Search results for "Antisense"

showing 10 items of 101 documents

Sequence-Specific Repression of Cotranslational Translocation of the Hepatitis B Virus Envelope Proteins Coincides with Binding of Heat Shock Protein…

1997

AbstractThe large L envelope protein of the hepatitis B virus has the peculiar capacity to adopt two transmembrane topologies. The N-terminal preS domain of L initially remains in the cytosol while the S domain is cotranslationally inserted into the endoplasmic reticulum membrane. The preS region of about half of the L molecules is posttranslationally translocated to the lumenal space. We now demonstrate that the repression of cotranslational translocation of preS is conferred by a preS1-specific sequence. By analysis of L deletion mutants, the cytosolic anchorage determinant was mapped to amino acid sequence 70 to 94 of L. The intrinsic potential of this determinant to suppress cotranslati…

Hepatitis B virusHSC70 Heat-Shock ProteinsRecombinant Fusion ProteinsPlasma protein bindingBiologyGenes envCytosolViral Envelope ProteinsHeat shock proteinVirologyHumansHSP70 Heat-Shock ProteinsBinding sitePromoter Regions GeneticPeptide sequenceBinding SitesBase SequenceCell-Free SystemEndoplasmic reticulumHSC70 Heat-Shock ProteinsOligonucleotides AntisenseMolecular biologyTransmembrane proteinChaperone (protein)Protein Biosynthesisbiology.proteinMutagenesis Site-DirectedMetallothioneinCarrier ProteinsProtein BindingVirology
researchProduct

Naturally occurring testis-specific histone H3 antisense transcripts inDrosophila

1997

While analysing the transcription of the cluster of cell-cycle regulated histone genes in Drosophila hydei, we have found transcripts spanned both histone H3 and H4 genes and were antisense for histone H3. As the two histone genes are in opposite orientation, these transcripts contained the sense strand of the histone H4 gene. Such transcripts were present in both poly(A) + and poly(A) - RNA fractions. The polyadenylated molecules contained a poly(A) tail at the 3' end of the stem-loop structure, which is characteristic for cell-cycle regulated histone mRNAs. The antisense RNA of histone H3 is synthesized exclusively in testes. By developing an improved protocol of in situ hybridization to …

Histone H4Histone H3Histone H1Histone methyltransferaseHistone methylationHistone H2AGeneticsCell BiologyBiologySAP30Molecular biologyDevelopmental BiologyAntisense RNAMolecular Reproduction and Development
researchProduct

Predominant role of NF-kappa B p65 in the pathogenesis of chronic intestinal inflammation.

1998

NF-kappa B is a key transcription factor of lymphocytes and macrophages with important regulatory functions in the immune system and inflammatory processes. These functions are at least partially based on its ability to regulate the promoters of a variety of genes whose products, such as cytokines, adhesion molecules and acute phase proteins, are critical for inflammatory processes. In the present study, we describe a method to treat established intestinal inflammation by local or systemic application of antisense phosphorothioate oligonucleotides targeting the translation start site of the p65 subunit of NF-kappa B. Specific downregulation of p65 by administration of antisense phosphorothi…

ImmunologyInflammationBiologyPathogenesisMiceImmune systemDownregulation and upregulationCrohn DiseasemedicineImmunology and AllergyAnimalsHumansCells CulturedInflammationPhosphorothioate OligonucleotidesOligonucleotideInterleukin-6Tumor Necrosis Factor-alphaMacrophagesAcute-phase proteinNF-kappa BTranscription Factor RelAHematologyOligonucleotides AntisenseNFKB1ColitisIntestinesDisease Models AnimalImmunologyChronic DiseaseCancer researchFemalemedicine.symptomInterleukin-1Immunobiology
researchProduct

Local administration of antisense phosphorothioate oligonucleotides to the c-kit ligand, stem cell factor, suppresses airway inflammation and IL-4 pr…

2001

Abstract Background: The c-kit ligand, stem cell factor (SCF), is an important activating and chemotactic factor for both mast cells and eosinophils. These cells are known to play a fundamental role in the pathogenesis of asthma. Objective: Our goal was to analyze the functional role of SCF in the pathogenesis of asthma. Methods: The expression of SCF was targeted in fibroblasts, epithelial cells, and locally in a murine model of asthma in mice induced by ovalbumin sensitization with an antisense DNA strategy. Results: We could suppress SCF expression in NIH 3T3 fibroblasts and SP1 epithelial cells by a specific antisense phosphorothioate oligonucleotide overlapping the translation start si…

