Search results for "guanidine"

showing 10 items of 78 documents

Nuclear Translocation of Mismatch Repair Proteins MSH2 and MSH6 as a Response of Cells to Alkylating Agents

2000

Mammalian mismatch repair has been implicated in mismatch correction, the prevention of mutagenesis and cancer, and the induction of genotoxicity and apoptosis. Here, we show that treatment of cells specifically with agents inducing O(6)-methylguanine in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea, elevates the level of MSH2 and MSH6 and increases GT mismatch binding activity in the nucleus. This inducible response occurs immediately after alkylation, is long-lasting and dose-dependent, and results from translocation of the preformed MutSalpha complex (composed of MSH2 and MSH6) from the cytoplasm into the nucleus. It is not caused by an increase in MSH2 gen…

CytoplasmDNA RepairBase Pair MismatchRNA StabilityChromosomal translocationmedicine.disease_causeBiochemistrychemistry.chemical_compoundMismatch Repair Endonuclease PMS2Adenosine TriphosphatasesNuclear ProteinsMethylnitrosoureaNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinDNA mismatch repairMutL Protein Homolog 1Protein BindingAlkylating AgentsMethylnitronitrosoguanidinecongenital hereditary and neonatal diseases and abnormalitiesGuanineActive Transport Cell NucleusBiologyCell LineO(6)-Methylguanine-DNA MethyltransferaseProto-Oncogene ProteinsDNA Repair ProteinmedicineHumansRNA MessengerneoplasmsMolecular BiologyAdaptor Proteins Signal TransducingCell NucleusMutagenesisnutritional and metabolic diseasesDNACell BiologyDNA MethylationMolecular biologydigestive system diseasesMSH6DNA Repair EnzymesGene Expression RegulationchemistryMSH2Carrier ProteinsGenotoxicityDNADNA DamageHeLa CellsJournal of Biological Chemistry
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Chromosomal instability, reproductive cell death and apoptosis induced by O6-methylguanine in Mex−, Mex+ and methylation-tolerant mismatch repair com…

1998

O6-Methylguanine (O6-MeG) is induced in DNA by methylating environmental carcinogens and various cytostatic drugs. It is repaired by O6-methylguanine-DNA methyltransferase (MGMT). If not repaired prior to replication, the lesion generates gene mutations and leads to cell death, sister chromatid exchanges (SCEs), chromosomal aberrations and malignant transformation. To address the question of how O6-MeG is transformed into genotoxic effects, isogenic Chinese hamster cell lines either not expressing MGMT (phenotypically Mex-), expressing MGMT (Mex+) or exhibiting the tolerance phenotype (Mex-, methylation resistant) were compared as to their clastogenic response. Mex- cells were more sensitiv…

DNA ReplicationMethylnitronitrosoguanidineGuanineDNA RepairDNA damageHealth Toxicology and MutagenesisDrug ResistanceApoptosisCHO CellsGene mutationBiologyChromosomesDNA AdductsO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeChromosome instabilityGeneticsAnimalsSister chromatidsMolecular BiologyMitosisChromosome AberrationsCell DeathModels GeneticMutagenicity TestsDNA replicationDNA MethylationMolecular biologyDNA methylationDNA mismatch repairSister Chromatid ExchangeMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Processing of O6-methylguanine into DNA double-strand breaks requires two rounds of replication whereas apoptosis is also induced in subsequent cell …

2009

The DNA adduct O(6)-methylguanine (O(6)MeG) induced by environmental genotoxins and anticancer drugs is a highly mutagenic, genotoxic and apoptotic lesion. Apoptosis induced by O(6)MeG requires mismatch repair (MMR) and proliferation. Models of O(6)MeG-triggered cell death postulate that O(6)MeG/T mispairs activate MMR giving rise to either direct genotoxic signaling or secondary lesions that trigger apoptotic signaling in the 2(nd) replication cycle. To test these hypotheses, we used a highly synchronized cell system competent and deficient for the repair of O(6)MeG adducts, which were induced by the S(N)1 methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We show that DNA doub…

DNA ReplicationProgrammed cell deathMethylnitronitrosoguanidineCell cycle checkpointGuanineDNA repairBlotting WesternSuccinimidesApoptosisCHO CellsBiologychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductAnimalsDNA Breaks Double-StrandedMolecular BiologyCell CycleCell BiologyCell cycleFlow CytometryFluoresceinsMolecular biologyCell biologychemistryMicroscopy FluorescenceApoptosisDNA mismatch repairDNADevelopmental BiologyCell cycle (Georgetown, Tex.)
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Association of hepatitis Be antigen (HBeAg) with the core of the hepatitis B virus (HBcAg).

