Search results for "knockdown"

showing 10 items of 178 documents

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
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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Mutation ofPOC1Bin a Severe Syndromic Retinal Ciliopathy

2014

We describe a consanguineous Iraqi family with Leber congenital amaurosis (LCA), Joubert syndrome (JBTS), and polycystic kidney disease (PKD). Targeted next-generation sequencing for excluding mutations in known LCA and JBTS genes, homozygosity mapping, and whole-exome sequencing identified a homozygous missense variant, c.317G>C (p.Arg106Pro), in POC1B, a gene essential for ciliogenesis, basal body, and centrosome integrity. In silico modeling suggested a requirement of p.Arg106 for the formation of the third WD40 repeat and a protein interaction interface. In human and mouse retina, POC1B localized to the basal body and centriole adjacent to the connecting cilium of photoreceptors and in …

MaleRetinal degenerationgenetic structuresAmino Acid MotifsLeber Congenital AmaurosisMolecular Sequence DataCell Cycle ProteinsBiologyKidneyArticleRetinaJoubert syndromeMiceCerebellar DiseasesCerebellumCiliogenesisRetinitis pigmentosaGeneticsmedicineAnimalsHumansAbnormalities MultipleAmino Acid SequenceCiliaEye AbnormalitiesChildZebrafishGenetics (clinical)Cystic kidneyGeneticsCiliumKidney Diseases Cysticmedicine.diseaseDisease gene identificationeye diseasesPedigreeCiliopathyGene Knockdown TechniquesIraqMutationsense organsHuman Mutation
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Hypothalamic eIF2 alpha signaling regulates food intake

2014

International audience; The reversible phosphorylation of the a subunit of eukaryotic initiation factor 2 (eIF2 alpha) is a highly conserved signal implicated in the cellular adaptation to numerous stresses such as the one caused by amino acid limitation. In response to dietary amino acid deficiency, the brain-specific activation of the eIF2 alpha kinase GCN2 leads to food intake inhibition. We report here that GCN2 is rapidly activated in the mediobasal hypothalamus (MBH) after consumption of a leucine-deficient diet. Furthermore, knockdown of GCN2 in this particular area shows that MBH GCN2 activity controls the onset of the aversive response. Importantly, pharmacological experiments demo…

Male[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEukaryotic Initiation Factor-2neuronsEatingMicepiriform cortex0302 clinical medicineGene Knockdown Techniquesarcuate nucleusamino-acid deficiency;arcuate nucleus;translational control;energy homeostasis;piriform cortex;cancer cachexia;protein-intake;transfer-rna;mechanism;neuronsPhosphorylationlcsh:QH301-705.52. Zero hungerchemistry.chemical_classification0303 health sciencesGene knockdownalimentationtranslational controlamino-acid deficiencyEukaryotic Initiation Factor-2Amino acidtransfer-rnaGene Knockdown TechniquesAlimentation et NutritionPhosphorylation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Signal transductionmedicine.symptomSignal Transductioncancer cachexiamedicine.medical_specialtyCellular adaptationHypothalamusmechanismAnorexiaBiologyProtein Serine-Threonine KinasesGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesLeucineInternal medicinemedicineFood and NutritionAnimalsenergy homeostasis030304 developmental biologyNeurosciencesArcuate Nucleus of Hypothalamusprotein-intakeMice Inbred C57BL[SDV.AEN] Life Sciences [q-bio]/Food and NutritionEndocrinologychemistrylcsh:Biology (General)Neurons and Cognition[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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Dexamethasone upregulates Nox1 expression in vascular smooth muscle cells.

