Search results for "Transfection"

showing 10 items of 581 documents

PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Interactions of human P-glycoprotein transport substrates and inhibitors at the drug binding domain: Functional and molecular docking analyses

2015

Rhodamine 123 (R123) transport substrate sensitizes P-glycoprotein (P-gp) to inhibition by compound 2c (cis-cis) N,N-bis(cyclohexanolamine)aryl ester isomer in a concentration-dependent manner in human MDR1-gene transfected mouse T-lymphoma L5178 cells as shown previously. By contrast, epirubicin (EPI) concentration changes left unaltered 2c IC50 values of EPI efflux. To clarify this discrepancy, defined molecular docking (DMD) analyses of 12 N,N-bis(cyclohexanolamine)aryl esters, the highly flexible aryl ester analog 4, and several P-gp substrate/non-substrate inhibitors were performed on human P-gp drug- or nucleotide-binding domains (DBD or NBD). DMD measurements yielded lowest binding e…

0301 basic medicineStereochemistryCell Culture TechniquesCancer drug resistance; Molecular docking; NN-Bis(cyclohexanolamine)aryl ester; P-glycoproteinPlasma protein bindingP-glycoproteinTransfectionBiochemistryRhodamine 123Substrate Specificity03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineCell Line TumorAnimalsRhodamine 123ATP Binding Cassette Transporter Subfamily B Member 1Binding siteP-glycoproteinEpirubicinPharmacologyBinding SitesbiologyMolecular StructureArylEstersCancer drug resistanceNCyclohexanolsMolecular Docking SimulationProtein Transport030104 developmental biologychemistryDocking (molecular)030220 oncology & carcinogenesisMolecular dockingbiology.proteinN-Bis(cyclohexanolamine)aryl esterEffluxBinding domainProtein Binding
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Rett Syndrome Mutant Neural Cells Lacks MeCP2 Immunoreactive Bands.

2016

Dysfunctions of MeCP2 protein lead to various neurological disorders such as Rett syndrome and Autism. The exact functions of MeCP2 protein is still far from clear. At a molecular level, there exist contradictory data. MeCP2 protein is considered a single immunoreactive band around 75 kDa by western-blot analysis but several reports have revealed the existence of multiple MeCP2 immunoreactive bands above and below the level where MeCP2 is expected. MeCP2 immunoreactive bands have been interpreted in different ways. Some researchers suggest that multiple MeCP2 immunoreactive bands are unidentified proteins that cross-react with the MeCP2 antibody or degradation product of MeCP2, while others…

0301 basic medicineThreonineHeredityMethyl-CpG-Binding Protein 2Genetic LinkageMutantFluorescent Antibody TechniqueSocial Scienceslcsh:MedicinePC12 CellsBiochemistryEpitopeImmunoenzyme TechniquesCell FusionNeuroblastomaFluorescence MicroscopyAnimal CellsMedicine and Health SciencesPsychologyPost-Translational ModificationPhosphorylationAmino Acidslcsh:ScienceCells CulturedCross ReactivityNeuronsStainingMicroscopyMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionOrganic CompoundsCell StainingLight MicroscopyTransfectionChemistryX-Linked TraitsSex LinkagePhysical SciencesCellular TypesResearch ArticleCell signalingCell Physiologycongenital hereditary and neonatal diseases and abnormalitiesBlotting WesternImmunologyRett syndromeBiologyReal-Time Polymerase Chain ReactionResearch and Analysis MethodsMECP203 medical and health sciencesNeurologiaAntigenHydroxyl Amino Acidsmental disordersmedicineRett SyndromeGeneticsAnimalsHumansRNA MessengerClinical GeneticsHEK 293 cellsOrganic Chemistrylcsh:RChemical CompoundsBiology and Life SciencesProteinsCell Biologymedicine.diseaseMolecular biologyRatsnervous system diseases030104 developmental biologyHEK293 CellsSpecimen Preparation and TreatmentCellular NeuroscienceMutationDevelopmental PsychologyMalaltieslcsh:QNeuroscience
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Transient postnatal over nutrition induces long-term alterations in cardiac NLRP3-inflammasome pathway.