KeratinocytesLung DiseasesOvalbuminAdministration TopicalImmunologyInflammationStem cell factorBiology3T3 cellsAllergic inflammationLeukocyte CountMicemedicineImmunology and AllergyAnimalsInterleukin 4InflammationStem Cell FactorOligonucleotide3T3 CellsAllergensFibroblastsOligonucleotides AntisenseThionucleotidesMast cellAsthmaEosinophilsOvalbuminDisease Models Animalmedicine.anatomical_structureembryonic structuresImmunologybiology.proteinInterleukin-4medicine.symptomBronchoalveolar Lavage FluidThe Journal of allergy and clinical immunology
researchProduct

Regulation of hematopoietic growth factor production by genetically modified human bone marrow stromal cells expressing interleukin-1beta antisense R…

2001

Interleukin-1 (IL-1) plays a major role in the regulation of bone marrow stromal cell function and hematopoiesis. It is known to induce secretion of the hematopoietic growth factors granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), IL-6, and IL-8 as well as IL-1 itself in stromal cells. We investigated the role of IL-1beta-mediated growth factor production in the human stromal cell line L88/5. Using liposome-mediated DNA transfer, two stromal cell transfectants that constitutively express IL-1beta antisense (AS) RNA were generated. Expression of IL-1beta AS RNA and IL-1beta RNA was determined by RT-PCR. The stromal cell transfectants were strongly impaired …

LipopolysaccharidesStromal cellHematopoietic growth factormedicine.medical_treatmentImmunologyBone Marrow CellsBiologyTransfectionCell LineVirologyLymph node stromal cellmedicineHumansRNA AntisenseRNA MessengerBase SequenceInterleukin-6Tumor Necrosis Factor-alphaGrowth factorInterleukin-8RNAGranulocyte-Macrophage Colony-Stimulating FactorCell BiologyMolecular biologyAntisense RNACell biologyHaematopoiesisTumor necrosis factor alphaStromal CellsInterleukin-1Journal of interferoncytokine research : the official journal of the International Society for Interferon and Cytokine Research
researchProduct

TGF-β2 silencing to target biliary-derived liver diseases

2020

ObjectiveTGF-β2 (TGF-β, transforming growth factor beta), the less-investigated sibling of TGF-β1, is deregulated in rodent and human liver diseases. Former data from bile duct ligated and MDR2 knockout (KO) mouse models for human cholestatic liver disease suggested an involvement of TGF-β2 in biliary-derived liver diseases.DesignAs we also found upregulated TGFB2 in liver tissue of patients with primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC), we now fathomed the positive prospects of targeting TGF-β2 in early stage biliary liver disease using the MDR2-KO mice. Specifically, the influence of TgfB2 silencing on the fibrotic and inflammatory niche was analysed on m…

Liver CirrhosisATP Binding Cassette Transporter Subfamily B2312Cholangitis SclerosingPrimary sclerosing cholangitisMiceTransforming Growth Factor beta2Liver diseasePrimary biliary cirrhosisCholestasisFibrosisDrug DiscoveryTGF beta signaling pathwayHepatic Stellate CellsAnimalsHumansMedicineGene silencingGene Silencing1506TGF-betaddc:610Mice KnockoutHepatologybiologyLiver Cirrhosis Biliarybusiness.industryfibrosisGastroenterologyprimary sclerosing cholangitisTransforming growth factor betaOligonucleotides Antisensemedicine.diseaseUp-Regulationprimary biliary cirrhosisDisease Models AnimalGene Expression RegulationCancer researchbiology.proteincholestasisbusinessGut
researchProduct

CD38 expression enhances sensitivity of lymphoma T and B cell lines to biochemical and receptor-mediated apoptosis

2006

CD38 has been widely characterised both as an ectoenzyme and as a receptor. In the present paper, we investigated the role of CD38 as possible modulator of apoptosis. CD38-positive (CD38(+)) and negative (CD38(-)) fractions, obtained by sorting CD38(+) cells from lymphoma T (Jurkat) and lymphoma B (Raji) and by transfecting lymphoma LG14 and myeloid leukemia K562 cell lines, were used. Cellular subpopulations were exposed to different triggers (H(2)O(2), UV-B, alpha-TOS and hrTRAIL) and the extent of apoptosis was determined by Annexin V-FITC/PI assay. Our data showed that, in lymphoma cells, propensity to apoptosis was significantly linked to CD38 expression and that, remarkably, such resp…

Lymphoma B-CellCD30Ultraviolet RaysTocopherolsApoptosisCD38BiologyLymphoma T-CellJurkat cellsTNF-Related Apoptosis-Inducing LigandJurkat Cellsimmune system diseasesAnnexinCell Line Tumorhemic and lymphatic diseasesmedicineHumansVitamin EAnnexin A5B cellhemic and immune systemsHydrogen PeroxideCell BiologyGeneral MedicineOligonucleotides AntisenseFlow CytometryADP-ribosyl Cyclase 1Antigens DifferentiationMolecular biologyBCL10medicine.anatomical_structureApoptosisAnnexin A5K562 CellsFluorescein-5-isothiocyanateCell Biology International
researchProduct

Targeting PCSK9 for therapeutic gains: Have we addressed all the concerns?

