Search results for "RNA interference"

showing 10 items of 202 documents

IP 3 signalling regulates exogenous RNA i in C aenorhabditis elegans

2015

RNA interference (RNAi) is a widespread and widely exploited phenomenon. Here, we show that changing inositol 1,4,5-trisphosphate (IP3) signalling alters RNAi sensitivity in Caenorhabditis elegans. Reducing IP3 signalling enhances sensitivity to RNAi in a broad range of genes and tissues. Conversely up-regulating IP3 signalling decreases sensitivity. Tissue-specific rescue experiments suggest IP3 functions in the intestine. We also exploit IP3 signalling mutants to further enhance the sensitivity of RNAi hypersensitive strains. These results demonstrate that conserved cell signalling pathways can modify RNAi responses, implying that RNAi responses may be influenced by an animal's physiology…

inorganic chemicalscalcium signallingCell signalingMutantInositol 145-TrisphosphateBiologyModels BiologicalBiochemistryRNA interferenceRNA interferenceImage Processing Computer-AssistedGeneticsAnimalsIntestinal MucosaCaenorhabditis elegansMolecular BiologyCaenorhabditis elegansRNA Double-StrandedCalcium signalingenhanced RNAiScientific Reportsfungiinositol 145‐trisphosphateRNAbiology.organism_classificationC. elegansCell biologySignallingMicroscopy FluorescenceSignal transductionSignal TransductionEMBO reports
researchProduct

Mutant HRAS as novel target for MEK and mTOR inhibitors.

2015

HRAS is a frequently mutated oncogene in cancer. However, mutant HRAS as drug target has not been investigated so far. Here, we show that mutant HRAS hyperactivates the RAS and the mTOR pathway in various cancer cell lines including lung, bladder and esophageal cancer. HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901. Further, we found that MEK inhibitors induce apoptosis in mutant HRAS cell lines but not in cell lines lacking RAS mutations. In addition, knockdown of HRAS by siRNA blocked cell growth in mutant HRAS cell lines. Inhibition of the PI3K pathway alone or in combination with MEK inhibitors did not alter signaling nor had an imp…

mTOR inhibitorMutantBlotting Western610 Medicine & healthApoptosisMice SCIDCell LineProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundCell Line TumorNeoplasmsMedicineAnimalsHumansHRASHRAS mutationsProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationGeneticsMitogen-Activated Protein Kinase KinasesMEK inhibitorOncogeneCell growthbusiness.industryMEK inhibitorTOR Serine-Threonine KinasesDiphenylamineXenograft Model Antitumor AssaysTumor Burdenlung cancer10219 Clinic for Gastroenterology and HepatologyCell Transformation NeoplasticOncologychemistry10032 Clinic for Oncology and HematologyBenzamidesMutationCancer researchbladder cancer2730 OncologyBenzimidazolesRNA InterferenceSignal transductionGrowth inhibitionbusinessSignal TransductionResearch PaperOncotarget
researchProduct

Diacylglycerol kinase α mediatses 17-β-estradiol-induced proliferation, motility, and anchorage-independent growth of Hec-1A endometrial cancer cell …

2011

Increased levels of endogenous and/or exogenous estrogens are one of the well known risk factors of endometrial cancer. Diacylglycerol kinases (DGKs) are a family of enzymes which phosphorylate diacylglycerol (DAG) to produce phosphatidic acid (PA), thus turning off and on DAG-mediated and PA-mediated signaling pathways, respectively. DGK α activity is stimulated by growth factors and oncogenes and is required for chemotactic, proliferative, and angiogenic signaling in vitro. Herein, using either specific siRNAs or the pharmacological inhibitor R59949, we demonstrate that DGK α activity is required for 17-β-estradiol (E2)-induced proliferation, motility, and anchorage-independent growth of …

medicine.medical_specialtyGPR30medicine.drug_classCell SurvivalDiacylglycerol kinaseMotilityEstrogen receptorEnzyme AssayEndometrial carcinomaBiologyQuinazolinoneReceptors G-Protein-CoupledPiperidinePiperidinesCell MovementInternal medicineCell Line TumormedicineCell AdhesionHumansEndometrial NeoplasmEnzyme AssaysQuinazolinonesDiacylglycerol kinaseCell ProliferationEstradiolCell growthKinaseCell BiologyDiacylglycerol kinase; Endometrial carcinoma; Estrogen; GPR30; Cell BiologyEstrogenEndometrial NeoplasmsCell biologyEnzyme ActivationLipoprotein LipaseEndocrinologyReceptors EstrogenEstrogenGene Knockdown TechniquesGene Knockdown TechniqueFemaleRNA InterferenceSignal transductionGPERHuman
researchProduct

Downregulation of alpha-galactosidase A upregulates CD77: functional impact for Fabry nephropathy.

