Search results for "gene silencing"

showing 10 items of 216 documents

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]
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Aurora-A Is Essential for the Tumorigenic Capacity and Chemoresistance of Colorectal Cancer Stem Cells

2010

Abstract Colorectal cancer stem cells (CR-CSC) are responsible for the generation and maintenance of intestinal tumors and are highly resistant to conventional chemotherapeutic agents. Aurora-A, a serine-threonine kinase involved in mitosis regulation, plays multiple key functions in tumor initiation and progression. We found that Aurora-A is overexpressed in primary colorectal tumor cells, in the CR-CSC fraction, and in stem cell–derived differentiated cells, compared with normal colon tissue. Aurora-A expression was functionally linked to centrosome amplification in CR-CSC, as indicated by the decrease in cells with multiple centrosomes that followed Aurora-A silencing. Knockdown of Auror…

MaleOncologyCancer Researchmedicine.medical_specialtyColorectal cancerCellular differentiationcolorectal cancer stem cellsMice NudeCell Growth ProcessesTumor initiationProtein Serine-Threonine KinasesBiologyMiceAurora KinasesCell MovementCancer stem cellInternal medicinemedicineAnimalsHumansCytotoxic T cellGene silencingMitosisAgedAurora Kinase ACentrosomeCell CycleGene AmplificationMiddle Agedmedicine.diseaseOncologyDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsCancer researchFemalebiological phenomena cell phenomena and immunityStem cellColorectal NeoplasmsCancer Research
researchProduct

PED is overexpressed and mediates TRAIL resistance in human non-small cell lung cancer

2008

PED (phosphoprotein enriched in diabetes) is a death-effector domain (DED) family member with a broad anti-apoptotic action. PED inhibits the assembly of the death-inducing signalling complex (DISC) of death receptors following stimulation. Recently, we reported that the expression of PED is increased in breast cancer cells and determines the refractoriness of these cells to anticancer therapy. In the present study, we focused on the role of PED in non-small cell lung cancer (NSCLC), a tumour frequently characterized by evasion of apoptosis and drug resistance. Immunohistochemical analysis of a tissue microarray, containing 160 lung cancer samples, indicated that PED was strongly expressed …

MaleProgrammed cell deathLung NeoplasmsNecrosisProtein Array AnalysisBiologyTransfectionTNF-Related Apoptosis-Inducing LigandCarcinoma Non-Small-Cell LungCell Line TumormedicineHumansGene silencingRNA Small InterferingLung cancerAgedAged 80 and overTissue microarrayAKTapoptosisIntracellular Signaling Peptides and ProteinsArticlesCell BiologyTransfectionMiddle AgedPhosphoproteinsmedicine.diseaseMolecular biologyRecombinant ProteinsUp-Regulationlung cancerReceptors TNF-Related Apoptosis-Inducing LigandDrug Resistance NeoplasmCell cultureApoptosisMolecular MedicineFemalemedicine.symptomApoptosis Regulatory ProteinsJournal of Cellular and Molecular Medicine
researchProduct

MUC1 intracellular bioactivation mediates lung fibrosis

2019

BackgroundSerum KL6/mucin 1 (MUC1) has been identified as a potential biomarker in idiopathic pulmonary fibrosis (IPF), but the role of MUC1 intracellular bioactivation in IPF is unknown.ObjectiveTo characterise MUC1 intracellular bioactivation in IPF.Methods and resultsThe expression and phosphorylation of Thr41 and Tyr46 on the intracellular MUC1-cytoplasmic tail (CT) was increased in patients with IPF (n=22) compared with healthy subjects (n=21) and localised to fibroblasts and hyperplastic alveolar type II cells. Transforming growth factor (TGF)-β1 phosphorylated SMAD3 and thereby increased the phosphorylation of MUC1-CT Thr41 and Tyr46 in lung fibroblasts and alveolar type II cells, ac…

MalePulmonary and Respiratory MedicineCellRisk AssessmentTransforming Growth Factor beta1BleomycinMice03 medical and health sciencesIdiopathic pulmonary fibrosis0302 clinical medicinemedicineAnimalsHumansGene silencingMolecular Targeted TherapyRNA MessengerSmad3 ProteinFibroblastneoplasmsCells CulturedMUC1030304 developmental biologyMice Knockout0303 health sciencesbusiness.industryBiopsy NeedleMucin-1Fibroblastsmedicine.diseaseImmunohistochemistryIdiopathic Pulmonary Fibrosisdigestive system diseasesDisease Models Animalmedicine.anatomical_structureGene Expression Regulation030228 respiratory systemCancer researchFemalebusinessMyofibroblastIntracellularSignal TransductionTransforming growth factorThorax
researchProduct

Y chromosomes: born to be destroyed

2005

Suppression of recombination is the prerequisite for stable genetically determined sex systems. A consequence of suppression of recombination is the strong bias in the distribution of transposable elements (TEs), mostly retrotransposons. Our results and those from others indicate that the major force driving the degeneration of Y chromosomes are retrotransposons in remodelling former euchromatic chromosome structures into heterochromatic ones. We put forward the following hypotheses. (1) A massive accumulation of retrotransposons occurs early in non-recombining regions. (2) Heterochromatic nucleation centres are formed as a genomic defence mechanism against invasive parasitic elements. The …

MaleRecombination GeneticTransposable elementGeneticsDosage compensationRetroelementsEuchromatinHeterochromatinGene DosageRetrotransposonSex Determination ProcessesBiologyY chromosomeGene dosageGeneral Biochemistry Genetics and Molecular BiologyEvolution MolecularHeterochromatinY ChromosomeAnimalsHumansDrosophilaFemaleGene SilencingGeneBioEssays
researchProduct

XRCC5 as a Risk Gene for Alcohol Dependence : Evidence from a Genome-Wide Gene-Set-Based Analysis and Follow-up Studies in Drosophila and Humans

2015

Genetic factors play as large a role as environmental factors in the etiology of alcohol dependence. Although genome-wide association studies (GWAS) enable systematic searches for loci not hitherto implicated in the etiology of alcohol dependence, many true findings may be missed due to correction for multiple testing. The aim of the present study was to circumvent this limitation by searching for biological system-level differences, and then following up these findings in humans and animals. Gene-set based analysis of GWAS data from 1333 cases and 2168 controls identified 19 significantly associated gene-sets of which five could be replicated in an independent sample. Clustered in these ge…

MaleRiskAdolescentMedizinGenome-wide association studyBiologyPolymorphism Single NucleotideWhite PeopleAnimals Genetically ModifiedRNA interferenceGermanyGenetic variationAnimalsHumansGene silencingGenetic Predisposition to DiseaseKu AutoantigenGeneGenetic associationPharmacologyGeneticsEthanolAlcohol dependenceDNA HelicasesCentral Nervous System DepressantsPhenotypeAlcoholismPsychiatry and Mental healthDrosophila melanogasterFemaleOriginal ArticleFollow-Up StudiesGenome-Wide Association Study
researchProduct