Search results for "silencing"

showing 10 items of 253 documents

Trans-Reactivation: A New Epigenetic Phenomenon Underlying Transcriptional Reactivation of Silenced Genes

2015

In order to study the role played by cellular RNA pools produced by homologous genomic loci in defining the transcriptional state of a silenced gene, we tested the effect of non-functional alleles of the white gene in the presence of a functional copy of white, silenced by heterochromatin. We found that non-functional alleles of white, unable to produce a coding transcript, could reactivate in trans the expression of a wild type copy of the same gene silenced by heterochromatin. This new epigenetic phenomenon of transcriptional trans-reactivation is heritable, relies on the presence of homologous RNA’s and is affected by mutations in genes involved in post-transcriptional gene silencing. Ou…

MaleCancer ResearchPEV white Trans-reactivation Epigenetics Gynogenesis ncRNAsRNA Untranslatedlcsh:QH426-470Transcription GeneticHeterochromatinSettore BIO/11 - Biologia MolecolareGenes InsectBiologySettore MED/13 - EndocrinologiaRNA interferenceSettore BIO/10 - BiochimicaHeterochromatinGene clusterGene expressionGeneticsGene silencingAnimalsDrosophila ProteinsEpigeneticsCompound Eye ArthropodEye ProteinsMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and SystematicsAllelesGeneticsEye ColorRNAlcsh:GeneticsSettore BIO/18 - GeneticaDrosophila melanogasterATP-Binding Cassette TransportersFemaleRNA InterferenceResearch ArticlePLoS Genetics
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Functional Inactivation of the Genome-Wide Association Study Obesity Gene Neuronal Growth Regulator 1 in Mice Causes a Body Mass Phenotype

2012

To date, genome-wide association studies (GWAS) have identified at least 32 novel loci for obesity and body mass-related traits. However, the causal genetic variant and molecular mechanisms of specific susceptibility genes in relation to obesity are yet to be fully confirmed and characterised. Here, we examined whether the candidate gene NEGR1 encoding the neuronal growth regulator 1, also termed neurotractin or Kilon, accounts for the obesity association. To characterise the function of NEGR1 for body weight control in vivo, we generated two novel mutant mouse lines, including a constitutive NEGR1-deficient mouse line as well as an ENU-mutagenised line carrying a loss-of-function mutation …

MaleCandidate geneMutantlcsh:MedicineGenome-wide association studymedicine.disease_causeEndoplasmic ReticulumEatingGene Knockout TechniquesMice0302 clinical medicineEndocrinologylcsh:ScienceObesity; NEGR1; GWAS; body weight control2. Zero hungerGenetics0303 health sciencesMutationMultidisciplinaryNeuronal growth regulator 1GenomicsPhenotypePhenotypeMedicineFemaleFunction and Dysfunction of the Nervous SystemResearch ArticleGenotypeHypothalamusNerve Tissue ProteinsBiologyMotor ActivityDiet High-FatCell Line03 medical and health sciencesGenetic MutationGenome Analysis ToolsmedicineGeneticsGenome-Wide Association StudiesCell AdhesionNeuritesAnimalsHumansObesityGene SilencingGeneBiologyAlleles030304 developmental biologyNutritionlcsh:RBody WeightMembrane ProteinsHuman GeneticsNeuroendocrinologyBody HeightMetabolic DisordersGenetics of DiseaseLean body masslcsh:QEnergy Metabolism030217 neurology & neurosurgeryGenome-Wide Association StudyPLoS ONE
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Expression ofDNMT3A transcripts and nucleolar localization of DNMT3A protein in human testicular and fibroblast cells suggest a role for de novo DNA …

2006

Transcriptional silencing during differentiation of human male germ cells and serum starvation of human fibroblasts is controlled by epigenetic mechanisms that involve de novo DNA methylation. It is associated with high expression of different transcripts of the DNA methyltransferase 3A (DNMT3A) gene that encode two isoforms with de novo methyltransferase activity and one without catalytic activity. Western blots revealed that DNMT3A protein (with catalytic domain) is present at low levels in several tissues and at increased levels in testicular cells and growth-arrested fibroblasts. Immunofluorescence experiments localized DNMT3A to discrete nucleolar foci in B spermatogonia and resting fi…

MaleGene isoformMethyltransferaseNucleolusActive Transport Cell NucleusBiologyBiochemistryGene Expression Regulation EnzymologicDNA Methyltransferase 3ATestisHumansGene silencingDNA (Cytosine-5-)-MethyltransferasesGene SilencingRNA MessengerEpigeneticsMolecular BiologyGeneCells CulturedRegulation of gene expressionCell DifferentiationCell BiologyDNA MethylationFibroblastsMolecular biologySpermatogoniaIsoenzymesembryonic structuresDNA methylationCell NucleolusJournal of Cellular Biochemistry
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A novel mutation of gene CBFA1/RUNX2 in cleidocranial dysplasia.