2009

Anderson-Fabry disease, an inherited deficiency in the lysosomal enzyme alpha-galactosidase A, is characterized by the progressive accumulation of globotriaosylceramide (Gb3), also known as CD77. We sought to clarify the pathogenesis of Fabry disease by establishing a cell model of this disorder. The expression of alpha-galactosidase A was transiently silenced by RNA interference in HK2 and primary human renal epithelial cells and stably silenced in HK2 cells by retroviral transfection with small hairpin RNA. All of the silenced cells had histological similarities to cells of patients with Fabry disease. The cells had reduced viability, significant accumulation of intracellular Gb3, and a m…

medicine.medical_specialtyGlobotriaosylceramideGb3Cell LineSmall hairpin RNAchemistry.chemical_compoundRNA interferenceDownregulation and upregulationInternal medicineMedicineGene silencingHumansGene SilencingRNA Small InterferingAnderson–Fabry diseaseGlobosidesbusiness.industryTrihexosylceramidesEpithelial CellsTransfectionEnzyme replacement therapymedicine.diseaseFabry diseaseα-galactosidaseEndocrinologychemistryGene Expression RegulationNephrologyCell culturealpha-GalactosidaseCancer researchFabry DiseaseCD77businessenzyme replacement therapyKidney international
researchProduct

Embryonic adhesion is not affected by endometrial leptin receptor gene silencing.

2006

Objective In rodents, evidence suggests that the leptin system is mandatory for embryonic implantation. We aimed to investigate the functional relevance of the endometrial leptin receptor (OB-R) in the adhesion phase of human implantation. Design We used an in vitro model for embryonic adhesion, composed of a human endometrial cell line (HEC1-A) and B6C3F1 mouse embryos. The OB-R gene was silenced in a stable manner by RNA interference, and embryonic adhesion rates were analyzed. Setting Research laboratory at a university-affiliated center. Intervention(s) RNA interference. Main Outcome Measure(s) Embryonic adhesion in cells treated with OB-R RNAi. Result(s) The OB-R shRNA-transfected cell…

medicine.medical_specialtyReceptors Cell SurfaceBiologyCell LineSmall hairpin RNAEndometriumMiceRNA interferencePregnancyInternal medicinemedicineCell AdhesionGene silencingAnimalsHumansBlastocystEmbryo ImplantationGene SilencingCells CulturedLeptin receptorObstetrics and GynecologyTransfectionEmbryo MammalianEmbryonic stem cellCell biologymedicine.anatomical_structureEndocrinologyReproductive MedicineReceptors LeptinNeural cell adhesion moleculeFemaleFertility and sterility
researchProduct

Cigarette smoke alters non-neuronal cholinergic system components inducing MUC5AC production in the H292 cell line.

2013

Abstract Cigarette smoke extract (CSE) affects the expression of Choline Acetyl-Transferase (ChAT), muscarinic acetylcholine receptors, and mucin production in bronchial epithelial cells. Mucin 5AC (MUC5AC), muscarinic acetylcholine receptor M3, ChAT expression, acetylcholine levels and acetylcholine binding were measured in a human pulmonary mucoepidermoid carcinoma cell line (H292) stimulated with CSE. We performed ChAT/RNA interference experiments in H292 cells stimulated with CSE to study the role of ChAT/acetylcholine in MUC5AC production. The effects of Hemicholinium-3 (HCh-3) (50 μM) (a potent and selective choline uptake blocker) and Tiotropium bromide (Spiriva ® ) (100 nM), alone o…

