Search results for "Promoter"

showing 10 items of 584 documents

NFATc1 Induction in Peripheral T and B Lymphocytes

2013

Abstract NFAT transcription factors control the proliferation and survival of peripheral lymphocytes. We have reported previously that the short isoform NFATc1/αA whose generation is induced by immune receptor stimulation supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cells. We will show in this study that in novel bacterial artificial chromosome transgenic mice that express EGFP under the control of entire Nfatc1 locus the Nfatc1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripheral T and B cells. Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated in B, Th1, and Th2 cells, but…

LipopolysaccharidesGene isoformChromosomes Artificial BacterialProgrammed cell deathTransgeneGreen Fluorescent ProteinsImmunologyGene ExpressionMice TransgenicStimulationImmune receptorBiologyLymphocyte ActivationT-Lymphocytes RegulatoryAntibodiesMiceTh2 CellsGenes ReporterTransforming Growth Factor betaAnimalsProtein IsoformsImmunology and AllergyPromoter Regions GeneticTranscription factorCell ProliferationB-LymphocytesNFATC Transcription Factorsintegumentary systemNF-kappa BCD28NFATTh1 CellsMolecular biologyMice Inbred C57BLTh17 CellsThe Journal of Immunology
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IL-9 and IL-13 production by activated mast cells is strongly enhanced in the presence of lipopolysaccharide: NF-kappa B is decisively involved in th…

2001

Abstract Mast cells, due to their ability to produce a large panel of mediators and cytokines, participate in a variety of processes in adaptive and innate immunity. Herein we report that in primary murine bone marrow-derived mast cells activated with ionomycin or IgE-Ag the bacterial endotoxin LPS strongly enhances the expression of IL-9 and IL-13, but not IL-4. This costimulatory effect of LPS is absent in activated mast cells derived from the LPS-hyporesponsive mouse strain BALB/c-LPSd, although in these cells the proinflammatory cytokine IL-1 can still substitute for LPS. The enhanced production of mast cell-derived IL-13 in the presence of IL-1 is a novel observation. Coactivation of m…

LipopolysaccharidesImmunologyInflammationBone Marrow CellsBiologyProinflammatory cytokinechemistry.chemical_compoundMiceMice CongenicAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsMast CellsPromoter Regions GeneticCells CulturedReporter geneMice Inbred BALB CMice Inbred C3HInnate immune systemBinding SitesInterleukin-13Interleukin-9NF-kappa BNFKB1Cell biologyInterleukin 33chemistryGene Expression RegulationIonomycinInterleukin 13Immunologymedicine.symptomSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Identification and characterization of a novel Ets-2-related nuclear complex implicated in the activation of the human interleukin-12 p40 gene promot…

1997

Interleukin-12 (IL-12) is a proinflammatory cytokine produced by antigen-presenting cells in response to many microbial infections. IL-12 plays an important role in the generation of T helper type-1 cells, which favor cell-mediated immune response. IL-12 is composed of two different subunits, p40 and p35, whose expression can be regulated concomitantly or differentially. Monocytic cells, the major producers of IL-12, can be primed by interferon-gamma (IFN-gamma) to produce optimal amounts of IL-12 in response to LPS stimulation as a consequence of bacterial infection. The priming effect is exerted primarily at the transcriptional level on the p40 promoter in conjunction with the effects of …

LipopolysaccharidesTranscription GeneticSequence HomologyStimulationbiosynthesis/geneticsBiochemistryChromatography Affinitychemistry.chemical_compoundMiceAnimals Base Sequence Cell Line Cell Nucleus; metabolism Chromatography; Affinity DNA-Binding Proteins Humans Interferon-gamma; pharmacology Interleukin-12; biosynthesis/genetics Kinetics Lipopolysaccharides; pharmacology Mice Molecular Sequence Data Nuclear Proteins; isolation /&/ purification/metabolism Promoter Regions; Genetic Protein-Tyrosine Kinases; metabolism Proto-Oncogene Protein c-ets-2 Proto-Oncogene Proteins; isolation /&/ purification/metabolism Repressor Proteins Sequence Homology; Nucleic Acid Trans-Activators; isolation /&/ purification/metabolism Transcription Factors Transcription; Genetic; drug effectsPromoter Regions GeneticChromatographyNuclear ProteinsMethylationProtein-Tyrosine KinasesInterleukin-12DNA-Binding ProteinsTranscriptionMolecular Sequence DataBiologyProinflammatory cytokineCell LineProto-Oncogene Protein c-ets-2Promoter RegionsInterferon-gammaGeneticSequence Homology Nucleic AcidProto-Oncogene ProteinsAnimalsHumansMolecular BiologyTranscription factorCell NucleusMolecular massBase SequenceNucleic Acidisolation /&/ purification/metabolismPromoterCell BiologyMolecular biologyIn vitroRepressor ProteinsKineticschemistryAffinitydrug effectsTrans-ActivatorspharmacologymetabolismDNATranscription Factors
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Protection by nitric oxide against liver inflammatory injury in animals carrying a nitric oxide synthase-2 transgene

2001

22 pages, 7 figures, 1 table.

