Search results for "knockdown"

showing 10 items of 178 documents

Dimerization of the kinase ARAF promotes MAPK pathway activation and cell migration.

2014

The RAF family of kinases mediates RAS signaling, and RAF inhibitors can be effective for treating tumors with BRAF V600E mutant protein. However, RAF inhibitors paradoxically accelerate metastasis in RAS -mutant tumors and become ineffective in BRAF V600E tumors because of reactivation of downstream mitogen-activated protein kinase (MAPK) signaling. We found that the RAF isoform ARAF has an obligatory role in promoting MAPK activity and cell migration in a cell type–dependent manner. Knocking down ARAF prevented the activation of MAPK kinase 1 (MEK1) and extracellular signal–regulated kinase 1 and 2 (ERK1/2) and decreased the number of protrusions from tumor cell spheroids in three-dimensi…

MAPK/ERK pathwayScaffold proteinModels MolecularNiacinamideProto-Oncogene Proteins B-rafMAP Kinase Signaling SystemBlotting WesternMAP Kinase Kinase 1MAPK cascadeBiologyKSR1BiochemistryBinding CompetitiveProto-Oncogene Proteins A-rafTime-Lapse ImagingMutant proteinCell MovementTumor Cells CulturedHumansNeoplasm InvasivenessRNA Small InterferingProtein kinase AMolecular BiologyAnalysis of VarianceKinasePhenylurea CompoundsCell BiologySorafenibCell biologyEnzyme ActivationProto-Oncogene Proteins c-rafHEK293 CellsIndenesGene Knockdown TechniquesCancer researchPyrazolesElectrophoresis Polyacrylamide GelARAFDimerizationScience signaling
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Novel combination of celecoxib and proteasome inhibitor MG132 provides synergistic antiproliferative and proapoptotic effects in human liver tumor ce…

2010

Molecular targeted therapy has shown promise as a treatment for advanced hepatocellular carcinoma (HCC). Celecoxib (Celebrex®) exhibits antitumor effects in human HCC cells, and its mechanism of action is mediated either by its ability to inhibit cyclooxygenase 2 (COX-2) or by a number of various other COX-2 independent effects. Proteasome inhibitors (PIs) can exert cell growth inhibitory and apoptotic effects in different tumor cell types, including HCC cells. The present study examined the interaction between celecoxib and the PI MG132 in two human liver tumor cell lines HepG2 and HA22T/VGH. Our data showed that each inhibitor reduced proliferation and induced apoptosis in a dose-dependen…

MG132TRB3Programmed cell deathLeupeptinsBlotting WesternApoptosisUPRPharmacologyCysteine Proteinase Inhibitorschemistry.chemical_compoundMG132medicineHumansViability assayHCCMolecular BiologyCell ProliferationSettore MED/12 - GastroenterologiaGene knockdownSulfonamidesbiologyCyclooxygenase 2 InhibitorsCell growthReverse Transcriptase Polymerase Chain ReactionDrug SynergismCell BiologyHep G2 CellsCOX-2ER stress responseFlow CytometryapoptosiproteasomechemistryApoptosisCelecoxibSettore BIO/14 - Farmacologiabiology.proteinProteasome inhibitorPyrazolesCyclooxygenaseDevelopmental Biologymedicine.drug
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Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome

2020

Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an impri…

Male0301 basic medicinePotassium Channels[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyGeneral Physics and AstronomyDiseasePhenylenediamines[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCraniofacial AbnormalitiesHistonesMice0302 clinical medicineIntellectual disabilityImprinting (psychology)lcsh:ScienceMice KnockoutGeneticsMultidisciplinaryBehavior AnimalbiologyNeurodevelopmental disordersDevelopmental disordersQBrainPhenotypeUp-RegulationPhenotypeHistoneGene Knockdown TechniquesBenzamidesMuscle HypotoniaFemaleLocus CoeruleusEpigeneticsScienceArticleGeneral Biochemistry Genetics and Molecular BiologyGenomic Imprinting03 medical and health sciencesDevelopmental disorders ; Neurodevelopmental disorders ; EpigeneticsIntellectual DisabilitymedicineAnimalsHumansddc:610AlleleGene[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Chemistrymedicine.diseaseHistone Deacetylase InhibitorsMice Inbred C57BLDisease Models Animal030104 developmental biologyAcetylationMutationbiology.proteinlcsh:Q030217 neurology & neurosurgery
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SETD7 mediates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury

2019

Abstract Gene transcription regulation is critical for the development of spinal microgliosis and neuropathic pain after peripheral nerve injury. Using a model of chronic constriction injury (CCI) of the sciatic nerve, this study characterized the role of SET domain containing lysine methyltransferase 7 (SETD7) which monomethylates histone H3 lysine 4 (H3K4me1), a marker for active gene transcription. SETD7 protein expression in the spinal dorsal horn ipsilateral to nerve lesion was increased from one day to 14 days after CCI, concomitantly with the expression of inflammatory genes, Ccl2, Il-6 and Il-1β. The CCI-induced SETD7 expression was predominantly localized to microglia, as demonstra…

