Search results for "Sense"

showing 10 items of 3076 documents

Improvement of In Vivo Expression of Genes Delivered by Self-Amplifying RNA Using Vaccinia Virus Immune Evasion Proteins.

2017

Among nucleic acid–based delivery platforms, self-amplifying RNA (saRNA) vectors are of increasing interest for applications such as transient expression of recombinant proteins and vaccination. saRNA is safe and, due to its capability to amplify intracellularly, high protein levels can be produced from even minute amounts of transfected templates. However, it is an obstacle to full exploitation of this platform that saRNA induces a strong innate host immune response. In transfected cells, pattern recognition receptors sense double-stranded RNA intermediates and via activation of protein kinase R (PKR) and interferon signaling initiate host defense measures including a translational shutdow…

0301 basic medicineGenetic VectorsGene Expressionvaccinia virus E3Vaccinia virusBiologyCell Line03 medical and health sciencesMiceViral ProteinseIF-2 Kinase0302 clinical medicineImmune systemInterferonSense (molecular biology)GeneticsmedicineAnimalsHumansalphavirusMolecular BiologyResearch ArticlesImmune EvasionMessenger RNAMice Inbred BALB Cself-amplifying RNAPattern recognition receptorGene Transfer TechniquesRNAProtein kinase RVirology030104 developmental biologyvaccinia virus K3030220 oncology & carcinogenesisMolecular MedicineRNAFemalesaRNAmedicine.drugrepliconvaccinia virus B18Human gene therapy
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STAG1 mutations cause a novel cohesinopathy characterised by unspecific syndromic intellectual disability

2017

Item does not contain fulltext BACKGROUND: Cohesinopathies are rare neurodevelopmental disorders arising from a dysfunction in the cohesin pathway, which enables chromosome segregation and regulates gene transcription. So far, eight genes from this pathway have been reported in human disease. STAG1 belongs to the STAG subunit of the core cohesin complex, along with five other subunits. This work aimed to identify the phenotype ascribed to STAG1 mutations. METHODS: Among patients referred for intellectual disability (ID) in genetics departments worldwide, array-comparative genomic hybridisation (CGH), gene panel, whole-exome sequencing or whole-genome sequencing were performed following the …

0301 basic medicineGeneticsMutationCohesin complexPoint mutationBiologymedicine.diseasemedicine.disease_causeBioinformaticsFrameshift mutation03 medical and health sciences030104 developmental biology0302 clinical medicineIntellectual disabilityGeneticsmedicineJournal ArticleMissense mutationGene030217 neurology & neurosurgeryGenetics (clinical)Exome sequencingRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Journal of Medical Genetics
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A Novel Role for CSRP1 in a Lebanese Family with Congenital Cardiac Defects

2017

Despite an obvious role for consanguinity in congenital heart disease (CHD), most studies fail to document a monogenic model of inheritance except for few cases. We hereby describe a first-degree cousins consanguineous Lebanese family with 7 conceived children: 2 died in utero of unknown causes, 3 have CHD, and 4 have polydactyly. The aim of the study is to unveil the genetic variant(s) causing these phenotypes using next generation sequencing (NGS) technology. Targeted exome sequencing identified a heterozygous duplication in CSRP1 which leads to a potential frameshift mutation at position 154 of the protein. This mutation is inherited from the father, and segregates only with the CHD phen…

0301 basic medicineGeneticsPolydactylylcsh:QH426-470ConsanguinityBiologypolydactylymedicine.diseasecongenital heart diseaseFrameshift mutation03 medical and health scienceslcsh:Genetics030104 developmental biologyTRPS1Gene duplicationMutation (genetic algorithm)medicineGeneticsMolecular MedicineMissense mutationExomeGenetics (clinical)Exome sequencingOriginal ResearchCSRP1Frontiers in Genetics
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Rett‐like phenotypes: expanding the genetic heterogeneity to the KCNA2 gene and first familial case of CDKL5 ‐related disease

2016

Several genes have been implicated in Rett syndrome (RTT) in its typical and variant forms. We applied next-generation sequencing (NGS) to evaluate for mutations in known or new candidate genes in patients with variant forms of Rett or Rett-like phenotypes of unknown molecular aetiology. In the first step, we used NGS with a custom panel including MECP2, CDKL5, FOXG1, MEF2C and IQSEC2. In addition to a FOXG1 mutation in a patient with all core features of the congenital variant of RTT, we identified a missense (p.Ser240Thr) in CDKL5 in a patient who appeared to be seizure free. This missense was maternally inherited with opposite allele expression ratios in the proband and her mother. In th…

0301 basic medicineGeneticscongenital hereditary and neonatal diseases and abnormalitiesCandidate geneGenetic heterogeneityCDKL5Rett syndromeBiologymedicine.disease3. Good healthMECP203 medical and health sciences030104 developmental biology0302 clinical medicineGeneticsmedicineMissense mutationExome030217 neurology & neurosurgeryGenetics (clinical)Exome sequencingClinical Genetics
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Autosomal recessive mutations inTHOC6cause intellectual disability: syndrome delineation requiring forward and reverse phenotyping

2016

THOC6 is a part of the THO complex, which is involved in coordinating mRNA processing with export. The THO complex interacts with additional components to form the larger TREX complex (transcription export complex). Previously, a homozygous missense mutation in THOC6 in the Hutterite population was reported in association with syndromic intellectual disability. Using exome sequencing, we identified three unrelated patients with bi-allelic mutations in THOC6 associated with intellectual disability and additional clinical features. Two of the patients were compound heterozygous for a stop and a missense mutation, and the third was homozygous for a missense mutation; the missense mutations wer…

