Search results for "Nuclear proteins"

showing 10 items of 295 documents

MHC class II-expressing hepatocytes function as antigen-presenting cells and activate specific CD4 T lymphocyutes.

2003

The ability to activate CD4 T cells is restricted to antigen-presenting cells that express major histocompatibility complex (MHC) class II molecules. Parenchymal cells normally do not express MHC class II molecules; however, in clinical hepatitis, viral or autoimmune, hepatocytes often exhibit aberrant MHC class II expression. It is not known whether MHC class II-expressing hepatocytes can function as antigen-presenting cells, but it has been suggested that aberrant MHC class II expression by parenchymal cells may cause autoimmune disease. Therefore, we generated transgenic mice that specifically overexpress class II transactivator molecules in hepatocytes. Hepatocytes from these mice exhib…

CD4-Positive T-LymphocytesCD74Antigen presentationCD1Antigen-Presenting CellsGene ExpressionMice Inbred StrainsMice TransgenicLymphocyte ActivationHepatitisMiceMHC class ICytotoxic T cellAnimalsMHC class IIHepatologybiologyAntigen processingHistocompatibility Antigens Class IINuclear ProteinsMHC restrictionCell biologyImmunologybiology.proteinHepatocytesTrans-ActivatorsHepatology (Baltimore, Md.)
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NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

2005

The phenotype of NFATc2(-/-) c3(-/-) (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4(+) CD25(+) T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) and CD25. However, neither wild-type nor DKO CD4(+) CD25(+) regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4(+) CD25(-) T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4(+) CD25(+) T reg cells but renders c…

CD4-Positive T-LymphocytesT cellImmunologyPopulationchemical and pharmacologic phenomenaReceptors Nerve Growth FactorBiologyLymphocyte ActivationReceptors Tumor Necrosis FactorInterleukin 21MiceT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptoreducationTranscription factorMice Knockouteducation.field_of_studyNFATC Transcription FactorsZAP70Brief Definitive ReportNuclear Proteinshemic and immune systemsReceptors Interleukin-2Molecular biologyCoculture TechniquesDNA-Binding Proteinsmedicine.anatomical_structureTranscription FactorsThe Journal of Experimental Medicine
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H2-M, a facilitator of MHC class II peptide loading, and its negative modulator H2-O are differentially expressed in response to proinflammatory cyto…

2000

H2-M is a major histocompatibility complex (MHC) class II-like molecule that catalyzes peptide binding to MHC class II molecules. Recently, the H2-O heterodimer, encoded by H2-Oa and H2-Ob in the MHC class II region, has been shown to be physically associated with H2-M in B cells and to downregulate H2-M function. Examination of H2-O expression in freshly isolated mouse organs revealed that H2-Oa- and H2-Ob-specific transcripts are present in both lymphoid and nonlymphoid tissues. To evaluate the gene regulation and functional impact of H2-O on antigen presentation, we examined the effects on MHCII, invariant chain (Ii), H2-M, and H2-O gene expression of interleukin (IL)-4, IL-10, and inter…

CD74ImmunologyAntigen presentationchemical and pharmacologic phenomenaMajor histocompatibility complexInterferon-gammaMiceMHC class IGeneticsCIITAAnimalsTissue DistributionRNA MessengerAntigen PresentationHLA-D AntigensMHC class IIbiologyAntigen processingHistocompatibility Antigens Class IINuclear ProteinsMHC restrictionMolecular biologyInterleukin-10Antigens Differentiation B-LymphocyteGene Expression RegulationMice Inbred DBATrans-Activatorsbiology.proteinInterleukin-4PeptidesImmunogenetics
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The role of hypoxia-induced factors in tumor progression.

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Describe hypoxia-induced mechanisms for cell survival. Discuss hypoxia-induced gene expression. Relate hypoxia and glucose metabolism. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit atCME.TheOncologist.com Hypoxia is a common characteristic of locally advanced solid tumors that has been associated with diminished therapeutic response and, more recently, with malignant progression, that is, an increasing probability of recurrence, locoregional spread, and distant metastasis. Emerging evidence indicates that the effect of hypoxia on malignant progression is mediated by a…

Cancer ResearchAngiogenesisCell SurvivalRegulatorBiologyNeoplasmsmedicineHumansNuclear proteinSelection GeneticTranscription factorG alpha subunitRegulation of gene expressionHelix-Loop-Helix MotifsNuclear ProteinsHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaDNA-Binding ProteinsGene Expression Regulation NeoplasticCell Transformation NeoplasticGlucoseOncologyTumor progressionImmunologyCancer researchDisease ProgressionHypoxia-Inducible Factor 1medicine.symptomTranscription FactorsThe oncologist
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CtIP silencing as a novel mechanism of tamoxifen resistance in breast cancer.