2018

International audience; Background and aims: The prevalence of obesity is increasing worldwide at an alarming rate. Altered early nutrition, in particular postnatal overfeeding (PNOF), is a risk factor for impaired cardiac function in adulthood. In the understanding of the initiation or progression of heart diseases, NLRP3 inflammasome and non-coding RNAs have been proposed as key players. In this context, the aim of this study was to decipher the role of NLRP3 inflammasome and its post transcriptional control by micro-RNAs in the regulation of cardiac metabolic function induced by PNOF in mice. Methods and results: Based on a model of mice exposed to PNOF through litter size reduction, we …

0301 basic medicineTime FactorsLitter SizeInflammasomesEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMedicine (miscellaneous)InflammasomeOvernutritionInsulinNutrition and Dieteticsintegumentary systembiologyInflammasomeMicro-RNAsTransfection[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemAnimal Nutritional Physiological PhenomenaSignal transductionCardiology and Cardiovascular Medicinemedicine.drugSignal TransductionCardiac function curvemedicine.medical_specialtyHeart DiseasesCardiac dysfunctionsNutritional StatusContext (language use)Cell LineProto-Oncogene Protein c-ets-103 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsPost-transcriptional regulationNutritionbusiness.industryInsulinMyocardiumRatsMice Inbred C57BLInsulin receptorDisease Models AnimalMicroRNAs030104 developmental biologyEndocrinologyAnimals Newbornbiology.proteinbusinessNutrition, metabolism, and cardiovascular diseases : NMCD
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Induction of Chromosome Instability by Activation of Yes-Associated Protein and Forkhead Box M1 in Liver Cancer

2016

Background & Aims Many different types of cancer cells have chromosome instability. The hippo pathway leads to phosphorylation of the transcriptional activator yes-associated protein 1 (YAP1, YAP), which regulates proliferation and has been associated with the development of liver cancer. We investigated the effects of hippo signaling via YAP on chromosome stability and hepatocarcinogenesis in humans and mice. Methods We analyzed transcriptome data from 242 patients with hepatocellular carcinoma (HCC) to search for gene signatures associated with chromosomal instability (CIN); we investigated associations with overall survival time and cancer recurrence using Kaplan–Meier curves. We analyze…

0301 basic medicineTime FactorsMuscle ProteinsKaplan-Meier Estimatemedicine.disease_causeChromosome instabilityYAP1Liver NeoplasmsGastroenterologyTEA Domain Transcription FactorsHep G2 CellsPrognosisDNA-Binding ProteinsGene Expression Regulation NeoplasticPhenotypeHippo signalingRNA InterferenceSignal TransductionCarcinoma HepatocellularPorphyrinsAntineoplastic AgentsMice TransgenicBiologyTransfection03 medical and health sciencesChromosomal InstabilitymedicineAnimalsHumansGene silencingGenetic Predisposition to DiseaseAdaptor Proteins Signal TransducingHippo signaling pathwayHepatologyGene Expression ProfilingForkhead Box Protein M1VerteporfinYAP-Signaling ProteinsHCCSPhosphoproteinsThiostreptonMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyTissue Array AnalysisFOXM1Cancer researchTranscriptomeCarcinogenesisTranscription FactorsGastroenterology
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Human Upcyte Hepatocytes: Characterization of the Hepatic Phenotype and Evaluation for Acute and Long-Term Hepatotoxicity Routine Testing

2016

The capacity of human hepatic cell-based models to predict hepatotoxicity depends on the functional performance of cells. The major limitations of human hepatocytes include the scarce availability and rapid loss of the hepatic phenotype. Hepatoma cells are readily available and easy to handle, but are metabolically poor compared with hepatocytes. Recently developed human upcyte hepatocytes offer the advantage of combining many features of primary hepatocytes with the unlimited availability of hepatoma cells. We analyzed the phenotype of upcyte hepatocytes comparatively with HepG2 cells and adult primary human hepatocytes to characterize their functional features as a differentiated hepatic …

