Search results for "Repressor Protein"

showing 10 items of 169 documents

Evaluation of genetic stability of the SYT gene rearrangement by break-apart FISH in primary and xenotransplanted synovial sarcomas

2006

Synovial sarcomas (SS) are infrequent and morphologically heterogeneous soft tissue sarcomas. The t(X;18)(p11.2;q11.2), which results in fusion of the SYT gene at 18q11 with the SSX1, SSX2, or (rarely) SSX4 gene is a primary genetic event in 90% of SS. To determine whether the t(X;18) present in the original tumor is maintained in its passages, a dual-color break-apart FISH assay for SYT gene disruption was performed in two tissue microarrays (TMA) comprising eight molecularly confirmed primary SSs and their xenografts, which were followed for several generations. A simplified scoring system was applied to the FISH results of the primary and xenotransplanted SS to classify the FISH data int…

Cancer ResearchOncogene Proteins FusionXenotransplantationmedicine.medical_treatmentTransplantation HeterologousChromosomal translocationIn situ hybridizationBiologyTranslocation GeneticSarcoma SynovialProto-Oncogene ProteinsGeneticsmedicineAnimalsHumansMolecular BiologyGeneIn Situ Hybridization FluorescenceGene RearrangementGeneticsChromosomes Human XTissue microarrayGene rearrangementmedicine.diseaseMolecular biologyRepressor ProteinsTransplantationTissue Array AnalysisSarcomaChromosomes Human Pair 18Cancer Genetics and Cytogenetics
researchProduct

Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype

2007

Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.

Cancer ResearchTime FactorsCell of originCellular differentiationBrain tumormacromolecular substancesBiologyMiceProto-Oncogene ProteinsPrecursor cellmedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Cell ProliferationNeoplasm StagingMice KnockoutNeuronsPolycomb Repressive Complex 1Brain NeoplasmsCell growthStem CellsNuclear ProteinsCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseStem Cell Self-RenewalErbB ReceptorsGene Expression Regulation NeoplasticRepressor ProteinsCell Transformation NeoplasticPhenotypeOncologyBMI1AstrocytesMutationCancer cellCancer researchGlioblastomaSignal TransductionCancer Cell
researchProduct

pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
researchProduct

Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
researchProduct

Phenolic Acid-Mediated Regulation of the padC Gene, Encoding the Phenolic Acid Decarboxylase of Bacillus subtilis

2008

ABSTRACT In Bacillus subtilis , several phenolic acids specifically induce expression of padC , encoding a phenolic acid decarboxylase that converts these antimicrobial compounds into vinyl derivatives. padC forms an operon with a putative coding sequence of unknown function, yveFG , and this coding sequence does not appear to be involved in the phenolic acid stress response (PASR). To identify putative regulators involved in the PASR, random transposon mutagenesis, combined with two different screens, was performed. PadR, a negative transcriptional regulator of padC expression, was identified. padR is not located in the vicinity of padC , and the expression of padR is low and appears const…

Carboxy-lyasesCarboxy-LyasesOperonMolecular Sequence DataElectrophoretic Mobility Shift AssayBacillus subtilisBiologyMicrobiologyGene Expression Regulation Enzymologic03 medical and health scienceschemistry.chemical_compoundBacterial ProteinsHydroxybenzoatesGene RegulationElectrophoretic mobility shift assay[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceMolecular Biology030304 developmental biologychemistry.chemical_classification0303 health sciencesBase Sequence030306 microbiologyEffectorGene Expression Regulation BacterialPhenolic acidbiology.organism_classificationMolecular biologyRepressor ProteinsEnzymechemistryBiochemistryTransposon mutagenesisBacillus subtilis
researchProduct

Expression of WISPs and of their novel alternative variants in human hepatocellular carcinoma cells

2005

WISPs (Wnt-induced secreted proteins) are members of the CCN (CTGF/Cyr61/Nov) family involved in fibrotic disorders and tumorigenesis. They have a typical structure composed of four conserved cysteine-rich modular domains, but variants of CCN members lacking one or more modules, generated by alternative splicing or gene mutations, have been described in various pathological conditions. WISP genes were first described as downstream targets of the Wnt signaling pathway, which is frequently altered in human hepatocellular carcinoma (HCC). In the present study, WISP mRNA expression was analyzed by RT-PCR in four human HCC cell lines (HepG2, HuH-6, HuH-7, HA22T/VGH). Our results show for the fir…

Carcinoma HepatocellularWISPHepatocellular carcinomaApoptosisGene mutationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCCN Intercellular Signaling ProteinsWntalternative splicingHistory and Philosophy of ScienceCell Line TumorProto-Oncogene ProteinsCCN Intercellular Signaling ProteinsmedicineHumansRNA MessengerGeneDNA PrimersOncogene ProteinsGeneticsCCNModels GeneticReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceLiver NeoplasmsAlternative splicingIntracellular Signaling Peptides and ProteinsWnt signaling pathwaydigestive system diseasesNeoplasm ProteinsInsulin-Like Growth Factor Binding ProteinsRepressor ProteinsCTGFCYR61Cancer researchIntercellular Signaling Peptides and ProteinsRNACarcinogenesisWISPWntTranscription Factors
researchProduct