Male0301 basic medicineSpinal Cord Dorsal HornPathologymedicine.medical_specialtyImmunologyCCL2MicrogliosisRats Sprague-Dawley03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePeripheral Nerve InjuriesGanglia SpinalmedicineAnimalsGene knockdownMicrogliaEndocrine and Autonomic Systemsbusiness.industryHistone-Lysine N-MethyltransferaseNerve injurySciatic NerveSpineRats030104 developmental biologymedicine.anatomical_structureSpinal CordHyperalgesiaNeuropathic painPeripheral nerve injuryNeuralgiaFemaleMicrogliaSciatic nervemedicine.symptombusiness030217 neurology & neurosurgeryBrain, Behavior, and Immunity
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Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell–cell Adhesion in the Postnatal Brain

2018

In the rodent olfactory system, neuroblasts produced in the ventricular-subventricular zone of the postnatal brain migrate tangentially in chain-like cell aggregates toward the olfactory bulb (OB) through the rostral migratory stream (RMS). After reaching the OB, the chains are dissociated and the neuroblasts migrate individually and radially toward their final destination. The cellular and molecular mechanisms controlling cell–cell adhesion during this detachment remain unclear. Here we report that Fyn, a nonreceptor tyrosine kinase, regulates the detachment of neuroblasts from chains in the male and female mouse OB. By performing chemical screening andin vivoloss-of-function and gain-of-f…

Male0301 basic medicineanimal structuresRostral migratory streamNerve Tissue ProteinsProto-Oncogene Proteins c-fynAdherens junctionMice03 medical and health sciencesFYNNeural Stem CellsNeuroblastCell MovementCell AdhesionmedicineAnimalsCell adhesionResearch ArticlesChemistryGeneral NeurosciencefungiBrainCateninsCadherinsDAB1Granule cellOlfactory BulbOlfactory bulbCell biology030104 developmental biologymedicine.anatomical_structurenervous systemGene Knockdown Techniquesembryonic structuresFemaleThe Journal of Neuroscience
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RS1 (Rsc1A1) deficiency limits cerebral SGLT1 expression and delays brain damage after experimental traumatic brain injury

2018

Acute cerebral lesions are associated with dysregulation of brain glucose homeostasis. Previous studies showed that knockdown of Na+ -D-glucose cotransporter SGLT1 impaired outcome after middle cerebral artery occlusion and that widely expressed intracellular RS1 (RSC1A1) is involved in transcriptional and post-translational down-regulation of SGLT1. In the present study, we investigated whether SGLT1 is up-regulated during traumatic brain injury (TBI) and whether removal of RS1 in mice (RS1-KO) influences SGLT1 expression and outcome. Unexpectedly, brain SGLT1 mRNA in RS1-KO was similar to wild-type whereas it was increased in small intestine and decreased in kidney. One day after TBI, SGL…

Male0301 basic medicinemedicine.medical_specialtyTraumatic brain injuryGene ExpressionBrain EdemaBrain damageBiochemistryProinflammatory cytokineMice03 medical and health sciencesCellular and Molecular NeuroscienceSodium-Glucose Transporter 10302 clinical medicineInternal medicineCortex (anatomy)Brain Injuries TraumaticmedicineAnimalsGlucose homeostasisEye ProteinsBrain ChemistryCerebral CortexMice KnockoutGene knockdownKidneyMovement DisordersMicrogliabusiness.industrydigestive oral and skin physiologyBrainmedicine.diseaseUp-RegulationMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCytokinesMicrogliamedicine.symptombusinessCell Adhesion Molecules030217 neurology & neurosurgeryJournal of Neurochemistry
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Regulation of the proapoptotic functions of prostate apoptosis response-4 (Par-4) by casein kinase 2 in prostate cancer cells

2013

International audience; The proapoptotic protein, prostate apoptosis response-4 (Par-4), acts as a tumor suppressor in prostate cancer cells. The serine/threonine kinase casein kinase 2 (CK2) has a well-reported role in prostate cancer resistance to apoptotic agents or anticancer drugs. However, the mechanistic understanding on how CK2 supports survival is far from complete. In this work, we demonstrate both in rat and humans that (i) Par-4 is a new substrate of the survival kinase CK2 and (ii) phosphorylation by CK2 impairs Par-4 proapoptotic functions. We also unravel different levels of CK2-dependent regulation of Par-4 between species. In rats, the phosphorylation by CK2 at the major si…