0301 basic medicineTime FactorsPrimary Cell CultureTransfectionToxicologyRisk AssessmentTranscriptome03 medical and health sciences0302 clinical medicineMetabolomicsCytochrome P-450 Enzyme SystemIn vivoToxicity TestsmedicineHumansChildGlycogen synthaseDose-Response Relationship DrugbiologyInfant NewbornCytochrome P450Hep G2 CellsMiddle Agedmedicine.diseasePhenotypeHigh-Throughput Screening AssaysIsoenzymesOxidative StressPhenotype030104 developmental biologyGene Expression RegulationLiver030220 oncology & carcinogenesisHepatocytesbiology.proteinHepatic stellate cellCancer researchChemical and Drug Induced Liver InjurySteatosisTranscriptomeToxicological Sciences
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Hypoxia-Induced miR-675-5p Supports β-Catenin Nuclear Localization by Regulating GSK3-β  Activity in Colorectal Cancer Cell Lines

2020

The reduction of oxygen partial pressure in growing tumors triggers numerous survival strategies driven by the transcription factor complex HIF1 (Hypoxia Inducible Factor-1). Recent evidence revealed that HIF1 promotes rapid and effective phenotypic changes through the induction of non-coding RNAs, whose contribution has not yet been fully described. Here we investigated the role of the hypoxia-induced, long non-coding RNA H19 (lncH19) and its intragenic miRNA (miR-675-5p) into HIF1-Wnt crosstalk. During hypoxic stimulation, colorectal cancer cell lines up-regulated the levels of both the lncH19 and its intragenic miR-675-5p. Loss of expression experiments revealed that miR-675-5p inhibitio…

0301 basic medicineTranscription factor complexKaplan-Meier Estimatelcsh:Chemistry0302 clinical medicineGSK-3poxiahylcsh:QH301-705.5long non-coding H19Spectroscopybeta CateninKinaseChemistryGeneral MedicineCell HypoxiaComputer Science ApplicationsCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColorectal NeoplasmsProtein BindingActive Transport Cell Nucleuscolorectal cancermiR-675TransfectionCatalysisArticleInorganic Chemistry03 medical and health sciencesCell Line TumormicroRNAGene silencingHumansPhysical and Theoretical ChemistryMolecular BiologyGlycogen Synthase Kinase 3 betahypoxiaOrganic ChemistryRNAComputational Biologyβ-cateninHCT116 CellsMicroRNAs030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Microscopy FluorescenceCateninMutationNuclear localization sequenceInternational Journal of Molecular Sciences
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MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.

2018

The MID1 ubiquitin ligase activates mTOR signaling and regulates mRNA translation. Misregulation of MID1 expression is associated with various diseases including midline malformation syndromes, cancer and neurodegenerative diseases. While this indicates that MID1 expression must be tightly regulated to prevent disease states specific mechanisms involved have not been identified. We examined miRNAs to determine mechanisms that regulate MID1 expression. MicroRNAs (miRNA) are small non-coding RNAs that recognize specific sequences in their target mRNAs. Upon binding, miRNAs typically downregulate expression of these targets. Here, we identified four miRNAs, miR-19, miR-340, miR-374 and miR-542…

0301 basic medicineUntranslated regionSmall interfering RNAPhysiologymetabolism [Microtubule Proteins]Alzheimer's DiseaseBiochemistryImmune PhysiologyMedicine and Health SciencesSmall interfering RNAsmetabolism [Transcription Factors]3' Untranslated RegionsImmune System ProteinsMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionMessenger RNAQRNuclear ProteinsNeurodegenerative DiseasesTranslation (biology)EnzymesUbiquitin ligaseCell biologyNucleic acidsNeurologyMicrotubule ProteinsMedicineOxidoreductasesLuciferasemetabolism [Nuclear Proteins]Research ArticleScienceUbiquitin-Protein LigasesImmunologyTransfectionResearch and Analysis MethodsReal-Time Polymerase Chain ReactionAntibodies03 medical and health sciencesMental Health and PsychiatrymicroRNAGeneticsHumansddc:610Non-coding RNAMolecular Biology TechniquesMolecular BiologyMessenger RNABiology and life sciencesThree prime untranslated regionHEK 293 cellsProteinsGene regulationphysiology [MicroRNAs]MicroRNAs030104 developmental biologyHEK293 CellsEnzymologybiology.proteinRNAProtein TranslationDementiaGene expressionTranscription FactorsMid1 protein human
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Photocatalytic Activity of Polymer Nanoparticles Modulates Intracellular Calcium Dynamics and Reactive Oxygen Species in HEK-293 Cells

