Search results for "gene knockdown"

showing 10 items of 174 documents

ERK1/2 activation in human taste bud cells regulates fatty acid signaling and gustatory perception of fat in mice and humans

2016

Obesity is a major public health problem. An in-depth knowledge of the molecular mechanisms of oro-sensory detection of dietary lipids may help fight it. Humans and rodents can detect fatty acids via lipido-receptors, such as CD36 and GPR120. We studied the implication of the MAPK pathways, in particular, ERK1/2, in the gustatory detection of fatty acids. Linoleic acid, a dietary fatty acid, induced via CD36 the phosphorylation of MEK1/2-ERK1/2-ETS-like transcription factor-1 cascade, which requires Fyn-Src kinase and lipid rafts in human taste bud cells (TBCs). ERK1/2 cascade was activated by Ca2+ signaling via opening of the calcium-homeostasis modulator-1 (CALHM1) channel. Furthermore, f…

0301 basic medicineSmall interfering RNAMouseCD36BiochemistryMapkObesechemistry.chemical_compound0302 clinical medicinegpr120Cd36Mice Knockoutchemistry.chemical_classificationGene knockdownbiologyKinaseFatty AcidsTaste PerceptionGPR120Taste BudsLipidsProtein-tyrosine kinases3. Good healthTasteBenzamidesBiotechnologymedicine.medical_specialtyMAP Kinase Signaling SystemLinoleic acid[SDV.BC]Life Sciences [q-bio]/Cellular BiologyPreferenceFood Preferences03 medical and health sciencesCalhm1Internal medicineDietary-fatGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCalcium SignalingObesityMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyResearchDiphenylamineFatty acidDietary FatsMicroRNAs030104 developmental biologyEndocrinologychemistrybiology.proteinIon-channelCALHM1Src kinase030217 neurology & neurosurgery
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Impact of Elastin-Derived Peptide VGVAPG on Matrix Metalloprotease-2 and -9 and the Tissue Inhibitor of Metalloproteinase-1, -2, -3 and -4 mRNA Expre…

2018

Degradation products of elastin, i.e. elastin-derived peptides (EDPs), are involved in various physiological and pathological processes. EDPs are detectable in cerebrospinal fluid in healthy people and in patients after ischemic stroke. However, to date, no studies concerning the role of EDP in the nervous system were conducted. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) play important roles during the repair phases of cerebral ischemia, particularly during angiogenesis and reestablishment of cerebral blood flow. Therefore, the aim of this study was to investigate the impact of the specific elastin-derived peptide VGVAPG on Mmp-2, -9 and Timp-1, -2,…

0301 basic medicineTIMPsAngiogenesisGene ExpressionApoptosisReceptors Cell SurfaceMatrix metalloproteinaseToxicology03 medical and health sciencesMice0302 clinical medicineGlial cellsAnimalsRNA MessengerCells CulturedCerebral CortexGene knockdownbiologyL-Lactate DehydrogenaseMMP-2ChemistryCaspase 3General NeuroscienceTissue Inhibitor of MetalloproteinasesTissue inhibitor of metalloproteinasebeta-GalactosidaseIn vitroMatrix MetalloproteinasesCell biologyElastin-derived peptides030104 developmental biologyApoptosisVGVAPGbiology.proteinOriginal ArticleMMP-9ElastinNeurogliaOligopeptides030217 neurology & neurosurgeryFetal bovine serumNeurotoxicity research
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Co-chaperone Hsp70/Hsp90-organizing protein (Hop) is required for transposon silencing and Piwi-interacting RNA (piRNA) biogenesis

2017

Piwi-interacting RNAs (piRNAs) are 26–30-nucleotide germ line-specific small non-coding RNAs that have evolutionarily conserved function in mobile genetic element (transposons) silencing and maintenance of genome integrity. Drosophila Hsp70/90-organizing protein homolog (Hop), a co-chaperone, interacts with piRNA-binding protein Piwi and mediates silencing of phenotypic variations. However, it is not known whether Hop has a direct role in piRNA biogenesis and transposon silencing. Here, we show that knockdown of Hop in the germ line nurse cells (GLKD) of Drosophila ovaries leads to activation of transposons. Hop GLKD females can lay eggs at the same rate as wild-type counterparts, but the e…

0301 basic medicineTransposable elementendocrine systemPiwi-interacting RNABiologyBiochemistryGenomic InstabilityHop (networking)Animals Genetically Modified03 medical and health sciences0302 clinical medicineAnimalsDrosophila ProteinsGene silencingGene SilencingRNA Small InterferingMolecular BiologyJanus KinasesGeneticsGene knockdownurogenital systemOvaryRNACell BiologyPhenotypeDrosophila melanogasterGerm Cells030104 developmental biologyAccelerated CommunicationsArgonaute ProteinsDNA Transposable ElementsFemale030217 neurology & neurosurgeryBiogenesisDNA DamageTranscription FactorsJournal of Biological Chemistry
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Selective α-synuclein knockdown in monoamine neurons by intranasal oligonucleotide delivery: potential therapy for parkinson’s disease

