Search results for "helicases"

showing 10 items of 59 documents

Customised next-generation sequencing multigene panel to screen a large cohort of individuals with chromatin-related disorder

2020

BackgroundThe regulation of the chromatin state by epigenetic mechanisms plays a central role in gene expression, cell function, and maintenance of cell identity. Hereditary disorders of chromatin regulation are a group of conditions caused by abnormalities of the various components of the epigenetic machinery, namely writers, erasers, readers, and chromatin remodelers. Although neurological dysfunction is almost ubiquitous in these disorders, the constellation of additional features characterizing many of these genes and the emerging clinical overlap among them indicate the existence of a community of syndromes. The introduction of high-throughput next generation sequencing (NGS) methods f…

Adenosine TriphosphataseAdultMaleCCCTC-Binding FactorTranscription FactorDNA-Binding Proteinchromatin disorderComputational biologyBiologyDNA HelicaseDNA sequencingEpigenesis GeneticMendelian chromatin disordersLocus heterogeneityDe Lange SyndromeGeneticsmedicineCoffin-Lowry SyndromeHumansGenetic Predisposition to DiseaseEpigeneticsGenetic TestingChildGeneGenetics (clinical)Adenosine Triphosphatasesnext generation sequencingepigeneticsGenetic heterogeneityDNA HelicasesMendelian chromatin disorderHistone-Lysine N-Methyltransferasemedicine.diseaseChromatinChromatinDNA-Binding ProteinsMendelian chromatin disorders; epigenetics; next generation sequencingCohortMutationRelated disorderFemaleMyeloid-Lymphoid Leukemia ProteinepigeneticTranscription FactorsHuman
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Oxidative stress and antioxidant response in fibroblasts from Werner and Atypical Werner Syndromes

2014

Werner Syndrome (WS, ICD-10 E34.8, ORPHA902) and Atypical Werner Syndrome (AWS, ICD-10 E34.8, ORPHA79474) are very rare inherited syndromes characterized by premature aging. While approximately 90% of WS individuals have any of a range of mutations in theWRN gene, there exists a clinical subgroup in which the mutation occurs in the LMNA/C gene in heterozygosity. Although both syndromes exhibit an age-related pleiotropic phenotype, AWS manifests the onset of the disease during childhood, while major symptoms in WS appear between the ages of 20 and 30. To study the molecular mechanisms of progeroid diseases provides a useful insight into the normal aging process. Main changes found were the d…

AdultMalePremature agingAgingWerner Syndrome HelicaseAdolescentBiologymedicine.disease_causeAntioxidantsCell LineWerner Syndrome HelicaseLMNAProgeriaSuperoxide Dismutase-1antioxidant enzymesmedicineoxidative stressHumansRNA MessengerAtypical Werner syndromeChildeducationCell ProliferationWerner syndromeeducation.field_of_studyProgeriaAtypical Werner SyndromeRecQ Helicasespremature agingSuperoxide DismutaseAging PrematurethioredoxinglutaredoxinCell BiologyFibroblastsLamin Type Amedicine.diseaseGlutathioneMolecular biologyExodeoxyribonucleasesCase-Control StudiesMutationDNA damageFemaleWerner SyndromeThioredoxinOxidative stressResearch PaperAging
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Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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Senataxin defective in ataxia oculomotor apraxia type 2 is involved in the defence against oxidative DNA damage

2007

Adefective response to DNA damage is observed in several human autosomal recessive ataxias with oculomotor apraxia, including ataxia-telangiectasia. We report that senataxin, defective in ataxia oculomotor apraxia (AOA) type 2, is a nuclear protein involved in the DNA damage response. AOA2 cells are sensitive to H2O2, camptothecin, and mitomycin C, but not to ionizing radiation, and sensitivity was rescued with full-length SETX cDNA. AOA2 cells exhibited constitutive oxidative DNA damage and enhanced chromosomal instability in response to H2O2. Rejoining of H2O2-induced DNA double-strand breaks (DSBs) was significantly reduced in AOA2 cells compared to controls, and there was no evidence fo…

Ataxiagenetic structuresDNA RepairDNA damageApraxiasBiologyArticlechemistry.chemical_compoundComplementary DNAChromosome instabilitymedicineHumansDNA Breaks Double-StrandedOculomotor apraxiaCells CulturedResearch ArticlesNeurodegenerationMitomycin CDNA HelicasesCell BiologyHydrogen Peroxidemedicine.diseaseMolecular biologyMultifunctional EnzymesOxidative StresschemistryAtaxiamedicine.symptomDNARNA HelicasesDNA Damage
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Regulation of human inducible nitric oxide synthase expression by an upstream open reading frame.

