Search results for "Small Interfering"

showing 10 items of 249 documents

Tackling the Limitations of Copolymeric Small Interfering RNA Delivery Agents by a Combined Experimental–Computational Approach

2019

Despite the first successful applications of nonviral delivery vectors for small interfering RNA in the treatment of illnesses, such as the respiratory syncytial virus infection, the preparation of a clinically suitable, safe, and efficient delivery system still remains a challenge. In this study, we tackle the drawbacks of the existing systems by a combined experimental-computational in-depth investigation of the influence of the polymer architecture over the binding and transfection efficiency. For that purpose, a library of diblock copolymers with a molar mass of 30 kDa and a narrow dispersity (Đ1.12) was synthesized. We studied in detail the impact of an altered block size and/or compos…

Small interfering RNAPolymers and PlasticsBioengineering02 engineering and technologyComputational biologyBiology010402 general chemistry01 natural sciencesVirusBiomaterialsDrug Delivery SystemsText miningMaterials ChemistryHumansComputer SimulationRNA Small Interferingbusiness.industryRNA021001 nanoscience & nanotechnology0104 chemical sciencesHEK293 CellsModels ChemicalMCF-7 Cells0210 nano-technologybusinessHeLa CellsBiomacromolecules
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Post-Transcriptional Regulation of Human Inducible Nitric-Oxide Synthase Expression by the Jun N-terminal Kinase

2007

Human inducible nitric-oxide synthase (iNOS) expression is regulated both at transcriptional and post-transcriptional levels. In the present study, the effect of Jun N-terminal kinase (JNK) on human iNOS expression was investigated. In A549/8 human alveolar epithelial cells, both the inhibition of JNK by a pharmacological inhibitor anthra[1,9-cd]pyrazol-6(2H)-one1,9-pyrazoloanthrone (SP600125) and small interfering RNA (siRNA)-mediated down-regulation of JNK led to a reduction of iNOS mRNA and protein expression. iNOS promoter activity was not affected by these treatments. Hence, JNK seems to regulate iNOS expression through post-transcriptional mechanisms by stabilizing iNOS mRNA. Our labo…

Small interfering RNARNA Stabilityp38 mitogen-activated protein kinasesDown-RegulationNitric Oxide Synthase Type IIRNA-binding proteinNitric Oxidep38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicCell LineTristetraprolinHumansPhosphorylationRNA Small InterferingPromoter Regions GeneticPost-transcriptional regulationAnthracenesPharmacologyRegulation of gene expressionMessenger RNAbiologyChemistryKinaseJNK Mitogen-Activated Protein KinasesEpithelial Cellsrespiratory systemMolecular biologyPulmonary AlveoliNitric oxide synthasebiology.proteinCytokinesMolecular MedicineSignal TransductionMolecular Pharmacology
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Internalization of coxsackievirus A9 is mediated by {beta}2-microglobulin, dynamin, and Arf6 but not by caveolin-1 or clathrin.

2010

ABSTRACT Coxsackievirus A9 (CAV9) is a member of the human enterovirus B species within the Enterovirus genus of the family Picornaviridae . It has been shown to utilize αV integrins, particularly αVβ6, as its receptors. The endocytic pathway by which CAV9 enters human cells after the initial attachment to the cell surface has so far been unknown. Here, we present a systematic study concerning the internalization mechanism of CAV9 to A549 human lung carcinoma cells. The small interfering RNA (siRNA) silencing of integrin β6 subunit inhibited virus proliferation, confirming that αVβ6 mediates the CAV9 infection. However, siRNAs against integrin-linked signaling molecules, such as Src, Fyn, R…

Small interfering RNAmedia_common.quotation_subjectImmunologyEndocytic cycleIntegrinCaveolin 1CoxsackievirusEndocytosisCaveolaeMicrobiologyClathrinAmilorideDynamin IIVirologyCell Line TumorHumansRNA Small InterferingInternalizationmedia_commonDynaminbiologyADP-Ribosylation FactorsVirus Internalizationbiology.organism_classificationMolecular biologyClathrinEndocytosisCell biologyEnterovirus B HumanVirus-Cell InteractionsADP-Ribosylation Factor 6Insect Sciencebiology.proteinPinocytosisbeta 2-MicroglobulinJournal of virology
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SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress.

