Search results for "Transform"

showing 10 items of 3975 documents

A tyrosinase peptide presented by HLA-B35 is recognized on a human melanoma by autologous cytotoxic T lymphocytes

1999

We previously described different cytotoxic T lymphocyte (CTL) clones isolated from the blood lymphocytes of a melanoma patient after in vitro stimulation with autologous tumor cells. These CTL clones recognized at least 2 distinct antigens on the melanoma cells. Here, we show that one of them consists of a peptide derived from tyrosinase and presented by HLA-B35. The peptide is 9 amino acids long and has the sequence LPSSADVEF. It can be presented by the 2 major B35 allelic subtypes, B*3501 and B*3503. As HLA-B35 is one of the most frequent HLA-B specificities, being present in about 20% of Caucasian individuals, it may be a useful target for peptide-based immunotherapy of melanoma.

Cytotoxicity ImmunologicHerpesvirus 4 HumanCancer Researchmedicine.medical_treatmentAntigen presentationTyrosinase PeptideBiologyTransfectionAntigenTumor Cells CulturedmedicineAnimalsHumansCytotoxic T cellAmino Acid SequenceMelanomaPeptide sequenceAllelesCell Line TransformedB-LymphocytesMonophenol MonooxygenaseMelanomaImmunotherapymedicine.diseasePeptide FragmentsRecombinant ProteinsCTL*OncologyCOS CellsImmunologyCancer researchHLA-B35 AntigenT-Lymphocytes CytotoxicInternational Journal of Cancer
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Low frequency of cytotoxic liver-infiltrating T lymphocytes specific for endogenous processed surface and core proteins in chronic hepatitis B.

1993

To investigate the role of hepatitis B virus (HBV)-specific CD8+ T cells in chronic hepatitis B, the lytic activity of peripheral blood mononuclear cells (PBMC) and liver-infiltrating T cell clones and cytotoxic T cell (CTL) lines stimulated by recombinant vaccinia virus-infected cells were analyzed. Autologous and allogeneic Epstein-Barr virus-transformed B cells infected with vaccinia vectors (VAC) that contain sequences of the surface (S), secretory core (E), cytoplasmatic core (C) VAC antigen of HBV, or the wild-type (WT) VAC served as target cells. ELISA and immunoblotting showed HBV antigen expression in infected cells. Neither PBMC nor C- or E-VAC-stimulated CTL lines showed specific…

Cytotoxicity ImmunologicHerpesvirus 4 HumanT cellGenes MHC Class IVaccinia virusBiologymedicine.disease_causeHepatitis B AntigensAntigenCell MovementmedicineImmunology and AllergyCytotoxic T cellHumansHepatitis B e AntigensHepatitis ChronicHepatitis B virusHepatitisB-LymphocytesHepatitis B Surface AntigensHepatitis Bmedicine.diseasebiology.organism_classificationCell Transformation ViralHepatitis BVirologyHepatitis B Core AntigensRecombinant ProteinsCTL*Infectious Diseasesmedicine.anatomical_structureHepadnaviridaeLiverProtein Processing Post-TranslationalT-Lymphocytes CytotoxicThe Journal of infectious diseases
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On the accuracy of the fast hierarchical DBEM for the analysis of static and dynamic crack problems

2010

In this paper the main features of a fast dual boundary element method based on the use of hierarchical matrices and iterative solvers are described and its effectiveness for fracture mechanics problems, both in the static and dynamic case, is demonstrated. The fast solver is built by representing the collocation matrix in hierarchical format and by using a preconditioned GMRES for the solution of the algebraic system. The preconditioner is computed in hierarchical format by LU decomposition of a coarse hierarchical representation of the collocation matrix. The method is applied to elastostatic problems and to elastodynamic cases represented in the Laplace transform domain. The application …

DBEM Adaptive Cross Approximation Hierarchical Matrices Fast BEM solvers Elastodynamics Laplace Transform Method Stress Intensity Factors.Settore ING-IND/04 - Costruzioni E Strutture Aerospaziali
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Synthesis, chemical characterization, computational studies and biological activity of new DNA methyltransferases (DNMTs) specific inhibitor. Epigene…