2007

AbstractAcquired resistance to the antiestrogen tamoxifen constitutes a major clinical challenge in breast cancer therapy. However, the mechanisms involved are still poorly understood. Using serial analysis of gene expression, we identified CtIP, a BRCA1- and CtBP-interacting protein, as one of the most significantly down-regulated transcripts in estrogen receptor α–positive (ER+) MCF-7 tamoxifen-resistant breast cancer cells. We further confirmed the association of CtIP down-regulation with tamoxifen resistance in an additional ER+ breast cancer line (T47D), strengthening the relevance of the phenomenon observed. In additional studies, we found CtIP protein expression in a majority of ER+ …

Cancer ResearchAntineoplastic Agents HormonalEstrogen receptorDown-RegulationBreast NeoplasmsDisease-Free SurvivalBreast cancerCell Line TumormedicineGene silencingHumansSerial analysis of gene expressionGene Silencingskin and connective tissue diseasesMolecular BiologyEndodeoxyribonucleasesbusiness.industryCancerNuclear ProteinsAntiestrogenmedicine.diseaseGrowth InhibitorsGene Expression Regulation NeoplasticTamoxifenOncologyDrug Resistance NeoplasmCancer researchFemalebusinessCarrier ProteinsTamoxifenProgressive diseasemedicine.drugMolecular cancer research : MCR
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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
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Why do results conflict regarding the prognostic value of the methylation status in colon cancers? The role of the preservation method.

2012

Abstract Background In colorectal carcinoma, extensive gene promoter hypermethylation is called the CpG island methylator phenotype (CIMP). Explaining why studies on CIMP and survival yield conflicting results is essential. Most experiments to measure DNA methylation rely on the sodium bisulfite conversion of unmethylated cytosines into uracils. No study has evaluated the performance of bisulfite conversion and methylation levels from matched cryo-preserved and Formalin-Fixed Paraffin Embedded (FFPE) samples using pyrosequencing. Methods Couples of matched cryo-preserved and FFPE samples from 40 colon adenocarcinomas were analyzed. Rates of bisulfite conversion and levels of methylation of …

Cancer ResearchBisulfite sequencing[SDV.CAN]Life Sciences [q-bio]/CancerAdenocarcinomaBiologyMLH1lcsh:RC254-282[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound[SDV.CAN] Life Sciences [q-bio]/CancerPredictive Value of TestsBiomarkers TumorGeneticsHumansSulfitesDNA Modification MethylasesAdaptor Proteins Signal TransducingCryopreservationParaffin EmbeddingTumor Suppressor ProteinsNuclear ProteinsReproducibility of ResultsDNA NeoplasmMethylationDNA MethylationPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologydigestive system diseasesNeoplasm ProteinsBisulfiteDNA Repair EnzymesLong Interspersed Nucleotide ElementsPhenotypeOncologyCpG sitechemistrySodium bisulfiteColonic NeoplasmsDNA methylationFeasibility StudiesPyrosequencingCpG IslandsMutL Protein Homolog 1Research Article
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Hepatitis C Virus Core Protein Inhibits Tumor Suppressor Protein Promyelocytic Leukemia Function in Human Hepatoma Cells

2005

Abstract Tumor suppressor protein promyelocytic leukemia (PML) is implicated in apoptosis regulation and antiviral response. PML localizes predominantly to PML-nuclear bodies (PML-NB), nuclear macromolecular complexes regulating tumor suppressor protein p53 activity. Consistent with the function of PML in the cellular antiviral response, PML-NBs represent preferential targets in viral infections. In the case of hepatitis C virus (HCV) infection, important characteristics are nonresponsiveness to IFN therapy and development of hepatocellular carcinoma. However, the mechanisms which lead to the development of hepatocellular carcinoma are largely unknown. Here, we show that HCV core protein lo…

Cancer ResearchCarcinoma HepatocellularTumor suppressor genevirusesApoptosisPromyelocytic Leukemia ProteinBiologyTransfectionmedicine.disease_causePromyelocytic leukemia proteinCell Line TumorCoactivatormedicineHumansProtein IsoformsPhosphorylationCell NucleusTumor Suppressor ProteinsViral Core ProteinsLiver NeoplasmsNuclear Proteinsvirus diseasesAcetylationFas receptorHepatitis Cdigestive system diseasesNeoplasm ProteinsOncologyApoptosisAcetylationbiology.proteinCancer researchPhosphorylationTumor Suppressor Protein p53CarcinogenesisTranscription FactorsCancer Research
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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
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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
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