Search results for "Polymerase"

showing 10 items of 2127 documents

EcFLO, a FLORICAULA-like gene from Eschscholzia californica is expressed during organogenesis at the vegetative shoot apex.

2003

FLORICAULA/ LEAFY-like genes were initially characterized as flower meristem identity genes. In a range of angiosperms, expression occurs also in vegetative shoot apices and developing leaves, and in some species with dissected leaves expression is perpetuated during organogenesis at the leaf marginal blastozone. The evolution of these expression patterns and associated functions is not well understood. We have isolated and characterized a FLORICAULA-like gene from California Poppy, Eschscholzia californica Cham. (Papaveraceae), a species belonging to the basal eudicot clade Ranunculales. EcFLO encodes a putative 416-amino-acid protein with highest similarity to homologous genes from Trocho…

California PoppyMolecular Sequence DataOrganogenesisPlant ScienceEschscholziaBotanyGeneticsPapaveraceaePrimordiumAmino Acid SequenceLeafyIn Situ HybridizationPhylogenyDNA PrimersPlant ProteinsEschscholziabiologyBase SequenceSequence Homology Amino AcidReverse Transcriptase Polymerase Chain Reactionfungifood and beveragesRNA ProbesMeristembiology.organism_classificationRanunculalesSequence AlignmentPlanta
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A urochordate putative homolog of human EB1, the protein which binds APC1

1996

Abstract The human EB1 protein has been cloned by virtue of its interaction with the C-terminus of the APC (adenomatous polyposis coli) protein, whose C-terminal truncated forms have been shown to accompany sporadic and familial forms of colorectal cancer. We have cloned a putative EB1 homolog from Botryllus schlosseri (Urochordata, Ascidiacea). The deduced protein is 287 amino acids long, and is identical with 48% of the residues in human EB1 and 24–25% in two yeast hypothetical proteins. We propose that such a high degree of conservation among EB1 homologs is indicative of an essential regulatory mechanism in eukaryotic cells.

Cancer ResearchAdenomatous polyposis coliMolecular Sequence Datamacromolecular substancesBotryllus schlosseriPolymerase Chain ReactionHomology (biology)Conserved sequenceBacterial ProteinsComplementary DNAAnimalsHumansAmino Acid SequenceUrochordataGeneticschemistry.chemical_classificationBase SequencebiologyfungiNucleic acid sequenceProteinsSequence Analysis DNAbiology.organism_classificationYeastAmino acidOncologychemistrybiology.proteinSequence AlignmentCancer Letters
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Induction of the alkyltransferase (MGMT) gene by DNA damaging agents and the glucocorticoid dexamethasone and comparison with the response of base ex…

1996

Repair of alkylated bases in DNA is performed by O6-methylguanine-DNA methyltransferase (MGMT) and a set of enzymes of the base excision repair pathway involving N-methylpurine-DNA glycosylase (MPG), apurinic endonuclease (APE), DNA polymerase beta (Pol beta) and DNA ligase. The level of expression of these enzymes may exert a profound effect on resistance of cells towards alkylating drugs. We have comparatively analyzed the expression of MGMT and the different base excision repair genes in rat hepatoma cells (line H4IIE) after exposure to alkylating agents, X-rays and the glucocorticoid hormone dexamethasone. Furthermore, the effect of these agents on the activity of the cloned human MGMT …

Cancer ResearchAlkylationDNA RepairDNA damageDNA polymerase betaBiologyDexamethasoneGene Expression Regulation Enzymologicchemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalAnimalsRNA MessengerPromoter Regions GeneticneoplasmsAntineoplastic Agents AlkylatingGlucocorticoidschemistry.chemical_classificationDNA ligaseO-6-methylguanine-DNA methyltransferaseGeneral MedicineBase excision repairDNA NeoplasmMethyltransferasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyasedigestive system diseasesRatsUp-RegulationGene Expression Regulation NeoplasticKineticschemistryDNA glycosylaseEnzyme InductionAlkyltransferaseDNA DamageCarcinogenesis
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Deficient expression of components of the MHC class I antigen processing machinery in human cervical carcinoma.

