StatesMeta-analysisVemurafenibDrug Resistance NeoplasmMutationNeoplasmBiomarkersEuropean journal of cancer (Oxford, England : 1990)
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