2016

Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) regulates the expression of low-density lipoprotein (LDL)-receptors, through reducing their recycling by binding to the receptor along with LDL and targeting it for lysosomal destruction. PCSK9 also enhances the degradation of very-low-density-lipoprotein receptor (VLDLR) and lipoprotein receptor-related protein 1 (LRP-1) in a LDL-receptor independent manner. This role in lipid homeostasis presents PCSK9 as an attractive target for the therapeutic management of familial hypercholesterolemia as well as other refractory dyslipidaemias. However, PCSK9 mediates multifarious functions independent of its role in lipid homeostasis, which can be…

Male0301 basic medicineCell signalingHIPERCOLESTEROLEMIALow-density lipoprotein receptor gene familyHypercholesterolemiaMice TransgenicFamilial hypercholesterolemiaBiologyAntiviral AgentsPermeabilityMice03 medical and health sciencesAlzheimer DiseasemedicineAnimalsHomeostasisHumansGlucose homeostasisRNA Small InterferingEpithelial Sodium ChannelsGlycoproteinsNeuronsPCSK9PCSK9 InhibitorsAntibodies MonoclonalCell DifferentiationOligonucleotides Antisensemedicine.diseaseProprotein convertaseLipidsCircadian RhythmLiver RegenerationCell biology030104 developmental biologyReceptors LDLBiochemistryLDL receptorKexinFemalelipids (amino acids peptides and proteins)CRISPR-Cas SystemsProprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
researchProduct

Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cyto…

2005

Highly metastatic B16 melanoma (B16M)-F10 cells, as compared with the low metastatic B16M-F1 line, have higher GSH content and preferentially overexpress BCL-2. In addition to its anti-apoptotic properties, BCL-2 inhibits efflux of GSH from B16M-F10 cells and thereby may facilitate metastatic cell resistance against endothelium-induced oxidative/nitrosative stress. Thus, we investigated in B16M-F10 cells which molecular mechanisms channel GSH release and whether their modulation may influence metastatic activity. GSH efflux was abolished in multidrug resistance protein 1 knock-out (MRP-/-1) B16M-F10 transfected with the Bcl-2 gene or in MRP-/-1 B16M-F10 cells incubated with l-methionine, wh…

MaleMelanoma ExperimentalCystic Fibrosis Transmembrane Conductance RegulatorApoptosisBiochemistryOligodeoxyribonucleotides Antisensechemistry.chemical_compoundMiceCell AdhesionAnimalsEndotheliumNeoplasm MetastasisCytotoxicityCell adhesionMolecular BiologybiologyActivator (genetics)Cell BiologyGlutathioneTransfectiongamma-GlutamyltransferaseMolecular biologyGlutathioneCystic fibrosis transmembrane conductance regulatorMice Inbred C57BLKineticsOxidative StresschemistryProto-Oncogene Proteins c-bcl-2VerapamilApoptosisbiology.proteinEffluxMultidrug Resistance-Associated ProteinsThe Journal of biological chemistry
researchProduct

Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter.

1991

Glucose/galactose malabsorption (GGM) is an autosomal recessive disease manifesting within the first weeks of life and characterized by a selective failure to absorb dietary glucose and galactose from the intestine. The consequent severe diarrhoea and dehydration are usually fatal unless these sugars are eliminated from the diet. Intestinal biopsies of GGM patients have revealed a specific defect in Na(+)-dependent absorption of glucose in the brush border. Normal glucose absorption is mediated by the Na+/glucose cotransporter in the brush border membrane of the intestinal epithelium. Cellular influx is driven by the transmembrane Na+ electrochemical potential gradient; thereafter the sugar…

MaleModels MolecularBrush borderMonosaccharide Transport ProteinsProtein ConformationMolecular Sequence DataCarbohydrate metabolismPolymerase Chain Reactionchemistry.chemical_compoundMalabsorption SyndromesReference ValuesmedicineHumansMultidisciplinarySLC5A1biologyBase SequenceGlucose transporterGalactoseDNACarbohydratemedicine.diseaseMolecular biologyAntisense Elements (Genetics)GlucosechemistryBiochemistryGlucose-galactose malabsorptionGalactoseChild PreschoolMutationbiology.proteinFemaleCotransporterOligonucleotide ProbesNature
researchProduct