Search results for "binding proteins"

showing 10 items of 911 documents

Glioblastoma cells induce differential glutamatergic gene expressions in human tumor-associated microglia/macrophages and monocyte-derived macrophages

2015

Glioblastoma cells produce and release high amounts of glutamate into the extracellular milieu and subsequently can trigger seizure in patients. Tumor-associated microglia/macrophages (TAMs), consisting of both parenchymal microglia and monocytes-derived macrophages (MDMs) recruited from the blood, are known to populate up to 1/3 of the glioblastoma tumor environment and exhibit an alternative, tumor-promoting and supporting phenotype. However, it is unknown how TAMs respond to the excess extracellular glutamate in the glioblastoma microenvironment. We investigated the expressions of genes related to glutamate transport and metabolism in human TAMs freshly isolated from glioblastoma resecti…

Cancer ResearchAntigens Differentiation MyelomonocyticGlutamic AcidglutamateAMPA receptorSLC7A11Antigens CDTumor Cells CulturedExtracellularmedicineHumansReceptors AMPAGRIA2PharmacologyCD11b AntigenbiologyMicrogliaBrain NeoplasmsMacrophagesmonocyte-derived macrophagesCalcium-Binding ProteinsMicrofilament Proteinsglioblastomatumor-associated microglia/macrophagesGlutamate receptorSLC1A2Coculture TechniquesDNA-Binding ProteinsGlutaminemedicine.anatomical_structureGene Expression RegulationOncologyAstrocytesImmunologybiology.proteinCancer researchLeukocyte Common AntigensMolecular MedicineMicrogliaResearch PaperCancer Biology & Therapy
researchProduct

MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
researchProduct

The Muscleblind family of proteins: an emerging class of regulators of developmentally programmed alternative splicing.

2006

Alternative splicing is widely used to generate protein diversity and to control gene expression in many biological processes, including cell fate determination and apoptosis. In this review, we focus on the Muscleblind family of tissue-specific alternative splicing regulators. Muscleblind proteins bind pre-mRNA through an evolutionarily conserved tandem CCCH zinc finger domain. Human Muscleblind homologs MBNL1, MBNL2 and MBNL3 promote inclusion or exclusion of specific exons on different pre-mRNAs by antagonizing the activity of CUG-BP and ETR-3-like factors (CELF proteins) bound to distinct intronic sites. The relative activities of Muscleblind and CELF proteins control a key developmenta…

Cancer ResearchCellular differentiationMolecular Sequence DataRNA-binding proteinCell fate determinationBiologychemistry.chemical_compoundExonMiceMBNL1AnimalsHumansMyotonic DystrophyAmino Acid SequenceMolecular BiologyGeneticsZinc fingerAlternative splicingGene Expression Regulation DevelopmentalRNA-Binding ProteinsCell DifferentiationZinc FingersCell BiologyAlternative SplicingchemistryRNA splicingDevelopmental BiologyDifferentiation; research in biological diversity
researchProduct

Dual regulation of SPI1/PU.1 transcription factor by heat shock factor 1 (HSF1) during macrophage differentiation of monocytes

2014

International audience; : In addition to their cytoprotective role in stressful conditions, heat shock proteins (HSPs) are involved in specific differentiation pathways, e.g. we have identified a role for HSP90 in macrophage differentiation of human peripheral blood monocytes exposed to Macrophage Colony-Stimulating Factor (M-CSF). Here, we show that deletion of the main transcription factor involved in heat shock gene regulation, heat shock factor 1 (HSF1), affects M-CSF-driven differentiation of mouse bone marrow cells. HSF1 transiently accumulates in the nucleus of human monocytes undergoing macrophage differentiation, including M-CSF-treated peripheral blood monocytes and phorbol ester-…

Cancer ResearchCellular differentiation[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mice0302 clinical medicineHeat Shock Transcription FactorsHSF1[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells CulturedComputingMilieux_MISCELLANEOUSRegulation of gene expression0303 health sciencesMice Inbred BALB C[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]3. Good healthDNA-Binding ProteinsOncology030220 oncology & carcinogenesismonocytesProteasome Endopeptidase ComplexAntigens Differentiation MyelomonocyticReceptors Cell Surface[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesAntigens CDHeat shock proteinProto-Oncogene Proteinstranscription factorsAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyTranscription factor030304 developmental biologySPI1Macrophagesheat-shock proteinsfungi[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMolecular biologyHsp70Heat shock factorMice Inbred C57BLcell differentiationGene Expression RegulationTrans-Activators[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

Expression of DNA repair proteins hMSH2, hMSH6, hMLH1,O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in melanoma cells wit…