2008

— Three substances (pronase E, sodium dodecylsulfate (SDS) and guanidine hydrochloride) with different chemical actions partially convert HBcAg to HBeAg. This process retains the integrity of the HBcAg particle, which was not different between HBcAg subpopulations, and does not generate HBcAg or HBeAg sub-units. DNA polymerase activity was destroyed by SDS and guanidine hydrochloride, but not by pronase E. Serum HBeAg could not be converted into HBcAg, suggesting that this might be an irreversible process. The data are consistent with the assumption that HBcAg and HBeAg are coded for by the same gene (C gene of the HBV-DNA).

DNA polymerasePronaseDNA-Directed DNA Polymerasemedicine.disease_causeGuanidinesHepatitis B Antigenschemistry.chemical_compoundAntigenmedicineHumansHepatitis B e AntigensGuanidineGuanidineHepatitisHepatitis B virusHepatologybiologyChemistryvirus diseasesSodium Dodecyl Sulfatemedicine.diseaseHepatitis BVirologyHepatitis B Core Antigensdigestive system diseasesHBcAgHBeAgPronasebiology.proteinLiver
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Transglutaminase and polyamine dependence of effector functions of human immunocompetent cells

1982

AbstractThe effects of the transglutaminase inhibitor dansyl cadaverine (DC) and the polyamine antagonist methyl glyoxal-bis-(guanylhydrazone) (MeGbG) on the response of lymphocytes towards allogeneic and lectin stimulation and on the zymosan-induced chemiluminescence of neutrophilic granulocytes was studied. Application of DC resulted in dose-dependent suppression of chemiluminiscence and lymphocyte proliferation; no difference of inhibitory potential occurred with variation of incubation time in the latter system. MeGbG was inactive in granulocytes, but inhibited lymphocyte proliferation; its effect increased with time. The experiments provide further evidence for the importance of transg…

Dansyl cadaverineDNA ReplicationPolyamineLuminescenceMitoguazoneTissue transglutaminaseLymphocyteBiophysicsStimulationLymphocyte proliferationDiaminesGranulocyteBiologyLymphocyte ActivationGuanidinesBiochemistrylaw.inventionMeGbGchemistry.chemical_compoundStructural BiologylawCadaverinePolyaminesGeneticsmedicineHumansLymphocytesMolecular BiologyChemiluminescenceCadaverineTransglutaminasesGranulocyteCell BiologyTransglutaminaseMolecular biologyKineticsmedicine.anatomical_structurechemistryBiochemistrybiology.proteinLymphocytePolyamineAcyltransferasesGranulocytesFEBS Letters
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Enhanced flow-injection–chemiluminometric determination of sulphonamides by on-line photochemical reaction

2003

Abstract The viability of the tandem photochemical reaction-chemiluminescence detection has been studied for an heterogeneous group of sulphonamides (sulphamethoxazole, sulphadiazine, sulphamerazine, sulphamethoxypyridazine, sulphacetamide, sulphadimidine, sulphanilamide, sulphathiazole and sulphaguanidine) using sulphamethoxazole (whose chemiluminescent behaviour has not been previously reported) as a test substance. The ‘on-line’ photochemical-reaction of sulphonamides provides an enhancing influence on the chemiluminometric response of the drugs during their oxidation by potassium permanganate in sulphuric acid medium (sulphamethoxazole, sulphacetamide, sulphadimidine and sulphanilamide …

Detection limitChromatographyFluorescence spectrometryPhotochemistryBiochemistryOrders of magnitude (mass)Analytical Chemistrylaw.inventionStandard curvePotassium permanganatechemistry.chemical_compoundchemistrylawSulphaguanidineEnvironmental ChemistryPhotodegradationSpectroscopyChemiluminescenceAnalytica Chimica Acta
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Coexpression of inducible NO synthase and soluble guanylyl cyclase in colonic enterocytes: a pathophysiologic signaling pathway for the initiation of…

1998

Infectious diarrhea is often caused by the exotoxins of gram-negative bacteria such as Escherichia coli. However, these organisms also contain lipopolysaccharide (LPS) endotoxin. LPS induces nitric oxide synthase II (NOS II, inducible NOS) in various types of cells. We now demonstrate by RNase protection analysis, Western blot, and immunohistochemistry that the expression of NOS II mRNA and protein is markedly induced in colonic enterocytes of mice that ingest LPS with their drinking water. Using the same techniques, significant levels of soluble guanylyl cyclase (GC-S), the effector enzyme of NO, were found constitutively expressed in the mucosa. This creates a pathophysiologic autocrine p…