medicine.medical_specialtyScopolamine DerivativesBronchiComplex MixturesMucin 5ACCholinergic AntagonistsCholine O-Acetyltransferasechemistry.chemical_compoundAcetylcholine bindingInternal medicineCell Line TumorSmokeparasitic diseasesMuscarinic acetylcholine receptorTobaccomedicineCholineHumansSecretionAlbuterolNeurotransmitter Uptake InhibitorsTiotropium BromideAutocrine signallingSalmeterol XinafoatePharmacologyReceptor Muscarinic M3Epithelial CellsHemicholinium 3respiratory systemCholine acetyltransferaseAcetylcholineBronchodilator AgentsAndrostadienesEndocrinologychemistryCell cultureFluticasoneRNA InterferenceAcetylcholinemedicine.drugEuropean journal of pharmacology
researchProduct

Muscleblind, BSF and TBPH are mislocalized in the muscle sarcomere of a Drosophila myotonic dystrophy model

2012

SummaryMyotonic dystrophy type 1 (DM1) is a genetic disease caused by the pathological expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene. In the DMPK transcripts, the CUG expansions sequester RNA-binding proteins into nuclear foci, including transcription factors and alternative splicing regulators such as MBNL1. MBNL1 sequestration has been associated with key features of DM1. However, the basis behind a number of molecular and histological alterations in DM1 remain unclear. To help identify new pathogenic components of the disease, we carried out a genetic screen using a Drosophila model of DM1 that expresses 480 interrupted CTG repeats, i(CTG)480, and a collection of…

musculoskeletal diseasesSarcomerescongenital hereditary and neonatal diseases and abnormalitiesNeuroscience (miscellaneous)lcsh:MedicineMedicine (miscellaneous)RNA-binding proteinGenes InsectBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically Modifiedchemistry.chemical_compoundImmunology and Microbiology (miscellaneous)RNA interferencelcsh:PathologymedicineMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophyGeneticsMuscleslcsh:RAlternative splicingNuclear ProteinsRNA-Binding ProteinsEpistasis Geneticmedicine.diseaseDisease Models AnimalchemistryGene Knockdown TechniquesDrosophilaFemaleRNA InterferenceTrinucleotide repeat expansionTrinucleotide Repeat ExpansionDrosophila Proteinlcsh:RB1-214Genetic screenResearch ArticleDisease Models & Mechanisms
researchProduct

Apollon gene silencing induces apoptosis in breast cancer cells via p53 stabilisation and caspase-3 activation

2009

We analysed the effects of small interfering RNA (siRNA)-mediated silencing of Apollon, a member of the inhibitors of apoptosis protein family, on the proliferative potential and ability of human breast cancer cell lines to undergo apoptosis. In wild-type p53 ZR75.1 cells, Apollon knockdown resulted in a marked, time-dependent decline of cell growth and an increased rate of apoptosis, which was associated with p53 stabilisation and activation of the mitochondrial-dependent apoptotic pathway. Pre-incubation of cells with a p53-specific siRNA resulted in a partial rescue of cell growth inhibition, as well as in a marked reduction of the apoptotic response, indicating p53 as a major player in …

p53Cancer ResearchSmall interfering RNAProgrammed cell deathcaspase-3ApollonCaspase 3Breast NeoplasmsApollon gene apoptosisBiologyModels BiologicalInhibitor of Apoptosis ProteinsRNA interferenceTumor Cells CulturedGene silencingHumansGene SilencingRNA Small InterferingCell Proliferationhuman breast cancerGene knockdownCell growthCaspase 3Protein StabilityapoptosisEnzyme ActivationOncologyApoptosissiRNACancer researchSettore BIO/14 - FarmacologiaFemaleTumor Suppressor Protein p53Translational Therapeutics
researchProduct

Induction of body weight loss through RNAi-knockdown of APOBEC1 gene expression in transgenic rabbits

