Search results for " Suppressor"

showing 10 items of 462 documents

Enhancement of cytotoxicity of artemisinins toward cancer cells by ferrous iron

2004

Abstract Iron(II) heme-mediated activation of the peroxide bond of artemisinins is thought to generate the radical oxygen species responsible for their antimalarial activity. We analyzed the role of ferrous iron in the cytotoxicity of artemisinins toward tumor cells. Iron(II)–glycine sulfate (Ferrosanol) and transferrin increased the cytotoxicity of free artesunate, artesunate microencapsulated in maltosyl-β-cyclodextrin, and artemisinin toward CCRF-CEM leukemia and U373 astrocytoma cells 1.5- to 10.3-fold compared with that of artemisinins applied without iron. Growth inhibition by artesunate and ferrous iron correlated with induction of apoptosis. Cell cycle perturbations by artesunate an…

ArtemisininsIronPopulationTransferrin receptorBiochemistryFerrousInhibitory Concentration 50chemistry.chemical_compoundAntigens CDCell Line TumorNeoplasmsPhysiology (medical)Receptors TransferrinHumansFerrous CompoundsRNA MessengereducationCell Proliferationchemistry.chemical_classificationeducation.field_of_studybiologyMolecular biologyArtemisininsAntigens Differentiation B-LymphocyteGene Expression RegulationBiochemistrychemistryTransferrinArtesunateCancer cellbiology.proteinTumor Suppressor Protein p53CeruloplasminFree Radical Biology and Medicine
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Translational readthrough of ciliopathy genes BBS2 and ALMS1 restores protein, ciliogenesis and function in patient fibroblasts

2021

Abstract Background Ciliary dysfunction underlies a range of genetic disorders collectively termed ciliopathies, for which there are no treatments available. Bardet-Biedl syndrome (BBS) is characterised by multisystemic involvement, including rod-cone dystrophy and renal abnormalities. Together with Alstrom syndrome (AS), they are known as the ‘obesity ciliopathies’ due to their common phenotype. Nonsense mutations are responsible for approximately 11% and 40% of BBS and AS cases, respectively. Translational readthrough inducing drugs (TRIDs) can restore full-length protein bypassing in-frame premature termination codons, and are a potential therapeutic approach for nonsense-mediated ciliop…

BBS2AdultMaleMedicine (General)AdolescentNonsense mutationAminopyridinesCell Cycle ProteinsCiliopathiesGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundR5-920AtalurenCiliogenesismedicineHumansReceptors SomatostatinBardet-Biedl SyndromeAlstrom SyndromeCells CulturedOxadiazolesbusiness.industryTumor Suppressor ProteinsTranslational readthroughRProteinsGeneral MedicineFibroblastsmedicine.diseaseNonsense suppressionCiliopathiesAtalurenCiliopathyALMS1chemistryCodon NonsenseAmlexanoxCancer researchMedicineBBS2businessAlström syndromeResearch PaperEBioMedicine
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Toward the development of metal-based synthetic nucleases: DNA binding and oxidative DNA cleavage of a mixed copper(II) complex with N-(9H-purin-6-yl…

2009

Abstract The complex [Cu(N9-ABS)(phen) 2 ]·3.6H 2 O, H 2 N9-ABS  = N -(9 H -purin-6-yl)benzenesulfonamide and phen = 1,10-phenanthroline, has been synthesized and then characterized with the aid of X-ray diffraction, analytical, and spectroscopic techniques. The geometry of Cu(II) is distorted square pyramidal with the equatorial positions occupied by three N atoms from two phenantroline molecules and one N atom from the adenine ring of the sulfonamide ligand. The interaction of the complex with DNA was studied by means of viscosity measurements and fluorescence spectroscopy. The results pointed to a classic intercalation of the complex between the DNA base pairs. The complex was found to b…

Base pairStereochemistryIntercalation (chemistry)Antineoplastic AgentsApoptosisCleavage (embryo)BiochemistryJurkat cellsInorganic ChemistryJurkat Cellschemistry.chemical_compoundOrganometallic CompoundsHumansDNA CleavageCytotoxicitySulfonamidesChemistryDNASquare pyramidal molecular geometryProto-Oncogene Proteins c-bcl-2ApoptosisCaco-2 CellsTumor Suppressor Protein p53CopperDNAPhenanthrolinesJournal of Inorganic Biochemistry
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Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas

2007

AbstractIntegrative genomic and gene-expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored. Array-based comparative genomic hybridization (CGH) and gene-expression microarray analysis of 48 cell lines derived from patients with different B-NHLs delineated 20 homozygous deletions at 7 chromosome areas, all of which contained tumor suppressor gene targets. Further investigation revealed that only a fraction of primary biopsies presented inactivation of these genes by point mutation or intragenic deletion, but instead some of them w…