2018

Progressive neuronal death in brainstem nuclei and widespread accumulation of α-synuclein are neuropathological hallmarks of Parkinson’s disease (PD). Reduction of α-synuclein levels is therefore a potential therapy for PD. However, because α-synuclein is essential for neuronal development and function, α-synuclein elimination would dramatically impact brain function. We previously developed conjugated small interfering RNA (siRNA) sequences that selectively target serotonin (5-HT) or norepinephrine (NE) neurons after intranasal administration. Here, we used this strategy to conjugate inhibitory oligonucleotides, siRNA and antisense oligonucleotide (ASO), with the triple monoamine reuptake …

0301 basic medicineanimal diseasesDopamineOligonucleotidesGene ExpressionPharmacologySynaptic TransmissionPrefrontal cortexMiceDA neurotransmission0302 clinical medicineDrug DiscoveryMonoaminergicNeural PathwaysRNA Small InterferingCells Cultured5-HT neurotransmissionChemistryGene Transfer TechniquesParkinson DiseaseVentral tegmental areaSubstantia Nigramedicine.anatomical_structureCaudate putamenGene Knockdown Techniquesalpha-SynucleinMolecular MedicineRNA InterferenceOriginal ArticleMonoamine reuptake inhibitormedicine.drugSignal TransductionSerotoninSubstantia nigraASO03 medical and health sciencesProsencephalonα-synucleinDopamineIntranasal administrationGeneticsmedicineAnimalsHumansMolecular BiologyAdministration IntranasalPharmacologyPars compactaDopaminergic NeuronsGenetic TherapyCorpus Striatumnervous system diseases030104 developmental biologyMonoamine neurotransmitterGene Expression Regulationnervous systemsiRNAParkinson’s diseaseLocus coeruleus030217 neurology & neurosurgery
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Novel Modulators of Proteostasis: RNAi Screen of Chromosome I in a Heat Stress Paradigm in C. elegans

2018

Proteostasis is of vital importance for cellular function and it is challenged upon exposure to acute or chronic insults during neurodegeneration and aging. The proteostasis network is relevant for the maintenance of proteome integrity and mainly comprises molecular chaperones and two degradation pathways, namely, autophagy and the ubiquitin proteasome system. This network is characterized by an impressive functional interrelation and complexity, and occasionally novel factors are discovered that modulate proteostasis. Here, we present an RNAi screen in C. elegans, which aimed to identify modulators of proteostasis in a heat stress paradigm. The screen comprised genes that are located on ch…

0301 basic medicineautophagyproteostasis networkUPSArticle03 medical and health sciences0302 clinical medicinemedicinechaperonelcsh:QH301-705.5GeneRNAi screenGene knockdownproteostasisbiologyAutophagyNeurodegenerationneurodegenerationGeneral Medicinemedicine.diseaseCell biology030104 developmental biologyProteostasislcsh:Biology (General)ProteasomeChaperone (protein)Proteomebiology.proteinC. elegans<i>C. elegans</i>; RNAi screen; proteostasis; proteostasis network; autophagy; UPS; chaperone; neurodegeneration030217 neurology & neurosurgeryCells
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MECP2 impairs neuronal structure by regulating KIBRA

2016

Using a Drosophila model of MECP2 gain-of-function, we identified memory associated KIBRA as a target of MECP2 in regulating dendritic growth. We found that expression of human MECP2 increased kibra expression in Drosophila, and targeted RNAi knockdown of kibra in identified neurons fully rescued dendritic defects as induced by MECP2 gain-of-function. Validation in mouse confirmed that Kibra is similarly regulated by Mecp2 in a mammalian system. We found that Mecp2 gain-of-function in cultured mouse cortical neurons caused dendritic impairments and increased Kibra levels. Accordingly, Mecp2 loss-of-function in vivo led to decreased Kibra levels in hippocampus, cortex, and cerebellum. Togeth…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesCerebellumMethyl-CpG-Binding Protein 2Dendritic morphologyHippocampusDisease modelsHippocampusArticlelcsh:RC321-571MECP2Mice03 medical and health sciencesMemoryRNA interferencemental disordersmedicineAnimalsHumanslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCerebral CortexNeuronsGene knockdownMECP2 duplication syndromebiologybiology.organism_classificationMECP2nervous system diseasesCortex (botany)Disease Models AnimalDrosophila melanogaster030104 developmental biologymedicine.anatomical_structureNeurologyCerebral cortexDrosophilaDrosophila melanogasterNeuroscienceNeurobiology of Disease
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Mapping gene regulatory circuitry of Pax6 during neurogenesis.