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharideTransgeneBlotting WesternNitric Oxide Synthase Type IIApoptosisGalactosamineMice TransgenicLipopolysaccharideNitric OxideBiochemistryLiver cellsProinflammatory cytokineNitric oxidechemistry.chemical_compoundMiceInternal medicineGeneticsmedicineAnimalsTransgenesPromoter Regions GeneticMolecular BiologyLiver injurybiologyTumor Necrosis Factor-alphaNF-kappa BNitric oxide synthase 2medicine.diseaseEndotoxinsEndocrinologychemistryLiverbiology.proteinTumor necrosis factor alphaNitric Oxide SynthasePhosphoenolpyruvate carboxykinaseFood DeprivationBiotechnologyInterleukin-1
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Anandamide inhibits IL-12p40 production by acting on the promoter repressor element GA-12: Possible involvement of the COX-2 metabolite prostamide E 2

2007

The eCB [endoCB (cannabinoid)] system is being considered as a novel therapeutic target for immune disorders. Cytokines of the IL-12 (interleukin-12) family have essential functions in cell-mediated immunity. In the present study, we have addressed the mechanisms of action of the eCB AEA (anandamide) on the regulation of IL-12p40 in activated microglia/macrophages. We demonstrated that AEA can inhibit the expression of p35, p19 and p40 subunits, which form the biologically-active cytokines IL-12 and IL-23 in microglia stimulated with LPS (lipopolysaccharide)/IFNγ (interferon γ). Additionally, we have provided evidence that AEA reduces the transcriptional activity of the IL-12p40 gene in LPS…

Lipopolysaccharidesmedicine.medical_specialtyPolyunsaturated Alkamidesmedicine.medical_treatmentMolecular Sequence DataRepressorArachidonic AcidsBiologyInterleukin-23BiochemistryDinoprostoneInterferon-gammaMicechemistry.chemical_compoundInternal medicinemedicineAnimalsEthanolamidePromoter Regions GeneticReceptors CannabinoidMolecular BiologyCells CulturedRegulation of gene expressionMice Inbred BALB CInterleukin-12 Subunit p40Cell BiologyAnandamideEndocannabinoid systemCell biologyProtein SubunitsEndocrinologyGene Expression RegulationchemistryCyclooxygenase 2lipids (amino acids peptides and proteins)MicrogliaCannabinoidSignal transductionEndocannabinoidsSignal TransductionProstaglandin E
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Dominant negative MORT1/FADD rescues mice from CD95 and TNF-induced liver failure

2002

Derangement of the apoptotic program is considered an important cause of liver disease. It became clear that receptor-mediated apoptosis is of specific interest in this context, and CD95 and CD120a, both members of the tumor necrosis factor (TNF) receptor superfamily, are the most prominent cell death receptors involved. The death signal is induced upon ligand binding by recruitment of caspases via the adapter molecule MORT1/FADD to the receptor and their subsequent activation. To investigate the role of MORT1/FADD in hepatocyte apoptosis, we generated transgenic mice expressing liver-specific dominant negative mutant. Mice looked grossly normal; breeding and liver development were not diff…

Lipopolysaccharidesmedicine.medical_specialtyProgrammed cell deathFas-Associated Death Domain ProteinOligonucleotidesMice TransgenicAntibodiesReceptors Tumor Necrosis FactorMiceLiver diseaseAntigens CDAlbuminsInternal medicinemedicineAnimalsfas ReceptorFADDPromoter Regions GeneticAdaptor Proteins Signal TransducingLiver injuryHepatitisMice Inbred BALB CHepatologybiologyTumor Necrosis Factor-alphamedicine.diseaseFas receptorMice Inbred C57BLEndocrinologyReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinTumor necrosis factor alphaCarrier ProteinsLiver FailureHepatology
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IL-6 -174G/C polymorphism and IL-6 serum levels in patients with liver cirrhosis and hepatocellular carcinoma.

2011

Recently, a link between high levels of circulating IL-6 and hepatocellular carcinoma (HCC) has been proposed. In addition, single nucleotide polymorphisms (SNPs) in the promoter region of the IL-6 gene have been reported to be related to several inflammatory-related conditions, including cancer. The purpose of this article is: (1) to evaluate the frequencies of SNPs in the IL-6 promoter region at position -174 and IL-6 serum levels in a group of patients with HCC and underlying liver cirrhosis (LC), and compare them with a group of LC patients without HCC; (2) to determine whether a possible correlation exists between the allelic variations, IL-6 serum levels, and the risk of developing HC…