2014

<b><i>Background/Aim:</i></b> It has been demonstrated that dexamethasone-induced hypertension can be prevented by the NADPH oxidase inhibitor apocynin. The effect of dexamethasone on NADPH oxidase, however, is unknown. The present study was conducted to investigate the effect of dexamethasone on the gene expression of Nox1, the major NADPH oxidase isoform in vascular smooth muscle cells. <b><i>Results:</i></b> Oral treatment of Wistar-Kyoto rats with dexamethasone (0.03 mg/kg/day) for 12 days led to an upregulation of Nox1 mRNA expression in the aorta. In cultured A7r5 rat aortic smooth muscle cells, dexamethasone increased Nox1 mRNA expressi…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsMyocytes Smooth Musclemedicine.disease_causeRats Inbred WKYDexamethasoneHistone DeacetylasesMuscle Smooth Vascularchemistry.chemical_compoundReceptors GlucocorticoidInternal medicinemedicineAnimalsNADH NADPH Oxidoreductasescardiovascular diseasesRNA MessengerGlucocorticoidsDexamethasoneAortaPharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyDose-Response Relationship DrugChemistryfungifood and beveragesGeneral MedicineRatsUp-RegulationEndocrinologyNOX1Gene Knockdown TechniquesApocynincardiovascular systembiology.proteinNADPH Oxidase 1Oxidative stresscirculatory and respiratory physiologymedicine.drugPharmacology
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Genomic run-on evaluates transcription rates for all yeast genes and identifies gene regulatory mechanisms

2004

Most studies of eukaryotic gene regulation have been done looking at mature mRNA levels. Nevertheless, the steady-state mRNA level is the result of two opposing factors: transcription rate (TR) and mRNA degradation. Both can be important points to regulate gene expression. Here we show a new method that combines the use of nylon macroarrays and in vivo radioactive labeling of nascent RNA to quantify TRs, mRNA levels, and mRNA stabilities for all the S. cerevisiae genes. We found that during the shift from glucose to galactose, most genes undergo drastic changes in TR and mRNA stability. However, changes in mRNA levels are less pronounced. Some genes, such as those encoding mitochondrial pro…

Mature messenger RNATranscription GeneticRNA StabilityGenes FungalMolecular Sequence DataBiologySaccharomycesTranscripció genèticaTranscription (biology)Gene Expression Regulation FungalGene expressionP-bodiesRNA MessengerMolecular BiologyGenePhylogenyRegulation of gene expressionMessenger RNAGene knockdownGenomeGene Expression ProfilingGalactoseRNA FungalCell BiologyBlotting NorthernMolecular biologyCell biologyGenòmicaGlucose
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Glial expression of Swiss cheese (SWS), the Drosophila orthologue of neuropathy target esterase (NTE), is required for neuronal ensheathment and func…

2016

ABSTRACT Mutations in Drosophila Swiss cheese (SWS) or its vertebrate orthologue neuropathy target esterase (NTE), respectively, cause progressive neuronal degeneration in Drosophila and mice and a complex syndrome in humans that includes mental retardation, spastic paraplegia and blindness. SWS and NTE are widely expressed in neurons but can also be found in glia; however, their function in glia has, until now, remained unknown. We have used a knockdown approach to specifically address SWS function in glia and to probe for resulting neuronal dysfunctions. This revealed that loss of SWS in pseudocartridge glia causes the formation of multi-layered glial whorls in the lamina cortex, the firs…

Medicine (miscellaneous)lcsh:MedicineAxonal degenerationSynaptic Transmission0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsNeurons0303 health sciencesGene knockdownCell Deathmusculoskeletal neural and ocular physiologyPhototaxisAnatomyCell biologymedicine.anatomical_structureDrosophila melanogasterPhospholipasesGene Knockdown TechniquesNeurogliaNeurogliaDrosophila Proteinpsychological phenomena and processesResearch Articlelcsh:RB1-214Programmed cell deathNeuriteNeuroscience (miscellaneous)Nerve Tissue ProteinsNeuropathy target esteraseNeurotransmissionBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesPNPLA6mental disordersNeuropilmedicineNeuriteslcsh:PathologyAnimalsPhospholipaseCell Shape030304 developmental biologySequence Homology Amino AcidSpastic paraplegialcsh:R302Reproducibility of ResultsEnsheathing gliabody regionsnervous systemVacuolesbiology.proteinCarboxylic Ester Hydrolases030217 neurology & neurosurgeryDisease Models & Mechanisms
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FSHD muscular dystrophy region gene 1 binds Suv4-20h1 histone methyltransferase and impairs myogenesis.