1999

Malignant melanoma is well known for its primary unresponsiveness to chemotherapy. The mechanisms conferring this intrinsic resistance are unclear. In this study, we investigated the role of genes involved in DNA repair in a panel of human melanoma cell variants exhibiting low and high levels of resistance to 4 commonly used drugs in melanoma treatment, i.e., vindesine, etoposide, fotemustine and cisplatin. We show that in melanoma cells exhibiting resistance to cisplatin, etoposide and vindesine, the nuclear content of each of the DNA mismatch repair (MMR) proteins hMLH1, hMSH2 and hMSH6 was reduced by 30–70%. A decreased expression level of up to 80% of mRNAs encoding hMLH1 and hMSH2 was …

Cancer ResearchDNA RepairTranscription GeneticVindesineDNA repairAntineoplastic AgentsBiologyNitrosourea CompoundsDNA GlycosylasesO(6)-Methylguanine-DNA MethyltransferaseOrganophosphorus CompoundsProto-Oncogene ProteinsmedicineHumansRNA MessengerPromoter Regions GeneticMelanomaN-Glycosyl HydrolasesneoplasmsEtoposideAdaptor Proteins Signal TransducingEtoposideCisplatinMelanomaNuclear Proteinsmedicine.diseaseMolecular biologyDrug Resistance Multipledigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinOncologyDNA glycosylaseFotemustineVindesineDNA mismatch repairCisplatinCarrier ProteinsMutL Protein Homolog 1medicine.drugInternational Journal of Cancer
researchProduct

T Cells Expressing Receptor Recombination/Revision Machinery Are Detected in the Tumor Microenvironment and Expanded in Genomically Over-unstable Mod…

2021

AbstractTumors undergo dynamic immunoediting as part of a process that balances immunologic sensing of emerging neoantigens and evasion from immune responses. Tumor-infiltrating lymphocytes (TIL) comprise heterogeneous subsets of peripheral T cells characterized by diverse functional differentiation states and dependence on T-cell receptor (TCR) specificity gained through recombination events during their development. We hypothesized that within the tumor microenvironment (TME), an antigenic milieu and immunologic interface, tumor-infiltrating peripheral T cells could reexpress key elements of the TCR recombination machinery, namely, Rag1 and Rag2 recombinases and Tdt polymerase, as a poten…

Cancer ResearchDatasets as TopicT-Cell Antigen Receptor SpecificityCD8-Positive T-LymphocytesMice0302 clinical medicineTumor MicroenvironmentRecombinaseT-cell receptorBreastRNA-SeqT Cells T Cell Receptor Recombination/Revision Machinery Tumor MicroenvironmentCancerAged 80 and overMice KnockoutRecombination GeneticNuclear Proteinshemic and immune systemsMiddle AgedDNA-Binding Proteins030220 oncology & carcinogenesisFemaleSingle-Cell AnalysisMutL Protein Homolog 1AdultImmunologyReceptors Antigen T-CellT cellsBreast Neoplasmschemical and pharmacologic phenomenaSettore MED/08 - Anatomia PatologicaBiologyRecombination-activating gene03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemAntigenDNA NucleotidylexotransferaseRAG2AnimalsHumansSettore MED/05 - Patologia ClinicaAgedHomeodomain ProteinsTumor microenvironmentT-cell receptorDisease Models AnimalImmunoeditingCancer researchDNA Damage030215 immunology
researchProduct

The Peroxisome Proliferator WY-14,643 Promotes Hepatocarcinogenesis Caused by Endogenously Generated Oxidative DNA Base Modifications in Repair-Defic…

2007

Abstract Basal levels of endogenously generated oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are present in apparently all mammalian cells, but their relevance for the generation of spontaneous cancers remains to be established. Both the 8-oxoG levels and the resulting spontaneous mutations are increased in the livers of Csbm/m/Ogg1−/− mice, which are deficient in the repair of 8-oxoG. In order to determine the consequences of these additional oxidative DNA modifications and mutations and thus assess the tumor initiating potency of this type of endogenous DNA damage, we treated Csbm/m/Ogg1−/− mice and repair-proficient controls with the peroxisome proliferator WY-14…

Cancer ResearchGuanineDNA RepairRatónDNA damageEndogenyOxidative phosphorylationBiologymedicine.disease_causeDNA GlycosylasesMicechemistry.chemical_compoundLiver Neoplasms ExperimentalmedicineAnimalsPoly-ADP-Ribose Binding ProteinsCocarcinogenesisCell growthLiver cellMolecular biologyMice Inbred C57BLOxidative StressDNA Repair EnzymesPyrimidinesLiverOncologyBiochemistrychemistryMutationPeroxisome ProliferatorsCarcinogenesisPrecancerous ConditionsDNADNA DamageCancer Research
researchProduct