2015

This work deals with the synthesis, the chemical characterization of dibutyltin(IV) complex of caffeic acid (Bu2Sn(IV)HCAF, caf1) and its cytotoxic action on tumor cells. The coordination environment at the tin center was investigated by FTIR, (119)Sn{(1)H} cross polarization magic angle spinning, electrospray ionization mass spectroscopy in the solid state and UV-vis, fluorescence and (1)H, (13)C and (119)Sn NMR spectroscopy in solution phases. Density functional theory study confirmed the proposed structures in solution phase and indicated the most probably stable conformation. The effects on viability of breast cancer MDA-MB231, colorectal cancer HCT116, hepatocellular carcinoma HepG2 an…

DNA (Cytosine-5-)-Methyltransferase 1Magnetic Resonance SpectroscopyMethyltransferaseAntineoplastic AgentsBiochemistryEpigenesis GeneticMembrane PotentialsInorganic Chemistrychemistry.chemical_compoundCaffeic AcidsCell Line TumorSettore BIO/10 - BiochimicaSpectroscopy Fourier Transform InfraredOrganotin CompoundsCaffeic acidHumansCytotoxic T cellDNA (Cytosine-5-)-MethyltransferasesEnzyme InhibitorsSettore CHIM/02 - Chimica FisicaChemistryOrganotin(IV) Caffeic acid DNMT1 DNA methylation CancerBiological activityDNA MethylationFlow CytometryMitochondriaModels ChemicalBiochemistryCell cultureSettore CHIM/03 - Chimica Generale E InorganicaDNA methylationHepatic stellate cellDNA
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Induction of DNA crosslinks and DNA strand lesions by cyclophosphamide after activation by cytochrome P450 2B1

1997

Cyclophosphamide requires metabolic activation by cytochrome P450 to exert its genotoxic effects. Therefore in vitro studies on its mechanism of action have been limited to the use of self-activating derivatives of cyclophosphamide or to hepatocytes as an activating system. In this study we used a cell line of Chinese hamster lung fibroblasts (V79 cells), genetically engineered to express active cytochrome P450 2B1 as the sole observable cytochrome P450 (SD1 cells). An increase in DNA strand lesions (SL: DNA single-strand breaks and alkali labile sites) was observed between 0.5 and 1.5 mM cyclophosphamide (24 h incubation) which could be classified as alkali labile sites using a modified al…

DNA RepairCyclophosphamideDNA repairDNA damageHealth Toxicology and MutagenesisHamsterBiologyTransfectionCell LineCricetulusCytochrome P-450 Enzyme SystemCricetinaeGeneticsmedicineAnimalsCyclophosphamideMolecular BiologyIncubationBiotransformationDose-Response Relationship Drug4-HydroxycyclophosphamideDNAPhosphoramide MustardBiochemistryCell culturePhosphoramide MustardsDNA Damagemedicine.drugMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Poly(ADP-ribosyl)ation accelerates DNA repair in a pathway dependent on Cockayne syndrome B protein

2003

Activation of poly(ADP-ribose)polymerases 1 and 2 (PARP-1 and PARP-2) is one of the earliest responses of mammalian cells to DNA damage by numerous genotoxic agents. We have analysed the influence of PARP inhibition, either achieved by over-expression of the DNA binding domain of PARP-1 or by treatment with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone, on the repair of single-strand breaks (SSB), pyrimidine dimers and oxidative base modifications sensitive to Fpg protein (mostly 8-hydroxyguanine) in mammalian cells at very low, non-cytotoxic levels of DNA damage. The data show that the repair rates of all three types of DNA damage are significantly lower in PARP-inhibited c…