0301 basic medicineGeneticseducation.field_of_studyMicrocephalybusiness.industryPopulationTranscription export complex030105 genetics & heredityCompound heterozygositymedicine.disease03 medical and health sciences030104 developmental biologyIntellectual disabilityGeneticsMedicineMissense mutationbusinesseducationExomeGenetics (clinical)Exome sequencingClinical Genetics
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Homozygous FIBP nonsense variant responsible of syndromic overgrowth, with overgrowth, macrocephaly, retinal coloboma and learning disabilities

2016

The acidic fibroblast growth factor (FGF) intracellular binding protein (FIBP) interacts directly with the fibroblast growth factor FGF1. Although FIBP is known to be implicated in the FGF signaling pathway, its precise function remains unclear. Gain-of-function variants in several FGF receptors (FGFRs) are implicated in a wide spectrum of growth disorders from achondroplasia to overgrowth syndromes. In a unique case from a consanguineous union presenting with overgrowth, macrocephaly, retinal coloboma, large thumbs, severe varicose veins and learning disabilities, exome sequencing identified a homozygous nonsense FIBP variant. The patient's fibroblasts exhibit FIBP cDNA degradation and an …

0301 basic medicineGeneticsmedia_common.quotation_subjectNonsenseMacrocephaly030105 genetics & heredityFGF1BiologyFibroblast growth factormedicine.diseasePhenotype03 medical and health sciences030104 developmental biologyFibroblast growth factor receptorGeneticsmedicinemedicine.symptomAchondroplasiaGenetics (clinical)Exome sequencingmedia_commonClinical Genetics
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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Clinical and molecular characterization of 112 single-center patients with Neurofibromatosis type 1.

2018

Abstract Background The aim of this retrospective study was to define clinical and molecular characteristics of a large sample of neurofibromatosis type 1 (NF1) patients, as well as to evaluate mutational spectrum and genotype-phenotype correlation. NF1 is a relatively common neurogenetic disorder (1:2500–1:3000 individuals). It is caused by mutations of the NF1 gene on chromosome 17ql1.2, with autosomal dominant pattern of inheritance and wide phenotypical variability. Café-au-lait spots (CALs), cutaneous and/or subcutaneous neurofibromas (CNFs/SCNFs), skinfold freckling, skeletal abnormalities, Lisch nodules of the iris and increased risk of learning and intellectual disabilities, as well…

0301 basic medicineGenotype-phenotype correlation; New mutation; NF1 gene; NF1 microdeletion syndrome; Adolescent; Adult; Age Factors; Child; Child Preschool; Cohort Studies; DNA Mutational Analysis; Female; Genes Neurofibromatosis 1; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Neurofibromatosis 1; Prevalence; Prognosis; Retrospective Studies; Risk Assessment; Sex Factors; Young Adult; Mutation MissenseMaleGenotype-phenotype correlationDNA Mutational AnalysisDiseaseCohort Studies0302 clinical medicineDNA Mutational AnalysisGenotypePrevalenceMedicineYoung adultChildNew mutationlcsh:RJ1-570Age FactorsMiddle AgedPrognosisItalyNF1 geneChild PreschoolCohortFemaleNF1 microdeletion syndromeCohort studyAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1AdolescentMutation MissenseRisk Assessment03 medical and health sciencesYoung AdultSex FactorsGenes Neurofibromatosis 1HumansGenetic Predisposition to DiseaseNeurofibromatosisPreschoolGenetic Association StudiesRetrospective Studiesbusiness.industryResearchRetrospective cohort studylcsh:Pediatricsmedicine.diseaseDermatology030104 developmental biologyGenesPediatrics Perinatology and Child HealthMutationMissensebusiness030217 neurology & neurosurgeryItalian journal of pediatrics
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Autoimmune aspects in glaucoma

2016

The pathogenesis of glaucoma, a common neurodegenerative disease, involves an immunologic component. Studies demonstrate changes of autoantibody concentrations against retinal and optic nerve head antigens in glaucoma patients. Furthermore we found antibody deposits in human glaucomatous retinae in a pro-inflammatory environment. Clinical studies showed up regulated, but also significantly down-regulated autoantibody levels. These antibodies belong to the natural autoimmunity. The upregulation of autoantibodies can be associated with fatal conditions, but several studies demonstrate that natural autoantibodies entail also neuroprotective characteristics and influence the protein expression …

0301 basic medicineGlaucomaAutoimmunityDiseasemedicine.disease_causeNeuroprotectionAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineAntigenmedicineAnimalsHumansAutoantibodiesPharmacologybusiness.industryAutoantibodyGlaucomamedicine.diseaseNeuroprotection030104 developmental biologyImmunology030221 ophthalmology & optometryBiomarker (medicine)sense organsbusinessEuropean Journal of Pharmacology
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Structures of collagen IV globular domains: insight into associated pathologies, folding and network assembly

2018

15 páginas, 6 figuras, 1 tabla.

0301 basic medicineGoodpasture’s diseaseAddenda and ErrataRandom hexamerBiochemistryEpitopelaw.invention03 medical and health sciencesAlport's syndrome0302 clinical medicineGoodpasture's diseaselawMissense mutationGeneral Materials ScienceAlport’s syndromeStructural motifNetwork assemblyCrystallographyGoodpasture's diseaseChemistry(IV)NC1 hexamersStructural proteinCollagen type IVGeneral ChemistryCondensed Matter PhysicsResearch PapersFolding (chemistry)030104 developmental biologyQD901-999BiophysicsRecombinant DNA030217 neurology & neurosurgeryAlport syndrome
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