2014

In the search of new strategies to fight against obesity, we targeted a gene pathway involved in energy uptake. We have thus investigated the APOB mRNA editing protein (APOBEC1) gene pathway that is involved in fat absorption in the intestine. The APOB gene encodes two proteins, APOB100 and APOB48, via the editing of a single nucleotide in the APOB mRNA by the APOBEC1 enzyme. The APOB48 protein is mandatory for the synthesis of chylomicrons by intestinal cells to transport dietary lipids and cholesterol. We produced transgenic rabbits expressing permanently and ubiquitously a small hairpin RNA targeting the rabbit APOBEC1 mRNA. These rabbits exhibited a moderately but significantly reduced …

perte de poidsobesityApolipoprotein BAgricultural BiotechnologyGene Expressionlcsh:MedicinetransgenesisSmall hairpin RNAAnimals Genetically Modified0302 clinical medicinesirnaRNA interferenceGene expressionGene Knockdown TechniquesBiologie de la reproductionMedicine and Health SciencesTransgenesIntestinal MucosaRNA Small Interferinglcsh:Science[SDV.BDD]Life Sciences [q-bio]/Development Biology2. Zero hunger0303 health sciencesGene knockdownReproductive BiologyMultidisciplinarybiologyGenetically Modified OrganismsBiologie du développementapobec1; obesity; editing apob; apob100; apob48; chylomicron; intestine; rabbit; sirna; transgenesis; knockdownchylomicronknockdownAgricultureInherited Metabolic DisordersDevelopment BiologyobésitéCholesterolPhenotypeTransgenic Engineering[ SDV.BDLR ] Life Sciences [q-bio]/Reproductive BiologyLiverapobapob48Gene Knockdown Techniquesanimal transgéniqueRNA Interferencelipids (amino acids peptides and proteins)RabbitsGenetic EngineeringResearch ArticleBiotechnologyexpression géniqueTransgeneAPOBEC-1 DeaminaseMolecular Sequence DatarabbitDiet High-Fat03 medical and health sciencesintestinCytidine DeaminaseWeight Loss[SDV.BDD] Life Sciences [q-bio]/Development BiologyAnimalsHumanslapinRNA Messenger[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyintestineTriglycerides[SDV.BDLR] Life Sciences [q-bio]/Reproductive Biology030304 developmental biologyapobec1Base SequenceGenetically Modified AnimalsAPOBEC1editinglcsh:RBiology and Life Sciences[SDV.BDLR]Life Sciences [q-bio]/Reproductive BiologyMolecular biologyapob100DyslipidemiaMetabolic Disordersbiology.proteinlcsh:QRNA EditingApolipoprotein B-48030217 neurology & neurosurgery
researchProduct

Single-cell analysis of population context advances RNAi screening at multiple levels

2012

Isogenic cells in culture show strong variability, which arises from dynamic adaptations to the microenvironment of individual cells. Here we study the influence of the cell population context, which determines a single cell's microenvironment, in image‐based RNAi screens. We developed a comprehensive computational approach that employs Bayesian and multivariate methods at the single‐cell level. We applied these methods to 45 RNA interference screens of various sizes, including 7 druggable genome and 2 genome‐wide screens, analysing 17 different mammalian virus infections and four related cell physiological processes. Analysing cell‐based screens at this depth reveals widespread RNAi‐induce…

toImage ProcessingDruggabilityGenomeImage analysis0302 clinical medicineComputer-AssistedSX00 SystemsX.ch2604 Applied MathematicsSingle-cell analysisRNA interferenceModels2400 General Immunology and MicrobiologyImage Processing Computer-AssistedViralRNA Small Interfering0303 health scienceseducation.field_of_studyApplied MathematicsSystems BiologyGenomics10124 Institute of Molecular Life SciencesCell biologycell variabilityComputational Theory and MathematicsCellular MicroenvironmentVirus DiseasesVirusesRNA ViralRNA InterferenceSingle-Cell AnalysisGeneral Agricultural and Biological SciencesInformation SystemsSystems biologyVirus infectionPopulationContext (language use)Genomics1100 General Agricultural and Biological SciencesBiologySmall InterferingModels BiologicalGeneral Biochemistry Genetics and Molecular BiologySX08 LipidX03 medical and health sciencesViral ProteinsCell-to-cell variability; Image analysis; Population context; RNAi; Virus infection1300 General Biochemistry Genetics and Molecular BiologyHumansComputer Simulationeducation030304 developmental biologyGeneral Immunology and MicrobiologyCell-to-cell variabilityReproducibility of ResultsBayes TheoremcellBiologicalPopulation contextRNAi570 Life sciences; biologyRNA030217 neurology & neurosurgeryHeLa CellsMolecular Systems Biology
researchProduct