Liver CirrhosisMaleCirrhosisCarcinoma HepatocellularGenotypeSNPSingle-nucleotide polymorphismEnzyme-Linked Immunosorbent AssayBioinformaticsBiochemistryPolymerase Chain ReactionPolymorphism Single NucleotideGene FrequencyGeneticsmedicineHumansAlleleHCCInterleukin 6Molecular BiologyGeneIL-6biologyInterleukin-6Liver NeoplasmsPromotermedicine.diseaseHepatocellular carcinomabiology.proteinCancer researchIL-6 -174G/C polymorphism liver cirrhosis hepatocellular carcinomaMolecular MedicineFemaleRestriction fragment length polymorphismPolymorphism Restriction Fragment LengthBiotechnology
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Reduced mRNA abundance of the main enzymes involved in methionine metabolism in human liver cirrhosis and hepatocellular carcinoma

2000

Abstract Background/Aims: It has been known for at least 50 years that alterations in methionine metabolism occur in human liver cirrhosis. However, the molecular basis of this alteration is not completely understood. In order to gain more insight into the mechanisms behind this condition, mRNA levels of methionine adenosyltransferase ( MAT1A ), glycine methyltransferase ( GNMT ), methionine synthase ( MS ), betaine homocysteine methyltransferase ( BHMT ) and cystathionine β-synthase ( CBS ) were examined in 26 cirrhotic livers, five hepatocellular carcinoma (HCC) tissues and ten control livers. Methods: The expression of the above-mentioned genes was determined by quantitative RT-PCR analy…

Liver Cirrhosismedicine.medical_specialtyCarcinoma HepatocellularMethyltransferaseBetaine—homocysteine S-methyltransferaseMethylationHepatocarcinemachemistry.chemical_compoundMethionineInternal medicinemedicineHumansRNA MessengerMethionine synthasePromoter Regions GeneticDNA methylationMethionineHepatologybiologyLiver NeoplasmsMethionine Adenosyltransferasemedicine.diseaseCystathionine beta synthaseEnzymesIsoenzymesEndocrinologyCirrhosisLiverchemistryMethionine AdenosyltransferaseGNMTbiology.proteinHypermethioninemia
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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A functional analysis of ACP-20, an adult-specific cuticular protein gene from the beetle Tenebrio. Role of an intronic sequence in transcriptional a…

2004

0962-1075 (Print) Comparative Study Journal Article Research Support, Non-U.S. Gov't; A gene encoding the adult cuticular protein ACP-20 was isolated in Tenebrio. It consists of three exons interspersed by two introns, intron 1 interrupting the signal peptide. To understand the regulatory mechanisms of ACP-20 expression, ACP-20 promoter-luciferase reporter gene constructs were transfected into cultured pharate adult wing epidermis. Transfection assays needed the presence of 20-hydroxyecdysone, confirming that ACP-20 is up-regulated by ecdysteroids. Analysis of 5' deletion constructs revealed that three regions are necessary for high levels of transcription. Interaction experiments between i…

MESH : Molecular Sequence Data[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionMESH : Genes Reporter/physiologyMESH : Transcriptional Activation/geneticsMESH : Introns/geneticsPromoter Regions (Genetics)/drug effects/physiologyExon0302 clinical medicineGenes ReporterTranscriptional regulationTrans-Activation (Genetics)/genetics/*physiologyMESH : Tenebrio/geneticsLuciferasesPromoter Regions GeneticTenebrioPeptide sequenceMESH : Metamorphosis Biological/geneticsComputingMilieux_MISCELLANEOUS0303 health sciencesMESH : Amino Acid SequenceMetamorphosis BiologicalMESH : Luciferases/metabolismEcdysone/metabolism/pharmacology3. Good healthInsect ProteinsMESH : TransfectionSequence AnalysisSignal peptideTranscriptional ActivationEcdysoneanimal structuresSequence analysisMolecular Sequence DataMESH : Transcriptional Activation/physiologyReporter/physiologyBiological/genetics/*physiologyMESH : Insect Proteins/physiologyBiologyLuciferases/metabolismTransfectionTenebrio/*genetics/physiologyMESH : Ecdysone/pharmacology03 medical and health sciencesGeneticsAnimalsAmino Acid Sequence[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyMolecular BiologyGeneMESH : Introns/physiology030304 developmental biologyGene LibraryMESH : Metamorphosis Biological/physiologyReporter gene[SDV.GEN.GPO]Life Sciences [q-bio]/Genetics/Populations and Evolution [q-bio.PE]Base SequenceMetamorphosisIntronIntrons/genetics/physiologyMESH : Ecdysone/metabolismSequence Analysis DNADNAMESH : Gene LibraryMolecular biologyIntronsGenesMESH : Tenebrio/physiologyEpidermis/metabolism Gene LibraryInsect ScienceMESH : Insect Proteins/geneticsMESH : Epidermis/metabolismMESH : Base SequenceMESH : AnimalsEpidermisMESH : Promoter Regions Genetic/drug effects[SDE.BE]Environmental Sciences/Biodiversity and EcologyInsect Proteins/*genetics/*physiology030217 neurology & neurosurgeryEpidermis/metabolismMESH : Promoter Regions Genetic/physiologyMESH : Sequence Analysis DNA
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