DiarrheaLipopolysaccharidesmedicine.medical_specialtyGram-negative bacteriaLipopolysaccharideColonNitric Oxide Synthase Type IImedicine.disease_causeGuanidinesBiochemistryDexamethasoneMicrobiologyMicechemistry.chemical_compoundWestern blotInternal medicineGeneticsmedicineAnimalsIntestinal MucosaAutocrine signallingMolecular BiologyEscherichia colibiologymedicine.diagnostic_testbiology.organism_classificationDiarrheaEndocrinologySolubilitychemistryGuanylate CyclaseNitric Oxide Synthasemedicine.symptomSignal transductionGram-Negative Bacterial InfectionsSoluble guanylyl cyclaseSignal TransductionBiotechnologyThe FASEB Journal
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Neue chemotherapeutisch-aktive 4-trifluormethylpyrimidine

1993

Abstract Condensation of N -(2-hydroxyethyl)- N -methylguanidine sulfate with various β-diketonesbearing 1,1,1-trifluoromethyl substituents leads to 2-[ N -(2-hydroxyethyl)-methylamino]-4-trifluoromethylpyrimidine derivatives. These compounds exhibit antimycotic, trichomonazide and anti-HIV properties.

DiketoneOrganic ChemistryCondensationHuman immunodeficiency virus (HIV)Biological activitymedicine.disease_causeBiochemistryInorganic Chemistrychemistry.chemical_compoundchemistrymedicineMethylguanidineEnvironmental ChemistryOrganic chemistryPhysical and Theoretical ChemistrySulfateJournal of Fluorine Chemistry
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Ammonium formate-Pd/C as a new reducing system for 1,2,4-oxadiazoles. Synthesis of guanidine derivatives and reductive rearrangement to quinazolin-4-…

2021

1,2,4-Oxadiazole is a heterocycle with wide reactivity and many useful applications. The reactive O-N bond is usually reduced using molecular hydrogen to obtain amidine derivatives. NH4CO2H-Pd/C is here demonstrated as a new system for the O-N reduction, allowing us to obtain differently substituted acylamidine, acylguanidine and diacylguanidine derivatives. The proposed system is also effective for the achievement of a reductive rearrangement of 5-(2′-aminophenyl)-1,2,4-oxadiazoles into 1-alkylquinazolin-4(1H)-ones. The alkaloid glycosine was also obtained with this method. The obtained compounds were preliminarily tested for their biological activity in terms of their cytotoxicity, induce…

Formatesquinazolin-4-onemedicine.disease_causeGuanidineschemistry.chemical_compoundBiology (General)CytotoxicityAmmonium formateSpectroscopyOxadiazolesMolecular StructureChemistryAlkaloidBiological activityGeneral MedicineComputer Science ApplicationsChemistryOxidation-ReductionPalladiumCell SurvivalQH301-705.5Dipeptidyl Peptidase 4chemistry.chemical_elementAntineoplastic AgentsreductionArticleCatalysisInorganic ChemistryAmidine4-oxadiazolereduction;Cell Line TumorDiabetes MellitusAmmonium formatemedicineHumansHypoglycemic AgentsReactivity (chemistry)Physical and Theoretical ChemistryMolecular BiologyQD1-999QuinazolinonesSettore MED/04 - Patologia GeneralediacylguanidineOrganic Chemistry124-oxadiazolealpha-GlucosidasesacylguanidineSettore CHIM/06 - Chimica OrganicapalladiumCombinatorial chemistryModels ChemicalA549 CellsOxidative stress
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Chemical skin carcinogenesis is prevented in mice by the induced expression of a TGF-β related transgene

1995

Skin papillomas and squamous cell carcinomas (SCCs) are induced in mice by tumor initiation with a carcinogen followed by tumor promotion with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). These usually arise from preneoplastic lesions characterized by epidermal proliferation and hyperplasia, dermal edema, and inflammation. To evaluate the role of polypeptide growth factors in chemically induced skin carcinogenesis, we used transgenic mice carrying the cDNA for a TGF-β related molecule, bone morphogenetic protein-4 (BMP-4), under the control of the regulatory elements of the cytokeratin IV* gene in a skin carcinogenesis protocol. Control non-transgenic littermates and BMP-4 …

Genetically modified mouseMethylnitronitrosoguanidinePathologymedicine.medical_specialtySkin NeoplasmsHealth Toxicology and MutagenesisTransgenemedicine.medical_treatmentMice TransgenicTumor initiationBiologyToxicologymedicine.disease_causeMiceTransforming Growth Factor betaGeneticsmedicineAnimalsGenetics (clinical)SkinPapillomaintegumentary systemEpidermis (botany)ProteinsHyperplasiamedicine.diseaseCytokineBromodeoxyuridineOncologyBone Morphogenetic ProteinsCarcinoma Squamous CellCancer researchTetradecanoylphorbol AcetateTumor promotionEpidermisCarcinogenesisCell DivisionTeratogenesis, Carcinogenesis, and Mutagenesis
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