2019

Abstract The human inducible nitric oxide synthase (iNOS) gene contains an upstream open reading frame (uORF) in its 5′-untranslated region (5′-UTR) implying a translational regulation of iNOS expression. Transfection experiments in human DLD-1 cells revealed that the uORF although translatable seems not to inhibit the translation start at the bona fide ATG. Our data clearly show that human iNOS translation is cap-dependent and that the 5′-UTR of the iNOS mRNA contains no internal ribosome entry site. Translation of the bona fide coding sequence is most likely mediated by a leaky scanning mechanism. The 5′-UTR is encoded by exon 1 and exon 2 of the iNOS gene with the uORF stop codon located…

Cancer ResearchFive prime untranslated regionPhysiologyClinical BiochemistryDown-RegulationNitric Oxide Synthase Type IILeaky scanningBiochemistryExonOpen Reading FramesCell Line TumorUpstream open reading frameTranslational regulationCoding regionHumansAmino Acid SequenceBase SequenceChemistryIntronExonsIntronsCell biologyNonsense Mediated mRNA DecayInternal ribosome entry siteGene Expression RegulationMutationTrans-ActivatorsRNA HelicasesNitric oxide : biology and chemistry
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Cytosolic RIG-I–like helicases act as negative regulators of sterile inflammation in the CNS

2011

The action of cytosolic RIG-I-like helicases (RLHs) in the CNS during autoimmunity is largely unknown. Using a mouse model of multiple sclerosis, we found that mice lacking the RLH adaptor IPS-1 developed exacerbated disease that was accompanied by markedly higher inflammation, increased axonal damage and elevated demyelination with increased encephalitogenic immune responses. Furthermore, activation of RLH ligands such as 5'-triphosphate RNA oligonucleotides decreased CNS inflammation and improved clinical signs of disease. RLH stimulation repressed the maintenance and expansion of committed T(H)1 and T(H)17 cells, whereas T-cell differentiation was not altered. Notably, T(H)1 and T(H)17 s…

Central Nervous SystemEncephalomyelitis Autoimmune ExperimentalCell SurvivalT-LymphocytesAutoimmunityInflammationStimulationReceptor Interferon alpha-betamedicine.disease_causeAutoimmunityMiceCytosolImmune systemmedicineAnimalsbiologyMicrogliaRIG-IGeneral NeuroscienceMultiple sclerosisHelicaseCell DifferentiationDendritic Cellsmedicine.diseasemedicine.anatomical_structurebiology.proteinmedicine.symptomNeuroscienceRNA HelicasesNature Neuroscience
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TFIIH Operates through an Expanded Proximal Promoter To Fine-Tune c-myc Expression

2004

A continuous stream of activating and repressing signals is processed by the transcription complex paused at the promoter of the c-myc proto-oncogene. The general transcription factor IIH (TFIIH) is held at promoters prior to promoter escape and so is well situated to channel the input of activators and repressors to modulate c-myc expression. We have compared cells expressing only a mutated p89 (xeroderma pigmentosum complementation group B [XPB]), the largest TFIIH subunit, with the same cells functionally complemented with the wild-type protein (XPB/wt-p89). Here, we show structural, compositional, and functional differences in transcription complexes between XPB and XPB/wt-89 cells at t…

Chromatin ImmunoprecipitationDNA ComplementaryCell SurvivalUltraviolet RaysBlotting WesternGreen Fluorescent ProteinsGene ExpressionRepressorCellular homeostasisBiologyTransfectionModels BiologicalProto-Oncogene MasProto-Oncogene Proteins c-mycTranscription Factors TFIIRibonucleasesPotassium PermanganateTranscription (biology)HumansRNA MessengerPromoter Regions GeneticMolecular BiologyModels GeneticGeneral transcription factorCell CycleGenetic Complementation TestDNA HelicasesPromoterCell BiologyFibroblastsFlow CytometryMolecular biologyDNA-Binding ProteinsKineticsTranscription Factor TFIIHMicroscopy FluorescenceMutationTranscription preinitiation complexTranscription factor II HTranscription Factor TFIIHPlasmidsMolecular and Cellular Biology
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Substrate determinants for cleavage in cis and in trans by the hepatitis C virus NS3 proteinase