2005

AbstractUnder hypertonic conditions the induction of SLC38A2/SNAT2 leads to the stimulation of transport system A and to the increase in the cell content of amino acids. In hypertonically stressed human fibroblasts transfection with two siRNAs for SNAT2 suppressed the increase in SNAT2 mRNA and the stimulation of system A transport activity. Under the same condition, the expansion of the intracellular amino acid pool was significantly lowered and cell volume recovery markedly delayed. It is concluded that the up-regulation of SNAT2 is essential for the rapid restoration of cell volume after hypertonic stress.

Small interfering RNAmedicine.medical_specialtyAmino Acid Transport System AGlutamineCellBiophysicsStimulationBiologyTransfectionBiochemistryStructural BiologyOsmotic PressureCell volumeInternal medicineGeneticsmedicineHumansRNA MessengerAmino AcidsRNA Small InterferingMolecular BiologyCell Sizechemistry.chemical_classificationSaline Solution HypertonicCell BiologyFibroblastsAmino acidCell biologyUp-RegulationGlutaminemedicine.anatomical_structureEndocrinologychemistryHypertonic StresssiRNATonicityRNA InterferenceIntracellularFEBS letters
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Neue Therapieoption für akute hepatische Porphyrien

2021

Was ist neu? Therapie mit Givosiran Givosiran ist ein kleines synthetisches doppelsträngiges siRNA-Fragment mit 20 Basenpaaren Länge. Eine prospektive, randomisierte multizentrische Studie (Envision) zeigte erstmalig die klinische Wirksamkeit von monatlich subkutan applizierten synthetischen RNA-Molekülen („small interfering“ RNA, siRNA) zur Prävention von Attacken bei akuten hepatischen Porphyrien (AHP) 2. Die Koppelung von siRNA-Molekülen an N-Acetyl-Galaktosamin (GalNAc) und die hierdurch leberspezifische Aufnahme durch den Asialoglykoprotein-Rezeptor auf Hepatozyten sind ein Meilenstein in der Hepatologie. Dies führt zu einer hochselektiven Inhibition der Translation der bei AHP überexp…

Small interfering RNAmedicine.medical_specialtybusiness.industryRenal functionGeneral MedicinePharmacologyHepatologymedicine.diseaseSubcutaneous injectionmedicine.anatomical_structurePorphyriaHepatocyteInternal medicinemedicineAsialoglycoprotein receptorClinical efficacybusinessDMW - Deutsche Medizinische Wochenschrift
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Tribolium castaneum immune defense genes are differentially expressed in response to Bacillus thuringiensis toxins sharing common receptor molecules …

2015

In Tribolium castaneum larvae we have demonstrated by RNA interference knockdown that the Bacillus thuringiensis Cry3Ba toxin receptors Cadherin-like and Sodium solute symporter proteins are also functional receptors of the less active Cry3Aa toxin. Differences in susceptibility to B. thuringiensis infection might not only rely on toxin-receptor interaction but also on host defense mechanisms. We compared the expression of the immune related genes encoding Apolipophorin-III and two antimicrobial peptides, Defensin3 and Defensin2 after B. thuringiensis challenge. All three genes were up-regulated following Cry3Ba spore-crystal intoxication whereas only Defensins gene expression was induced u…

Staphylococcus aureusImmunologyAntimicrobial peptidesBacterial ToxinsMolecular Sequence DataBacillus thuringiensisBiologymedicine.disease_causeMicrobiologyDefensinsHemolysin ProteinsImmune systemBacterial ProteinsRNA interferenceBacillus thuringiensisGene expressionCandida albicansmedicineEscherichia coliAnimalsAmino Acid SequenceRNA Small InterferingDefensinTriboliumInnate immune systemBacillus thuringiensis ToxinsSymportersToxinfungibiology.organism_classificationAnti-Bacterial AgentsEndotoxinsApolipoproteinsLarvaInsect ProteinsRNA InterferenceDevelopmental BiologyDevelopmental and comparative immunology
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Preeclampsia: a defect in decidualization is associated with deficiency of Annexin A2.