2007

Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal dysplasia characterised by abnormal clavicles, patent sutures and fontanelles, supernumerary teeth, short stature, and a variety of other skeletal changes. The disease gene is CBFA1/RUNX2, which is mapped to chromosome 6p21. Inactivation of the CBFA1/RUNX2 gene by mutations is involved in the skeletal defects that occur in patients with CCD. CBFA1/RUNX2 controls the differentiation of precursor cells into osteoblasts and is essential for membranous as well as endochondral bone formation. In this study of a 14-yr-old boy with typical CCD phenotype, the authors found a novel CBFA1/RUNX2 gene mutation. All of the amplified segment…

MaleHeterozygoteAdolescentDNA Mutational AnalysisCore Binding Factor Alpha 1 SubunitPolymerase Chain ReactionPedigreeAdolescent Chromosomes Human Pair 6 Cleidocranial Dysplasia/genetics* Cleidocranial Dysplasia/pathology Codon Nonsense/genetics* Core Binding Factor Alpha 1 Subunit/genetics* DNA Mutational Analysis DNA Primers/chemistry Female Gene Silencing Heterozygote Humans Male Pedigree Point Mutation* Polymerase Chain Reactioncleidocranial dysplasiaCodon NonsenseCBFA1/RUNX2HumansPoint MutationChromosomes Human Pair 6Femalegene mutationGene SilencingCleidocranial DysplasiaDNA Primers
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A high incidence of meiotic silencing of unsynapsed chromatin is not associated with substantial pachytene loss in heterozygous male mice carrying mu…

2009

Meiosis is a complex type of cell division that involves homologous chromosome pairing, synapsis, recombination, and segregation. When any of these processes is altered, cellular checkpoints arrest meiosis progression and induce cell elimination. Meiotic impairment is particularly frequent in organisms bearing chromosomal translocations. When chromosomal translocations appear in heterozygosis, the chromosomes involved may not correctly complete synapsis, recombination, and/or segregation, thus promoting the activation of checkpoints that lead to the death of the meiocytes. In mammals and other organisms, the unsynapsed chromosomal regions are subject to a process called meiotic silencing of…

MaleHeterozygoteCancer ResearchDevelopmental Biology/Germ Cellslcsh:QH426-470BiologíaCell Biology/Cell Growth and DivisionChromosomal translocationMeiocyteBiologyTranslocation GeneticMiceMeiosisSpermatocytesGeneticsHomologous chromosomeAnimalsGene SilencingMolecular BiologyMetaphaseGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsSex ChromosomesAutosomeSynapsisChromosomeSynapsisChromatinGenetics and Genomics/Chromosome BiologyChromosome PairingMeiosislcsh:GeneticsEvolutionary Biology/Nuclear Structure and FunctionFemalePachytene StageResearch ArticlePLoS Genetics
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A protein quality control pathway regulated by linear ubiquitination.

2019

Neurodegenerative diseases are characterized by the accumulation of misfolded proteins in the brain. Insights into protein quality control mechanisms to prevent neuronal dysfunction and cell death are crucial in developing causal therapies. Here, we report that various disease-associated protein aggregates are modified by the linear ubiquitin chain assembly complex (LUBAC). HOIP, the catalytic component of LUBAC, is recruited to misfolded Huntingtin in a p97/VCP-dependent manner, resulting in the assembly of linear polyubiquitin. As a consequence, the interactive surface of misfolded Huntingtin species is shielded from unwanted interactions, for example with the low complexity sequence doma…