1995

Processing of the hepatitis C virus polyprotein is accomplished by a series of cotranslational and posttranslational cleavages mediated by host cell signalases and two virally encoded proteinases. Of these the NS3 proteinase is essential for processing at the NS3/4A, NS4A/4B, NS4B/5A, and NS5A/5B junctions. Processing between NS3 and NS4A occurs in cis, implying an intramolecular reaction mechanism, whereas cleavage at the other sites can also be mediated in trans. Sequence analysis of the amino termini of mature cleavage products and comparisons of amino acid residues around the scissile bonds of various hepatitis C virus isolates identified amino acid residues which might contribute to su…

Cleavage factorvirusesMolecular Sequence DataImmunologyHepacivirusCleavage and polyadenylation specificity factorViral Nonstructural ProteinsBiologyCleavage (embryo)MicrobiologySubstrate SpecificityScissile bondVirologyHumansAmino Acid SequenceAmino AcidsPeptide sequencechemistry.chemical_classificationNS3Cleavage stimulation factorHydrolysisSerine Endopeptidasesbiochemical phenomena metabolism and nutritionAmino acidchemistryBiochemistryMutagenesisInsect ScienceProtein Processing Post-TranslationalRNA HelicasesHeLa CellsResearch ArticleJournal of Virology
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How to untie G-quadruplex knots and why?

2021

International audience; For over two decades, the prime objective of the chemical biology community studying G-quadruplexes (G4s) has been to use chemicals to interact with and stabilize G4s in cells to obtain mechanistic interpretations. This strategy has been undoubtedly successful, as demonstrated by recent advances. However, these insights have also led to a fundamental rethinking of G4-targeting strategies: due to the prevalence of G4s in the human genome, transcriptome, and ncRNAome (collectively referred to as the G4ome), and their involvement in human diseases, should we continue developing G4-stabilizing ligands or should we invest in designing molecular tools to unfold G4s? Here, …

Clinical BiochemistryChemical biologyComputational biology[CHIM.THER]Chemical Sciences/Medicinal ChemistryBiology010402 general chemistryG-quadruplex01 natural sciencesBiochemistry03 medical and health sciencesgenetic diseasesDrug DiscoveryHumansMolecular Biologyunfolding030304 developmental biologyPharmacology0303 health sciencesG-quadruplex[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM]Genome Humanhelicasesgenetic instability0104 chemical sciencesG-Quadruplexessmall moleculesMolecular Medicine
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Poly(ADP-ribosyl)ation accelerates DNA repair in a pathway dependent on Cockayne syndrome B protein

2003

Activation of poly(ADP-ribose)polymerases 1 and 2 (PARP-1 and PARP-2) is one of the earliest responses of mammalian cells to DNA damage by numerous genotoxic agents. We have analysed the influence of PARP inhibition, either achieved by over-expression of the DNA binding domain of PARP-1 or by treatment with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone, on the repair of single-strand breaks (SSB), pyrimidine dimers and oxidative base modifications sensitive to Fpg protein (mostly 8-hydroxyguanine) in mammalian cells at very low, non-cytotoxic levels of DNA damage. The data show that the repair rates of all three types of DNA damage are significantly lower in PARP-inhibited c…

DNA RepairDNA damageDNA repairPoly ADP ribose polymerase[SDV]Life Sciences [q-bio]Pyrimidine dimerBiologyPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorCockayne syndromeDexamethasone03 medical and health sciencesMice0302 clinical medicinePiperidinesCricetinaeGeneticsmedicineAnimalsPoly-ADP-Ribose Binding ProteinsComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Line TransformedMice Knockout0303 health sciencesDNA HelicasesArticlesDNADNA repair protein XRCC4Fibroblastsmedicine.diseaseIsoquinolinesMolecular biology3. Good healthDNA Repair Enzymes030220 oncology & carcinogenesisPoly(ADP-ribose) PolymerasesNucleotide excision repairDNA DamageSignal Transduction
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