2020

Background Decidualization defects in the endometrium have been demonstrated at the time of delivery in women with severe preeclampsia and to linger for years, which suggests a maternal contribution to the pathogenesis of this condition. Global transcriptional profiling reveals alterations in gene expression, which includes down-regulation of Annexin A2 in severe preeclampsia patients with decidualization resistance. Objective We investigated the functional role of Annexin A2 deficiency during endometrial decidualization and its potential contribution to shallow trophoblast invasion during implantation and subsequent placentation using in vitro and in vivo modeling. Study Design Annexin A2 …

Stromal cellGene ExpressionEndometriumAndrology03 medical and health sciencesMice0302 clinical medicinePre-EclampsiaAnnexinCell MovementPregnancymedicineDeciduaAnimalsHumans030212 general & internal medicineEmbryo ImplantationRNA Small InterferingAnnexin A2Cells Cultured030219 obstetrics & reproductive medicinemedicine.diagnostic_testbusiness.industryObstetrics and GynecologyDecidualizationPlacentationTrophoblastActinsPlacentationProlactinTrophoblastsInsulin-Like Growth Factor Binding Protein 1Disease Models Animalmedicine.anatomical_structureFemaleStromal CellsbusinessAnnexin A2Endometrial biopsyAmerican journal of obstetrics and gynecology
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Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
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cIAP1-dependent TRAF2 degradation regulates the differentiation of monocytes into macrophages and their response to CD40 ligand.

2008

AbstractPeripheral blood monocytes are plastic cells that migrate to tissues and differentiate into various cell types, including macrophages, dendritic cells, and osteoclasts. We have described the migration of cellular inhibitor of apoptosis protein 1 (cIAP1), a member of the IAP family of proteins, from the nucleus to the Golgi apparatus in monocytes undergoing differentiation into macrophages. Here we show that, once in the cytoplasm, cIAP1 is involved in the degradation of the adaptor protein tumor necrosis factor receptor–associated factor 2 (TRAF2) by the proteosomal machinery. Inhibition of cIAP1 prevents the decrease in TRAF2 expression that characterizes macrophage formation. We d…

TRAF2CytoplasmCellular differentiationImmunologyCD40 LigandDown-RegulationGene ExpressionGolgi ApparatusBiologyBiochemistryMonocytesProinflammatory cytokineInhibitor of Apoptosis ProteinsPhagocytes Granulocytes and MyelopoiesisPhagocytosisMacrophageHumansRNA Small InterferingCD40U937 cellMacrophagesSignal transducing adaptor proteinCell DifferentiationCell BiologyHematologyU937 CellsTNF Receptor-Associated Factor 2Molecular biologyCell biologybiology.proteinTumor necrosis factor alphaBlood
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Nickel induces intracellular calcium mobilization and pathophysiological responses in human cultured airway epithelial cells.

2009

Abstract Environmental exposure to nickel is associated to respiratory disorders and potential toxicity in the lung but molecular mechanisms remain incompletely explored. The extracellular Ca 2+ -sensing receptor (CaSR) is widely distributed and may be activated by divalent cations. In this study, we investigated the presence of CaSR in human cultured airway epithelial cells and its activation by nickel. Nickel transiently increased intracellular calcium (−log EC 50  = 4.67 ± 0.06) in A549 and human bronchial epithelial cells as measured by epifluorescence microscopy. Nickel (20 μM)-induced calcium responses were reduced after thapsigargin or ryanodine exposure but not by Ca 2+ -free medium…

ThapsigarginInterleukin-1betachemistry.chemical_elementRespiratory MucosaBiologyCalciumToxicologyCalcium in biologychemistry.chemical_compoundNickelExtracellularHumansRNA Small InterferingCells CulturedA549 cellRyanodine receptorRyanodineTumor Necrosis Factor-alphaInositol trisphosphateEpithelial CellsGeneral MedicineEnvironmental exposureIntercellular Adhesion Molecule-1Cell biologychemistryMicroscopy FluorescenceType C PhospholipasesImmunologyGTP-Binding Protein alpha Subunits Gq-G11ThapsigarginCalciumReceptors Calcium-SensingChemico-biological interactions
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