MaleCancer Researchanimal structuresCK2[SDV]Life Sciences [q-bio]ImmunologyAmino Acid MotifsPAWR[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Biology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology[SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and NephrologyCellular and Molecular NeuroscienceProstate cancer[SDV.CAN] Life Sciences [q-bio]/CancerProstateCell Line Tumor[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]medicineAnimalsHumansCasein Kinase IIComputingMilieux_MISCELLANEOUSGene knockdownKinasephosphorylationfungita1182apoptosisProstatic Neoplasms[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCell Biologymedicine.diseaseprostate cancer[SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and NephrologyRatsmedicine.anatomical_structureApoptosisembryonic structuresCancer researchPhosphorylationOriginal ArticleCasein kinase 2Apoptosis Regulatory ProteinsPar-4
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Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4

2019

Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive human HCC for macroH2A1 and CD44 CSC marker expression. We also knocked down (KD) macroH2A1 in HCC cells, and performed integrated transcriptomic and secretomic analyses. Results: Human HCC showed low macroH2A1 and high CD44 expression compared to control tissues. MacroH2A1 KD CSC-like cells transferred paracrinally their chemoresistant properties to parental HCC cells. MacroH2A1 KD conditioned media transcriptionally reprogrammed parental …

MaleCarcinoma HepatocellularT-Lymphocytes RegulatoryHistonesadaptive immune systemCell Line TumorParacrine CommunicationTumor MicroenvironmentHumansMetabolomicschemoresistance.neoplasmsLiver Neoplasmshistone macroH2A1Interleukin-2 Receptor alpha SubunitForkhead Transcription Factorshepatocellular carcinomaMiddle Ageddigestive system diseasesGene Expression Regulation NeoplasticHyaluronan ReceptorsDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsGlycolysisResearch PaperTheranostics
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Importance of mitochondrial dynamin-related protein 1 in hypothalamic glucose sensitivity in rats.

2012

International audience; AIMS: Hypothalamic mitochondrial reactive oxygen species (mROS)-mediated signaling has been recently shown to be involved in the regulation of energy homeostasis. However, the upstream signals that control this mechanism have not yet been determined. Here, we hypothesize that glucose-induced mitochondrial fission plays a significant role in mROS-dependent hypothalamic glucose sensing. RESULTS: Glucose-triggered translocation of the fission protein dynamin-related protein 1 (DRP1) to mitochondria was first investigated in vivo in hypothalamus. Thus, we show that intracarotid glucose injection induces the recruitment of DRP1 to VMH mitochondria in vivo. Then, expressio…

MaleEnergy-Generating Resourcesnervous-systemPhysiology[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionClinical BiochemistryneuronsMitochondrionBiochemistryinvolvementEnergy homeostasisDNM1L0302 clinical medicineInsulin-Secreting CellsInsulin SecretionInsulinGeneral Environmental Science2. Zero hungerchemistry.chemical_classification0303 health sciencesTransport proteinMitochondriaProtein TransportHypothalamusGene Knockdown TechniquesMitochondrial MembranesMitochondrial fissionRNA InterferenceDynaminsmedicine.medical_specialtyendocrine systembrainmechanismCarbohydrate metabolismBiology03 medical and health sciencesOxygen ConsumptionInternal medicineexpressionmedicineAnimalsRats WistarMolecular Biologyenergy homeostasis030304 developmental biologyReactive oxygen speciesAppetite RegulationArcuate Nucleus of HypothalamusCell Biologyislet blood-flowRatsEndocrinologyGlucosechemistryVentromedial Hypothalamic NucleusGeneral Earth and Planetary SciencesactivationReactive Oxygen Species[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryinsulin-secretion
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Antiatherosclerotic Effects of Small-Molecular-Weight Compounds Enhancing Endothelial Nitric-Oxide Synthase (eNOS) Expression and Preventing eNOS Unc…

2008

Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling). In human endothelial EA.hy 926 cells, two small-molecular-weight compounds with related structures, 4-fluoro-N-indan-2-yl-benzamide (CAS no. 291756-32-6; empirical formula C16H14FNO; AVE9488) and 2,2-difluoro-benzo[1,3]dioxole-5-carboxylic acid indan-2-ylamide (CAS no. 450348-85-3; empirical formula C17H13F2NO3; AVE3085), enhanced eNOS promoter activity in a concentration-dependent manner; with the responsible cis-element localized within the proximal 263 base pairs of the promoter region. RNA int…

MaleNeointimamedicine.medical_specialtyNitric Oxide Synthase Type IIINitric Oxide Synthase Type IINitric OxideProtective AgentsUmbilical veinCell LineNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosInternal medicinemedicineAnimalsHumansBenzodioxolesRNA MessengerAortaMice KnockoutPharmacologychemistry.chemical_classificationSp1 transcription factorReactive oxygen speciesGene knockdownbiologyEndothelial CellsAtherosclerosisbiology.organism_classificationVasoprotectiveMice Inbred C57BLMolecular WeightEndocrinologychemistryBenzamidesIndansMolecular MedicineJournal of Pharmacology and Experimental Therapeutics
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