A novel tumour associated leucine zipper protein targeting to sites of gene transcription and splicing

2002

We describe here the definition and characterization of antigen CT-8/HOM-TES-85 encoded by a previously unknown gene and identified by serological expression screening using antibodies from a seminoma patient. Intriguingly, the leucine zipper region of CT-8/HOM-TES-85 shows an atypical amphipathy with clusters of hydrophobic residues that is exclusively shared by the N-myc proto-oncogene. CT-8/HOM-TES-85 gene is tightly silenced in normal tissues except for testis. However, it is frequently activated in human neoplasms of different types including lung cancer, ovarian cancer, melanoma and glioma. Endogenous as well as heterogeneously expressed CT-8/HOM-TES-85 targets predominantly to the nu…

Cancer ResearchLeucine zipperDNA ComplementaryTranscription GeneticGreen Fluorescent ProteinsImmunoblottingBiologymedicine.disease_causeModels BiologicalProto-Oncogene MasAntigens NeoplasmTranscription (biology)Protein targetingTumor Cells CulturedGeneticsmedicineHumansTissue DistributionAntigensMolecular BiologyGeneLeucine ZippersATF3GenomeReverse Transcriptase Polymerase Chain ReactionAlternative splicingfood and beveragesBlotting NorthernPhenotypeProtein Structure TertiaryDNA-Binding ProteinsAlternative SplicingLuminescent ProteinsPhenotypeMicroscopy FluorescenceModels ChemicalRNA splicingCancer researchOncogene
researchProduct

The BCL6 gene in B-cell lymphomas with 3q27 translocations is expressed mainly from the rearranged allele irrespective of the partner gene

2003

The BCL6 gene, which functions as a transcription repressor, is the target of multiple chromosomal translocations in non-Hodgkin's lymphomas (NHL). These translocations occur in the nontranslated region of the BCL6 gene, juxtaposing regulatory sequences of the diverse partner genes to the open reading frame of the BCL6 gene and thus are thought to deregulate BCL6 gene expression. The levels of expression of the BCL6 gene and protein have been demonstrated to predict the clinical outcome of diffuse large B-cell lymphomas. By contrast, the prognostic significance of BCL6 gene translocations is unclear. In this study we have sought an explanation for this apparent discrepancy. We examined tumo…

Cancer ResearchLymphoma B-CellBiologyTranslocation Geneticimmune system diseasesProto-Oncogene Proteinshemic and lymphatic diseasesGene expressionTumor Cells CulturedHumansRNA MessengerAllelePromoter Regions GeneticGeneAllelesGene RearrangementGeneticsRegulation of gene expressionPromoterHematologyGene rearrangementBCL6Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsOncologyRegulatory sequenceMutationProto-Oncogene Proteins c-bcl-6Cancer researchChromosomes Human Pair 3Transcription FactorsLeukemia
researchProduct

Negative transcriptional control of ERBB2 gene by MBP-1 and HDAC1: diagnostic implications in breast cancer

2013

Abstract Background The human ERBB2 gene is frequently amplified in breast tumors, and its high expression is associated with poor prognosis. We previously reported a significant inverse correlation between Myc promoter-binding protein-1 (MBP-1) and ERBB2 expression in primary breast invasive ductal carcinoma (IDC). MBP-1 is a transcriptional repressor of the c-MYC gene that acts by binding to the P2 promoter; only one other direct target of MBP-1, the COX2 gene, has been identified so far. Methods To gain new insights into the functional relationship linking MBP-1 and ERBB2 in breast cancer, we have investigated the effects of MBP-1 expression on endogenous ERBB2 transcript and protein lev…

Cancer ResearchMBP-1/EnolaseReceptor ErbB-2Breast NeoplasmsHistone Deacetylase 1BiologyERBB geneBreast cancerTranscriptional regulationTranscription (biology)Histone DeacetylaseBreast CancermedicineTranscriptional regulationBiomarkers TumorTumor Cells CulturedGeneticsHumansMBP-1ERBB2Promoter Regions Geneticskin and connective tissue diseasesGeneReporter geneCarcinoma Ductal BreastCancerTransfectionGenes erbB-2medicine.diseaseImmunohistochemistryHDAC1Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticSettore BIO/18 - GeneticaOncologyCancer researchChromatin immunoprecipitationResearch ArticleBMC Cancer
researchProduct