2001

In cervical carcinomas abnormalities in the MHC class I surface expression are a frequent event, which are often associated with the deficient expression of the peptide transporter subunit TAP1 thereby resulting in impaired T cell response. In order to understand the role of other components of the MHC class I antigen processing machinery (APM) in the immune escape, 16 surgically removed primary cervical carcinoma lesions were analyzed for their mRNA expression of the heterodimeric peptide transporter TAP, the constitutive and interferon (IFN)-gamma inducible proteasome subunits and their activators PA28alpha/beta, various chaperones as well as MHC class I antigens. High expression levels o…

Cancer ResearchAntigen presentationBlotting WesternDown-RegulationGene ExpressionGenes MHC Class IUterine Cervical NeoplasmsHuman leukocyte antigenBiologyInterferon-gammaInterferonMHC class ImedicineBiomarkers TumorTumor Cells CulturedHumansRNA MessengerCells CulturedDNA PrimersAntigen PresentationAntigen processingMHC class I antigenReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class ITransporter associated with antigen processingNeoplasm ProteinsPhenotypeOncologyImmunologyCancer researchbiology.proteinFemaleTAP1medicine.drugInternational journal of oncology
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Role of glutathione in the induction of apoptosis and c-fos and c-jun mRNAs by oxidative stress in tumor cells.

2003

We have used two tumor cell clones (B9 and G2), derived from the methylcholanthrene-induced murine fibrosarcoma GR9 and normal BALB/c3T3 fibroblasts, to study the ability of t-BOOH derived reactive oxygen radicals to induce oxidative stress, apoptosis and c-fos and c-jun mRNA transcription. These clones differ in terms of their major histocompatibility complex (MHC) (H-2) class I genes expression, their tumor induction and metastatic potential and their reduced glutathione (GSH) levels. Incubation of both cell clones in the presence of t-BOOH results in the increase of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and malondialdehyde and the decrease of GSH. The xenobiotic also induces the transcripti…

Cancer ResearchBALB 3T3 CellsTranscription GeneticProto-Oncogene Proteins c-junFibrosarcomaCellApoptosisBiologymedicine.disease_causeAntioxidantsSuperoxide dismutasechemistry.chemical_compoundMicetert-ButylhydroperoxideCell CloneMalondialdehydemedicineTumor Cells CulturedAnimalsRNA MessengerDNA Primerschemistry.chemical_classificationReactive oxygen speciesReverse Transcriptase Polymerase Chain Reactionc-junHistocompatibility Antigens Class IDeoxyguanosineGlutathioneFibroblastsMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureOncologychemistryGene Expression RegulationApoptosis8-Hydroxy-2'-Deoxyguanosinebiology.proteinReactive Oxygen SpeciesProto-Oncogene Proteins c-fosOxidative stressCancer letters
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Expression of the IAPs in multidrug resistant tumor cells

2003

We have investigated the expression of the IAPs (inhibitory of apoptosis proteins) in the human HL-60 leukemia and in its multidrug resistant, P-glycoprotein (P-gp) over-expressing variant, HL-60R. HL-60R exhibits resistance to apoptosis induced from P-gp substrate drugs and also from other triggers (cisplatin, TNF-alpha, Fas ligation, TRAIL, IFN-gamma and serum starvation) not related to the multidrug transporter. Except for c-IAP-1 mRNA, HL-60R significantly over-expressed both the mRNAs and the proteins of all the IAPs studied, i.e. c-IAP-1, c-IAP-2, XIAP, NAIP and survivin. Determination of the DNA-binding capacity of NF-kappaB (p50 or p65 subunits) indicated that, while HL-60 cells sho…

Cancer ResearchBlotting WesternCellApoptosisHL-60 CellsBiologyInhibitor of Apoptosis Proteinsmultidrug resistanceSurvivinmedicineHumansRNA MessengerCisplatinOncogeneReverse Transcriptase Polymerase Chain ReactionNF-kappa BProteinsGeneral MedicineIAPCell cycleapoptosiMolecular biologyDrug Resistance MultipleXIAPGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyDrug Resistance NeoplasmApoptosisCancer researchNAIPmedicine.drugOncology Reports
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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Ultraviolet light-induced DNA damage triggers apoptosis in nucleotide excision repair-deficient cells via Bcl-2 decline and caspase-3/-8 activation.