BiopsyDNA Mutational AnalysisGene DosageVesicular Transport ProteinsApoptosisBiochemistryEpigenesis Geneticimmune system diseaseshemic and lymphatic diseasesChromosomes HumanGenes Tumor SuppressorPromoter Regions GeneticSorting NexinsOligonucleotide Array Sequence AnalysisSequence DeletionBcl-2-Like Protein 11HomozygoteChromosome MappingNuclear ProteinsNucleic Acid HybridizationRNA-Binding ProteinsHematologyDNA NeoplasmBCL10Gene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2DNA methylationLymphoma B-CellTumor suppressor geneImmunologyBiologyGene dosageCell Line TumorProto-Oncogene ProteinsmedicineCyclin-Dependent Kinase Inhibitor p18HumansPoint MutationGene SilencingB cellAdaptor Proteins Signal TransducingHomeodomain ProteinsMembrane ProteinsCell BiologyDNA Methylationmedicine.diseaseMolecular biologyLymphomaCancer researchMantle cell lymphomaApoptosis Regulatory ProteinsCarrier ProteinsDiffuse large B-cell lymphomaTranscription Factors
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Relationship Between Thymidylate Synthase and p53 and Response to FEC Versus Taxane Adjuvant Chemotherapy for Breast Carcinoma

2011

Many drugs can be used for adjuvant therapy of breast cancer, including anthracyclines, cyclophosphamide, 5-fluorouracil (5-fU) and, recently, taxanes (TXT) have shown promising results. 5-FU blocks thymidylate synthase (TS) which cross-links p53 mRNA, inhibiting its synthesis. TS overexpression is one of the main mechanisms involved in 5-FU drug resistance. Enough p53 mutations can confer resistance to chemotherapy using anthracyclines and 5-FU, while are associated with improved responses to TXT. The aim of this study was to examine the TS and p53 levels in tumor samples and to compare the efficacy of FEC (5-FU, epirubicin, cyclophosphamide) and TXT chemotherapy in a group of patients wit…

Bridged-Ring CompoundsOncologymedicine.medical_specialtyCyclophosphamidemedicine.medical_treatmentBreast NeoplasmsThymidylate synthaseBreast cancerInternal medicineAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineAdjuvant therapyHumansPharmacology (medical)CyclophosphamideEpirubicinNeoplasm StagingPharmacologyChemotherapyTaxanebiologybusiness.industryThymidylate SynthasePrognosismedicine.diseaseImmunohistochemistryInfectious DiseasesOncologyChemotherapy AdjuvantFluorouracilbiology.proteinCancer researchFemaleTaxoidsFluorouracilTumor Suppressor Protein p53businessmedicine.drugEpirubicinJournal of Chemotherapy
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Tumorigenic conversion of endothelial cells.

2003

Tumors of endothelial origin develop rarely. Until now, only two angiosarcoma (AS)-derived endothelial cell lines have been be isolated, ISO-HAS and AS-M. Both AS-derived endothelial cell lines presented the typical endothelial characteristics, such as the expression of CD31 and von Willebrand factor, but differed from normal endothelial cells in a nuclear expression of p53, in a delayed angiogenic reaction, and a reduced expression of caveolin. In addition, differences in the expression of cytokines and cell adhesion molecules responsive to proinflammatory stimuli were observed. While AS-M showed an expression pattern similar to that of human umbilical vein endothelial cells (HUVEC), ISO-H…

CD31AdultLipopolysaccharidesTelomerasePathologymedicine.medical_specialtyClinical BiochemistryCaveolin 1Vascular Cell Adhesion Molecule-1BiologyCaveolinsPathology and Forensic Medicinevon Willebrand FactormedicineCell AdhesionHumansMolecular BiologyTelomeraseCells CulturedCell NucleusCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionGranulocyte-Macrophage Colony-Stimulating FactorTelomereIntercellular Adhesion Molecule-1Cell biologyVascular endothelial growth factor BEndothelial stem cellDNA-Binding ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factor ACell Transformation NeoplasticVascular endothelial growth factor CCell cultureEndothelium VascularTumor Suppressor Protein p53Experimental and molecular pathology
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Cylindromatosis (Cyld) gene mutation in T cells promotes the development of an IL-9-dependent allergic phenotype in experimental asthma

2016

Cylindromatosis (CYLD) is a ubiquitously expressed deubiquitinating enzyme which removes activating ubiquitin residues from important signaling molecules of the NF-κB pathway. In CYLDex7/8 transgenic mice, a naturally occurring short isoform (sCYLD) is overexpressed in the absence of full length CYLD, leading to excessive NF-κB activity. Herein, we investigated the impact of the CYLDex7/8 mutation selectively in T cells on the development of experimental allergic airway disease induced by sensitization and challenge with ovalbumin. Compared with their wildtype littermates, mice bearing the T cell-specific mutation (CD4+CYLDex7/8) display stronger eosinophilia and mucus production in the lun…