EngineeredControl of Cell Morphology In Vivo Reveals Distinct Roles for Yeast andFilamentous Forms of Candida albicans duringInfection

2003

ABSTRACT It is widely assumed that the ability of Candida albicans to switch between different morphologies is required for pathogenesis. However, most virulence studies have used mutants that are permanently locked into either the yeast or filamentous forms which are avirulent but unsuitable for discerning the role of morphogenetic conversions at the various stages of the infectious process. We have constructed a strain in which this developmental transition can be externally modulated both in vitro and in vivo. This was achieved by placing one copy of the NRG1 gene (a negative regulator of filamentation) under the control of a tetracycline-regulatable promoter. This modified strain was th…

Cell divisionMutantHyphaeVirulenceBiologyKidneyCell morphologyMicrobiologyArticleMicrobiologyMiceIn vivoGene Expression Regulation FungalYeastsCandida albicansAnimalsPromoter Regions GeneticCandida albicansMolecular BiologyMice Inbred BALB CCandidiasisBrainGeneral Medicinebiology.organism_classificationYeastCorpus albicansRepressor ProteinsSurvival RateDoxycyclineFemaleGenetic EngineeringCell DivisionSpleenEukaryotic Cell
researchProduct

Analysis of Drosophila salivary gland, epidermis and CNS development suggests an additional function of brinker in anterior-posterior cell fate speci…

2000

Salivary glands are simple structured organs which can serve as a model system in the study of organogenesis. Following a large EMS mutagenesis we have identified a number of genes required for normal salivary gland development. Mutations in the locus small salivary glands-1 (ssg-1) lead to a drastic reduction in the size of the salivary glands. The gene ssg-1 was cloned and subsequent sequence and genetic analysis showed identity to the recently published gene brinker. The salivary gland placode in brinker mutants appears reduced along both the anterior-posterior and dorso-ventral axis. Analysis of the brinker cuticle phenotype revealed a similar loss of anterior-posterior as well as later…

Central Nervous SystemEmbryologyReceptors SteroidEmbryo NonmammalianMutantLocus (genetics)OrganogenesisBiologyCell fate determinationSalivary GlandsNeuroblastBacterial ProteinsmedicineAnimalsDrosophila ProteinsAdhesins BacterialGeneBody PatterningEmbryonic InductionHomeodomain ProteinsSalivary glandGenetic Complementation TestNeuropeptidesChromosome MappingGene Expression Regulation DevelopmentalCell DifferentiationAnatomyPhenotypeCell biologyRepressor Proteinsmedicine.anatomical_structureEpidermal CellsMutationInsect ProteinsDrosophilaEpidermisDevelopmental BiologyTranscription FactorsMechanisms of development
researchProduct

Generation of a DNA microarray for determination of E6 natural variants of human papillomavirus type 16.

2003

Infection with high-risk types of human papillomavirus (HPV) is necessary for the development of cervical cancer. However, the majority of the HPV infections are efficiently cleared by the immune system and only a minority persist and induce the development of malignant lesions. Several studies provided evidence that intratype genetic variations are implicated in determining the clinical outcome of HPV infections. In this study, we describe a DNA chip based on arrayed primer extension (APEX) for the analysis of the natural variants of HPV16, the most frequently detected type in cervical cancer world-wide. We show that HPV16 E6 variants are detected efficiently by APEX. In addition, APEX is …

Cervical cancerGeneticsMicroarrayvirus diseasesGenetic VariationOncogene Proteins ViralBiologymedicine.diseaseGenomefemale genital diseases and pregnancy complicationsDNA sequencingPrimer extensionVirusRepressor ProteinsVirologyGenetic variationDNA ViralmedicineHumansFemaleDNA microarrayOligonucleotide Array Sequence AnalysisJournal of virological methods
researchProduct

CtsR is the master regulator of stress response gene expression in Oenococcus oeni.

2005

ABSTRACT Although many stress response genes have been characterized in Oenococcus oeni , little is known about the regulation of stress response in this malolactic bacterium. The expression of eubacterial stress genes is controlled both positively and negatively at the transcriptional level. Overall, negative regulation of heat shock genes appears to be more widespread among gram-positive bacteria. We recently identified an ortholog of the ctsR gene in O. oeni . In Bacillus subtilis , CtsR negatively regulates expression of the clp genes, which belong to the class III family of heat shock genes. The ctsR gene of O. oeni is cotranscribed with the downstream clpC gene. Sequence analysis of t…

ChaperoninsOperonMolecular Sequence DataBiologyMicrobiologyGenome03 medical and health sciencesBacterial ProteinsSigma factorHeat shock proteinOperon[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyGene RegulationPromoter Regions GeneticMolecular BiologyGeneHeat-Shock Proteins030304 developmental biologyRegulator geneOenococcus oeniGeneticsRegulation of gene expressionAdenosine Triphosphatases0303 health sciencesBase Sequence030306 microbiologyCTSRGene Expression Regulation Bacterialbiology.organism_classificationDNA-Binding ProteinsGram-Positive CocciRepressor ProteinsMutagenesis Site-DirectedOenococcus oeniGenome BacterialHeat-Shock ResponseBacillus subtilisMolecular ChaperonesJournal of bacteriology
researchProduct