DNA RepairDNA damageDNA repairPoly ADP ribose polymerase[SDV]Life Sciences [q-bio]Pyrimidine dimerBiologyPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorCockayne syndromeDexamethasone03 medical and health sciencesMice0302 clinical medicinePiperidinesCricetinaeGeneticsmedicineAnimalsPoly-ADP-Ribose Binding ProteinsComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Line TransformedMice Knockout0303 health sciencesDNA HelicasesArticlesDNADNA repair protein XRCC4Fibroblastsmedicine.diseaseIsoquinolinesMolecular biology3. Good healthDNA Repair Enzymes030220 oncology & carcinogenesisPoly(ADP-ribose) PolymerasesNucleotide excision repairDNA DamageSignal Transduction
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Nucleotide excision repair of abasic DNA lesions

2019

AbstractApurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, w…

DNA RepairTranscription GeneticDNA damageDNA repairGenome Integrity Repair and ReplicationGene Knockout Techniques03 medical and health sciencesEndonucleasechemistry.chemical_compoundTranscription (biology)CRISPR-Associated Protein 9DNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansAP siteCell Line TransformedSkin030304 developmental biologyGene Editing0303 health sciencesBase SequencebiologyGenome Human030302 biochemistry & molecular biologyDNABase excision repairFibroblastsMolecular biologyXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinschemistryMutationbiology.proteinCRISPR-Cas SystemsDNADNA DamageProtein BindingNucleotide excision repairNucleic Acids Research
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Mechanisms and consequences of methylating agent-induced SCEs and chromosomal aberrations: a long road traveled and still a far way to go.

2003

Since the milestone work of Evans and Scott, demonstrating the replication dependence of alkylation-induced aberrations, and Obe and Natarajan, pointing to the critical role of DNA double-strand breaks (DSBs) as the ultimate trigger of aberrations, the field has grown extensively. A notable example is the identification of DNA methylation lesions provoking chromosome breakage (clastogenic) effects, which made it possible to model clastogenic pathways evoked by genotoxins. Experiments with repair-deficient mutants and transgenic cell lines revealed both O<sup>6</sup>-methylguanine (O<sup>6</sup>MeG) and N- methylpurines as critical lesions. For S<sub>N</sub&g…

DNA ReplicationAlkylating AgentsGuanineDNA RepairDNA damageDNA repairBase Pair MismatchApoptosisBiologyMethylationLesionAnimals Genetically ModifiedMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeGeneticsmedicineAnimalsHumansPoint MutationAP siteMolecular BiologyGenetics (clinical)Chromosome AberrationsRecombination GeneticGuanosineModels GeneticCell CycleDNA replicationDNAFibroblastsMolecular biologyCell killingCell Transformation NeoplasticCancer researchDNA mismatch repairChromosome breakagemedicine.symptomSister Chromatid ExchangeDNA DamageMutagensCytogenetic and genome research
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Transformation of Aspergillus parasiticus using autonomously replicating plasmids from Aspergillus nidulans.

1994

A genetic transformation system for the aflatoxin-producing fungus Aspergillus parasiticus using two autonomously replicating plasmids from A. nidulans (ARp1 and pDHG25) is reported. Transformation frequencies using the plasmid pDHG25 were from 5 x 10(2) to 2.5 x 10(4) transformants per 10(6) viable protoplasts and microgram DNA. The stability of the plasmids in the transformants was also studied. This transformation system offers a new opportunity to clone genes related to aflatoxin production using appropriate aflatoxin-defective mutants.

DNA ReplicationArginine BAutonomously replicating sequenceMitosisLaboratorium voor ErfelijkheidsleerMicrobiologyAspergillus parasiticusAspergillus nidulansMicrobiologyGenetic transformationchemistry.chemical_compoundPlasmidTransformation GeneticAutonomous replicationAspergillus nidulansGeneticsDNA FungalMolecular BiologyGeneGeneticsAspergillus nidulans autonomous replicating plasmidbiologyProtoplastsfood and beveragesProtoplastbiology.organism_classificationAspergillus parasiticusTransformation (genetics)AspergilluschemistryLaboratory of GeneticsDNAPlasmidsFEMS microbiology letters
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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