2013

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant myopathy with a strong epigenetic component. It is associated with deletion of a macrosatellite repeat leading to over-expression of the nearby genes. Among them, we focused on FSHD region gene 1 (FRG1) since its over-expression in mice, Xenopus laevis and Caenorhabditis elegans, leads to muscular dystrophy-like defects, suggesting that FRG1 plays a relevant role in muscle biology. Here we show that, when over-expressed, FRG1 binds and interferes with the activity of the histone methyltransferase Suv4-20h1 both in mammals and Drosophila. Accordingly, FRG1 over-expression or Suv4-20h1 knockdown inhibits myogenesis. Moreov…

Muscle DevelopmentEvolution Molecular03 medical and health sciencesMice0302 clinical medicineGeneticsmedicineFacioscapulohumeral muscular dystrophyMyocyteAnimalsHumansEpigeneticsMuscular dystrophyMyopathyMolecular Biology030304 developmental biologyCell NucleusMice Knockout0303 health sciencesMuscle CellsbiologyMyogenesisMicrofilament ProteinsNuclear ProteinsProteinsRNA-Binding ProteinsCell DifferentiationCell BiologyGeneral MedicineHistone-Lysine N-MethyltransferaseMuscular Dystrophy Animalmedicine.diseaseMolecular biologyHistoneDrosophila melanogasterHEK293 CellsPhenotypeOrgan SpecificityHistone methyltransferaseEpigenetic deregulation by FRG1Gene Knockdown Techniquesbiology.proteinmedicine.symptomCarrier Proteins030217 neurology & neurosurgeryProtein BindingJournal of molecular cell biology
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SIRT1 prevents genotoxic stress-induced p53 activation in acute myeloid leukemia

2014

SIRT1 is an important regulator of cellular stress response and genomic integrity. Its role in tumorigenesis is controversial. Whereas sirtuin 1 (SIRT1) can act as a tumor suppressor in some solid tumors, increased expression has been demonstrated in many cancers, including hematologic malignancies. In chronic myeloid leukemia, SIRT1 promoted leukemia development, and targeting SIRT1 sensitized chronic myeloid leukemia progenitors to tyrosine kinase inhibitor treatment. In this study, we investigated the role of SIRT1 in acute myeloid leukemia (AML). We show that SIRT1 protein, but not RNA levels, is overexpressed in AML samples harboring activating mutations in signaling pathways. In FMS-l…

Myeloidendocrine system diseasesmedicine.drug_classImmunologyBiologymedicine.disease_causeBiochemistryTyrosine-kinase inhibitorMiceSirtuin 1hemic and lymphatic diseasesmedicineAnimalsHumansGene Knock-In TechniquesKinase activityfood and beveragesMyeloid leukemiaCell BiologyHematologymedicine.diseaseEnzyme ActivationMice Inbred C57BLLeukemia Myeloid Acuteenzymes and coenzymes (carbohydrates)Leukemiamedicine.anatomical_structureGene Knockdown TechniquesCancer researchHeterograftsTumor Suppressor Protein p53Signal transductionCarcinogenesisTyrosine kinasehormones hormone substitutes and hormone antagonistsDNA DamageSignal TransductionBlood
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miR379-410 cluster miRNAs regulate neurogenesis and neuronal migration by fine-tuning N-cadherin

2014

N-cadherin-mediated adhesion is essential for maintaining the tissue architecture and stem cell niche in the developing neocortex. N-cadherin expression level is precisely and dynamically controlled throughout development; however, the underlying regulatory mechanisms remain largely unknown. MicroRNAs (miRNAs) play an important role in the regulation of protein expression and subcellular localisation. In this study, we show that three miRNAs belonging to the miR379–410 cluster regulate N-cadherin expression levels in neural stem cells and migrating neurons. The overexpression of these three miRNAs in radial glial cells repressed N-cadherin expression and increased neural stem cell different…

NeurogenesisCellular differentiationBiologyGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineNeural Stem CellsAntigens CDCell MovementmicroRNAmedicineAnimals10. No inequalityMolecular Biology030304 developmental biologyRegulation of gene expression0303 health sciencesGene knockdownNeocortexGeneral Immunology and MicrobiologyCadherinGeneral NeuroscienceNeurogenesisGene Expression Regulation DevelopmentalArticlesCadherinsNeural stem cellCell biologyMicroRNAsmedicine.anatomical_structure030217 neurology & neurosurgeryThe EMBO Journal
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