CD4-Positive T-Lymphocytes0301 basic medicineSkin Neoplasmsmedicine.medical_treatmentT cellImmunologyGene mutationImmunoglobulin Emedicine.disease_causeTh9 cellsDeubiquitinating enzymeMice03 medical and health sciencesNeoplastic Syndromes HereditaryHypersensitivitymedicineAnimalsHumansSensitizationMice KnockoutMutationbiologyTumor Suppressor ProteinsInterleukin-9Cylindromatosis (turban tumor syndrome) geneIL-9AsthmaDeubiquitinating Enzyme CYLDEosinophilsMice Inbred C57BLMucusOvalbumin030104 developmental biologymedicine.anatomical_structureCytokineModels AnimalMutationImmunologybiology.proteinCellular Immunology
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The gp130-stimulating designer cytokine hyper-IL-6 promotes the expansion of human hematopoietic progenitor cells capable to differentiate into funct…

2000

Abstract Objective . Hyper-IL-6, a fusion protein of interleukin-6 and its specific receptor, together with stem cell factor leads to the proliferation of primitive hematopoietic progenitor cells. Based on these findings, the current study examined whether hyper-IL-6 promotes the growth of precursor cells that can be further differentiated into dendritic cells in the presence of additional cytokines. Methods . Dendritic cell cultures were generated from CD34 + hematopoietic progenitor cells derived either from bone marrow or from peripheral blood. CD34 + cells were cultured in the presence of cytokines for 2 weeks and then used for phenotyping and T-cell stimulation assays. Results . Hyper-…

CD4-Positive T-LymphocytesCancer ResearchRecombinant Fusion ProteinsAntigen presentationBiologyDinoprostoneImmunophenotypingAntigens CDOxytocicsGeneticsCytokine Receptor gp130HumansProgenitor cellAntigen-presenting cellMolecular BiologyCells CulturedInterleukin 3Antigen PresentationStem Cell FactorMembrane GlycoproteinsFollicular dendritic cellsInterleukin-6Tumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationCell BiologyHematologyDendritic cellDendritic CellsReceptors InterleukinFlow CytometryHematopoietic Stem CellsHepatitis B Core AntigensReceptors Interleukin-6Recombinant ProteinsCell biologyEndothelial stem cellMyeloid-derived Suppressor CellInterleukin-4Cell DivisionInterleukin-1Experimental hematology
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Nitric oxide enhances Th9 cell differentiation and airway inflammation

2014

International audience; Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody.…

CD4-Positive T-LymphocytesInterleukin 2[SDV]Life Sciences [q-bio]Cellular differentiationNitric Oxide Synthase Type IIGeneral Physics and AstronomyMice TransgenicInflammationCell SeparationNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMicechemistry.chemical_compoundEosinophiliaSTAT5 Transcription FactormedicineAnimalsHumansInterleukin 9Cells CulturedInflammationMice Inbred BALB CMultidisciplinarybiologyNitrosylationInterleukin-9Cell DifferentiationGeneral Chemistryrespiratory systemFlow Cytometry3. Good healthCell biologyMice Inbred C57BLchemistryInterferon Regulatory FactorsImmunologyLeukocytes Mononuclearbiology.proteinInterleukin-2Mdm2Tumor Suppressor Protein p53medicine.symptomAntibodymedicine.drugNature Communications
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Cooperation of Human Tumor-Reactive CD4+ and CD8+ T Cells after Redirection of Their Specificity by a High-Affinity p53A2.1-Specific TCR

2004

Abstract Efficient immune attack of malignant disease requires the concerted action of both CD8 + CTL and CD4 + Th cells. We used human leukocyte antigen (HLA)-A*0201 (A2.1) transgenic mice, in which the mouse CD8 molecule cannot efficiently interact with the α3 domain of A2.1, to generate a high-affinity, CD8-independent T cell receptor (TCR) specific for a commonly expressed, tumor-associated cytotoxic T lymphocyte (CTL) epitope derived from the human p53 tumor suppressor protein. Retroviral expression of this CD8-independent, p53-specific TCR into human T cells imparted the CD8 + T lymphocytes with broad tumor-specific CTL activity and turned CD4 + T cells into potent tumor-reactive, p53…

CD4-Positive T-LymphocytesT cellImmunologyReceptors Antigen T-CellMice TransgenicT-Cell Antigen Receptor SpecificityCD8-Positive T-LymphocytesBiologyMiceInterleukin 21Transduction GeneticTumor Cells CulturedmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellCloning MolecularAntigen-presenting cellT-cell receptorFlow CytometryNatural killer T cellCell biologyCTL*Infectious Diseasesmedicine.anatomical_structureImmunologyTumor Suppressor Protein p53CD8T-Lymphocytes CytotoxicImmunity
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