2001

Ultraviolet (UV) light is a potent mutagenic and genotoxic agent. Whereas DNA damage induced by UV light is known to be responsible for UV-induced genotoxicity, its role in triggering apoptosis is still unclear. We addressed this issue by comparing nucleotide excision repair (NER) deficient 27-1 and 43-3B Chinese hamster (CHO) cells with the corresponding wild-type and ERCC-1 complemented cells. It is shown that NER deficient cells are dramatically hypersensitive to UV-C induced apoptosis, indicating that DNA damage is the major stimulus for the apoptotic response. Apoptosis triggered by UV-C induced DNA damage is related to caspase- and proteosome-dependent degradation of Bcl-2 protein. Th…

Cancer ResearchDNA RepairDNA repairDNA damageUltraviolet RaysPoly ADP ribose polymeraseFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsCaspase 8TransfectionFas ligandMembrane PotentialsCricetinaeGeneticsUltraviolet lightAnimalsRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingCaspase 8Caspase 3Fas receptorMolecular biologyCaspase InhibitorsCaspase 9MitochondriaEnzyme ActivationProto-Oncogene Proteins c-bcl-2CaspasesPoly(ADP-ribose) PolymerasesCarrier ProteinsNucleotide excision repairDNA DamageOncogene
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Spontaneous mutagenesis in Csb(m/m)Ogg1⁻(/)⁻ mice is attenuated by dietary resveratrol.

2010

Oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are generated endogenously in apparently all living cells. The defect of the repair of 8-oxoG in Csb m/m Ogg1 ―/― mice results in elevated basal levels of these lesions and increased frequencies of spontaneous mutations, which initiate tumorigenesis in the liver if cell proliferation is stimulated. Here, we describe that the phytoalexin resveratrol, applied either for 7 days per gavage (100 mg/kg body wt) or for 3―9 months in the diet (0.04% ad libitum), reduces the endogenous oxidative DNA base damage in the livers of the Csb m/m Ogg1 ―/― mice by 20―30% (P < 0.01). A small but consistent effect is also observed in the wi…

Cancer ResearchDNA damageSOD1SOD2Gene ExpressionMice TransgenicBiologyResveratrolSuperoxide dismutasechemistry.chemical_compoundMiceStilbenesAnimalschemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionGlutathione peroxidaseMutagenesisAntimutagenic AgentsGeneral MedicineMolecular biologyDietOxidative StressCell killingchemistryBiochemistryLiverMutagenesisResveratrolbiology.proteinDNA DamageCarcinogenesis
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Detection of the DCC gene product in normal and malignant colorectal tissues and its relation to a codon 201 mutation.

1998

Protein expression of the putative tumour-suppressor gene DCC on chromosome 18q was evaluated in a panel of 16 matched colorectal cancer and normal colonic tissue samples together with DCC mRNA expression and allelic deletions (loss of heterozygosity, LOH). Determined by a polymerase chain reaction (PCR)-LOH assay, 12 of the 16 (75%) cases were informative with LOH occurring in 2 of the 12 cases. For DCC mRNA, transcripts could be detected in all analysed normal tissues (eight out of eight) by RT-PCR, whereas 6 of the 15 tumours were negative. DCC protein expression, investigated by immunohistochemistry using the monoclonal antibody 15041 A directed against the intracellular domain, was hom…

Cancer ResearchDeleted in Colorectal CancerDNA Mutational AnalysisLoss of HeterozygosityReceptors Cell SurfaceBiologymedicine.disease_causePolymerase Chain ReactionLoss of heterozygosityGene productmedicineHumansGenes Tumor SuppressorRNA MessengerRNA NeoplasmCodonGeneMessenger RNAMutationTumor Suppressor ProteinsfungiDCC ReceptorImmunohistochemistryNeoplasm ProteinsBlotting SouthernOncologyCancer researchImmunohistochemistryColorectal NeoplasmsCell Adhesion MoleculesImmunostainingResearch ArticleBritish Journal of Cancer
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