MaleHuntingtinSp1 protein humanProtein aggregationHTT protein humanDeubiquitinating enzymegenetics [Huntington Disease]Micegenetics [Sp1 Transcription Factor]0302 clinical medicineUbiquitinpathology [Brain]Valosin Containing Proteincytology [Fibroblasts]pathology [Neurons]PolyubiquitinCells CulturedMice Knockout0303 health sciencesHuntingtin ProteinGeneral NeuroscienceNF-kappa Bgenetics [Huntingtin Protein]Middle AgedCell biologymetabolism [Polyubiquitin]pathology [Huntington Disease]metabolism [Neurons]metabolism [NF-kappa B]Protein foldingFemalemetabolism [Fibroblasts]Protein BindingSignal TransductionAdultmetabolism [Valosin Containing Protein]Sp1 Transcription Factorcytology [Embryo Mammalian]genetics [Valosin Containing Protein]BiologyGeneral Biochemistry Genetics and Molecular Biologymetabolism [Sp1 Transcription Factor]03 medical and health sciencesddc:570Gene silencingAnimalsHumansmetabolism [Huntington Disease]Protein Interaction Domains and MotifsMolecular Biologymetabolism [Embryo Mammalian]030304 developmental biologyAgedSp1 transcription factorGeneral Immunology and MicrobiologyUbiquitinationProteotoxicitymetabolism [Brain]Case-Control Studiesmetabolism [Huntingtin Protein]biology.proteinProtein Processing Post-Translational030217 neurology & neurosurgerygenetics [NF-kappa B]
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PBDEs affect inflammatory and oncosuppressive mechanisms via the EZH2 methyltransferase in airway epithelial cells

2021

Abstract Aims We aimed to investigate the effect of PBDEs (47, 99, 209) on cellular events involved in epigenetic modification, inflammation, and epithelial mesenchymal transition (EMT). Materials and methods We studied: 1) ERK1/2 phosphorylation; 2) Enhancer of Zester Homolog 2 (EZH2); 3) Histone H3 tri-methylated in lysine 27 (H3K27me3); 4) K-RAS; 5) silencing disabled homolog 2-interacting protein gene (DAB2IP), 6) let-7a; 7) Muc5AC/Muc5B, and 8) IL-8 in a 3D in vitro model of epithelium obtained with primary Normal Human Bronchial Epithelial cells (pNHBEs) or A549 cell line, chronically exposed to PBDEs (47, 99, 209). Key findings PBDEs (10 nM, 100 nM and 1 μM) increased ERK1/2 phosphor…

MaleLung NeoplasmsMethyltransferaseRespiratory Mucosamacromolecular substancesAirway epithelial cellsGeneral Biochemistry Genetics and Molecular BiologyHistone H3Airway epithelial cellHalogenated Diphenyl EthersPolybrominated diphenyl ethersHumansGene silencingEnhancer of Zeste Homolog 2 ProteinEpigeneticsEpithelial–mesenchymal transitionGeneral Pharmacology Toxicology and PharmaceuticsProtein gene (DAB2IP)AgedFlame RetardantsInflammationA549 cellChemistryEZH2Epithelial CellsLet-7aGeneral MedicineMiddle AgedNeoplasm ProteinsA549 CellsCancer researchDisabled homolog 2 interactingPhosphorylationFemaleLung cancerLife Sciences
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Understanding Cannabinoid Psychoactivity with Mouse Genetic Models

2007

Marijuana and its main psychotropic ingredient Δ9-tetrahydrocannabinol (THC) exert a plethora of psychoactive effects through the activation of the neuronal cannabinoid receptor type 1 (CB1), which is expressed by different neuronal subpopulations in the central nervous system. The exact neuroanatomical substrates underlying each effect of THC are, however, not known. We tested locomotor, hypothermic, analgesic, and cataleptic effects of THC in conditional knockout mouse lines, which lack the expression of CB1 in different neuronal subpopulations, including principal brain neurons, GABAergic neurons (those that release γ aminobutyric acid), cortical glutamatergic neurons, and neurons expres…