2018

Optical modulation of living cells activity by light-absorbing exogenous materials is gaining increasing interest, due to the possibility both to achieve high spatial and temporal resolution with a minimally invasive and reversible technique and to avoid the need of viral transfection with light-sensitive proteins. In this context, conjugated polymers represent ideal candidates for photo-transduction, due to their excellent optoelectronic and biocompatibility properties. In this work, we demonstrate that organic polymer nanoparticles, based on poly(3-hexylthiophene) conjugated polymer, establish a functional interaction with an in vitro cell model (Human Embryonic Kidney cells, HEK-293). Th…

0301 basic medicineconjugated polymerHistologylcsh:BiotechnologyCellBiomedical EngineeringBioengineeringContext (language use)02 engineering and technologyCalcium in biology03 medical and health sciencesCa2+ imaginglcsh:TP248.13-248.65medicineViability assaybio-organic electronicsOriginal Researchreactive oxygen specieschemistry.chemical_classificationReactive oxygen speciesorganic semiconductorHEK 293 cellsBioengineering and BiotechnologyPhotocatalytic ActivityTransfection021001 nanoscience & nanotechnologyConjugated Polymer NanoparticlesCytosol030104 developmental biologymedicine.anatomical_structurechemistryBiophysicsIntracellular Calcium Dynamicsphotomodulationlight0210 nano-technologycell optical stimulationBiotechnologyFrontiers in Bioengineering and Biotechnology
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Tissue factor prothrombotic activity is regulated by integrin-arf6 trafficking

2017

Objective— Coagulation initiation by tissue factor (TF) is regulated by cellular inhibitors, cell surface availability of procoagulant phosphatidylserine, and thiol-disulfide exchange. How these mechanisms contribute to keeping TF in a noncoagulant state and to generating prothrombotic TF remain incompletely understood. Approach and Results— Here, we study the activation of TF in primary macrophages by a combination of pharmacological, genetic, and biochemical approaches. We demonstrate that primed macrophages effectively control TF cell surface activity by receptor internalization. After cell injury, ATP signals through the purinergic receptor P2rx7 induce release of TF + microvesicles. T…

0301 basic medicinedynaminsIntegrin alpha4CellCardiorespiratory Medicine and Haematology030204 cardiovascular system & hematologyIntegrin alpha4beta1Inbred C57BLTransgenicMicechemistry.chemical_compound0302 clinical medicineAdenosine TriphosphateCell-Derived MicroparticlesReceptors2.1 Biological and endogenous factorsfibrinGene Knock-In TechniquesAetiologyPhospholipidsTumorbiologyChemistryADP-Ribosylation FactorsHematologyPhosphatidylserineCell biologyProtein Transportmedicine.anatomical_structurePhenotypeProteomeextracellular vesiclesCardiology and Cardiovascular MedicinePurinergic P2X7BiotechnologySignal TransductionGenotypeproteomeClinical SciencesIntegrinMice TransgenicFactor VIIaTransfectionExtracellular vesiclesFibrinArticleCell LineThromboplastin03 medical and health sciencesTissue factorCell Line TumormedicineAnimalsHumansBlood CoagulationMacrophagesThrombosisMice Inbred C57BL030104 developmental biologyCardiovascular System & HematologyADP-Ribosylation Factor 6biology.proteinReceptors Purinergic P2X7
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