2016

AbstractPax6 is a highly conserved transcription factor among vertebrates and is important in various aspects of the central nervous system development. However, the gene regulatory circuitry of Pax6 underlying these functions remains elusive. We find that Pax6 targets a large number of promoters in neural progenitors cells. Intriguingly, many of these sites are also bound by another progenitor factor, Sox2, which cooperates with Pax6 in gene regulation. A combinatorial analysis of Pax6-binding data set with transcriptome changes in Pax6-deficient neural progenitors reveals a dual role for Pax6, in which it activates the neuronal (ectodermal) genes while concurrently represses the mesoderma…

0301 basic medicineendocrine systemNeurogenesisBiologyBiochemistryArticle03 medical and health sciencesSOX2GeneticsMolecular BiologyTranscription factorGeneRegulation of gene expressionGeneticsGene knockdownNeurogenesisPromoterCell BiologyNeural progenitorseye diseasesChromatinCell biologyGene regulation030104 developmental biologyPAX6sense organsTranscription FactorsCell discovery
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Quantitative Assessment of Eye Phenotypes for Functional Genetic Studies Using Drosophila melanogaster

2016

AbstractAbout two-thirds of the vital genes in the Drosophila genome are involved in eye development, making the fly eye an excellent genetic system to study cellular function and development, neurodevelopment/degeneration, and complex diseases such as cancer and diabetes. We developed a novel computational method, implemented as Flynotyper software (http://flynotyper.sourceforge.net), to quantitatively assess the morphological defects in the Drosophila eye resulting from genetic alterations affecting basic cellular and developmental processes. Flynotyper utilizes a series of image processing operations to automatically detect the fly eye and the individual ommatidium, and calculates a phen…

0301 basic medicinegenetic structuresNeurogenesisComputational biologyInvestigationsQH426-470EyeAnimals Genetically Modified03 medical and health sciences0302 clinical medicineOmmatidiumGeneticsAnimalsDrosophila Proteinshuman disease modelsEnhancerMolecular BiologyGeneGenetics (clinical)Genetic Association StudiesGeneticsGene knockdownbiologyModels Geneticneurodevelopmental disordersReproducibility of Resultsbiology.organism_classificationommatidiaPhenotypeeye diseases030104 developmental biologyPhenotypeDrosophila melanogastermodifier screensrough eyeGene Knockdown TechniquesEye developmentsense organsDrosophila melanogaster030217 neurology & neurosurgeryDrosophila ProteinFunction (biology)AlgorithmsG3: Genes, Genomes, Genetics
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Long Non-coding Antisense RNA TNRC6C-AS1 Is Activated in Papillary Thyroid Cancer and Promotes Cancer Progression by Suppressing TNRC6C Expression

2018

Context: Evidences have shown the important role of long non-coding antisense RNAs in regulating its cognate sense gene in cancer biology. Objective: Investigate the regulatory role of a long non-coding antisense RNA TNRC6C-AS1 on its sense partner TNRC6C, and their effects on the aggressiveness and iodine-uptake ability of papillary thyroid cancer (PTC). Design: TNRC6C-AS1 was identified as the target long non-coding RNA in PTC by using microarray analysis and computational analysis. In vitro gain/loss-of-function experiments were performed to investigate the effects of TNRC6C-AS1 and TNRC6C on proliferation, apoptosis, migration, invasion and iodine-uptake ability of TPC1 cells. Expressio…

0301 basic medicinelong non-coding antisense RNAendocrine system diseasesEndocrinology Diabetes and MetabolismTNRC6C-AS1lcsh:Diseases of the endocrine glands. Clinical endocrinologyPapillary thyroid cancer03 medical and health sciencesEndocrinology0302 clinical medicineDownregulation and upregulationSense (molecular biology)medicinepapillary thyroid cancerTNRC6COriginal Researchiodine accumulationGene knockdownMessenger RNAlcsh:RC648-665ChemistryMicroarray analysis techniquesRNAmedicine.diseaseAntisense RNA030104 developmental biology030220 oncology & carcinogenesisCancer researchFrontiers in Endocrinology
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Insulin Dissociates the Effects of Liver X Receptor on Lipogenesis, Endoplasmic Reticulum Stress, and Inflammation

2016

IF 4.258; International audience; Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxr alpha in mice with hepatocytespecific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxr alpha …

0301 basic medicinemedicine.medical_treatmentLipid-metabolismResistanceBiochemistryHepatitisMESH: HepatitisMESH: Endoplasmic Reticulum Stresspolycyclic compoundsInsulinGene-expressionPhospholipidsLiver X ReceptorsMice KnockoutbiologyMESH : Gene Expression RegulationFatty-acid synthesisfood and beveragesEndoplasmic Reticulum StressOrphan Nuclear ReceptorsCultured-cellsLipidsMESH: Gene Expression RegulationMESH : Endoplasmic Reticulum StressMessenger-rnaLiverMESH: Orphan Nuclear ReceptorsGene Knockdown TechniquesLipogenesisFemalelipids (amino acids peptides and proteins)Signal Transductionliver X receptormedicine.medical_specialtyLxr-alphaMice Transgenicdigestive systemPhospholipid transfer proteinGene Expression Regulation Enzymologic03 medical and health sciencesInsulin resistanceMESH : HepatitisLysophosphatidylcholine acyltransferaseInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X receptorMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCrosses GeneticLipogenesisEndoplasmic reticulumInsulinElement-binding protein-1cMESH : LiverCell Biologymedicine.diseaseMESH : Orphan Nuclear ReceptorsReceptor InsulinMice Inbred C57BLInsulin receptor030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Gene Expression RegulationNuclear receptorbiology.proteinUnfolded protein responseInsulin ResistanceMESH: Liver
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