MaleMESH: Body TemperatureCannabinoid receptormedicine.medical_treatmentGene ExpressionMESH: Receptor Cannabinoid CB1NeocortexMESH: gamma-Aminobutyric AcidMESH: CatalepsyPharmacologyHippocampusMESH: Mice KnockoutMESH: Corpus StriatumBody TemperatureMESH: Autonomic Nervous SystemMESH: NeocortexMice0302 clinical medicineReceptor Cannabinoid CB1MESH: Behavior AnimalCannabinoid receptor type 1MESH: AnimalsMESH: Gene SilencingDronabinolMESH: NociceptorsBiology (General)gamma-Aminobutyric AcidMice Knockout0303 health sciencesBehavior Animalmusculoskeletal neural and ocular physiologyGeneral NeuroscienceMESH: Pain ThresholdNociceptorsMESH: Glutamic AcidMESH: InterneuronsMESH: Motor Activity3. Good healthGABAergicMESH: TetrahydrocannabinolGeneral Agricultural and Biological SciencesResearch Articlemedicine.drugPain ThresholdMESH: Gene ExpressionMESH: Psychotropic DrugsQH301-705.5Glutamic AcidMotor ActivityBiologyAutonomic Nervous SystemGeneral Biochemistry Genetics and Molecular Biologygamma-Aminobutyric acid03 medical and health sciencesGlutamatergicDopamine receptor D1InterneuronsCannabinoid Receptor Modulatorsmental disorders[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineAnimalsGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyGene SilencingTetrahydrocannabinolMESH: MiceAnesthesiology and Pain Management030304 developmental biologyPharmacologyCatalepsyPsychotropic DrugsModels GeneticGeneral Immunology and MicrobiologyCannabinoidsIllicit Drugsorganic chemicalsMESH: MaleCorpus StriatumPrimerDisease Models Animalnervous systemCannabinoidNervous System Diseases030217 neurology & neurosurgeryNeurosciencePLoS Biology
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Cytochrome P450-dependent metabolism of caffeine in [i]Drosophila melanogaster[/i]

2014

Caffeine (1, 3, 7-trimethylxanthine), an alkaloid produced by plants, has antioxidant and insecticide properties that can affect metabolism and cognition. In vertebrates, the metabolites derived from caffeine have been identified, and their functions have been characterized. However, the metabolites of caffeine in insects remain unknown. Thus, using radiolabelled caffeine, we have identified some of the primary caffeine metabolites produced in the body of Drosophila melanogaster males, including theobromine, paraxanthine and theophylline. In contrast to mammals, theobromine was the predominant metabolite (paraxanthine in humans; theophylline in monkeys; 1, 3, 7-trimethyluric acid in rodents…

MaleMetabolite[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionlcsh:MedicineéthanolPharmacology[ SDV.BA ] Life Sciences [q-bio]/Animal biologychemistry.chemical_compound0302 clinical medicineCytochrome P-450 Enzyme Systemmétabolitelcsh:SciencemetabolitesParaxanthinecaféinecaffeineAnimal biology0303 health sciencesMultidisciplinarybiologyAlkaloid[SDV.BA]Life Sciences [q-bio]/Animal biologymétabolisme des xénobiotiquesxenobiotic metabolism3. Good healthBiochemistryAlimentation et Nutritioncaffeine;xenobiotic metabolism;drug metabolism;metabolites;drosophila melanogaster;theobromine;ethanolCaffeinemedicine.drugResearch Articledrosophila melanogasterXenobioticsmétabolisme enzymatique03 medical and health sciencesBiologie animalemedicineAnimalsFood and NutritionTheophyllineGene SilencingTheobromine030304 developmental biologytheobrominelcsh:RfungiCytochrome P450drug metabolismchemistrybiology.proteinlcsh:Qethanol[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryDrug metabolism
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Inhibition of autophagy rescues muscle atrophy in a LGMDD2 Drosophila model

2021

Limb-girdle muscular dystrophy D2 (LGMDD2) is an ultrarare autosomal dominant myopathy caused by mutation of the normal stop codon of the TNPO3 nuclear importin. The mutant protein carries a 15 amino acid C-terminal extension associated with pathogenicity. Here we report the first animal model of the disease by expressing the human mutant TNPO3 gene in Drosophila musculature or motor neurons and concomitantly silencing the endogenous expression of the fly protein ortholog. A similar genotype expressing wildtype TNPO3 served as a control. Phenotypes characterization revealed that mutant TNPO3 expression targeted at muscles or motor neurons caused LGMDD2-like phenotypes such as muscle degener…

MaleMutantBiochemistryAnimals Genetically ModifiedMutant proteinAutophagyGeneticsmedicineAnimalsHumansGene silencingMuscular dystrophyMyopathyMolecular BiologyMotor NeuronsbiologyMusclesAutophagyChloroquinebeta Karyopherinsmedicine.diseasebiology.organism_classificationMuscle atrophyCell biologySurvival RateDisease Models AnimalMuscular AtrophyDrosophila melanogasterPhenotypeMuscular Dystrophies Limb-GirdleInsect HormonesFemalemedicine.symptomDrosophila melanogasterLocomotionBiotechnologyThe FASEB Journal
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