Search results for "Promoter Regions"

showing 10 items of 441 documents

Stat3 and Gfi-1 Transcription Factors Control Th17 Cell Immunosuppressive Activity via the Regulation of Ectonucleotidase Expression

2012

International audience; Although Th17 cells are known to promote tissue inflammation and autoimmunity, their role during cancer progression remains elusive. Here, we showed that in vitro Th17 cells generated with the cytokines IL-6 and TGF-β expressed CD39 and CD73 ectonucleotidases, leading to adenosine release and the subsequent suppression of CD4(+) and CD8(+) T cell effector functions. The IL-6-mediated activation of the transcription factor Stat3 and the TGF-β-driven downregulation of Gfi-1 transcription factor were both essential for the expression of ectonucleotidases during Th17 cell differentiation. Stat3 supported whereas Gfi-1 repressed CD39 and CD73 expression by binding to thei…

Adoptive cell transferMESH : Transcription FactorsCellular differentiationMESH: Th17 CellsT-LymphocytesCellMESH : Promoter Regions GeneticMESH : RNA Small InterferingMESH: Mice KnockoutMice0302 clinical medicineTransforming Growth Factor betaMESH: RNA Small InterferingMESH : STAT3 Transcription FactorImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyEctonucleotidaseMESH: AnimalsRNA Small InterferingSTAT3MESH: Lymphocytes Tumor-InfiltratingPromoter Regions GeneticMESH: Antigens CD5'-NucleotidaseRegulation of gene expressionMice Knockout0303 health sciencesMESH : Gene Expression RegulationApyraseMESH: STAT3 Transcription FactorMESH: Transcription FactorsMESH: Gene Expression RegulationMESH : Mice TransgenicCell biologyMESH : Lymphocytes Tumor-InfiltratingDNA-Binding ProteinsMESH : ApyraseInfectious Diseasesmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : DNA-Binding ProteinsMESH: ApyraseSTAT3 Transcription Factor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Interleukin-6MESH: Mice TransgenicT cellImmunologyMice TransgenicMESH : Mice Inbred C57BLBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingMESH: Mice Inbred C57BLAntigens CDMESH: Promoter Regions GeneticMESH : 5'-NucleotidaseMESH : MicemedicineMESH : Antigens CDMESH : Th17 CellsAnimalsTranscription factorMESH: MiceMESH: Transforming Growth Factor beta030304 developmental biologyMESH : T-LymphocytesBinding SitesInterleukin-6MESH: Interleukin-6Mice Inbred C57BLMESH: T-LymphocytesMESH : Transforming Growth Factor betaMESH: Binding SitesGene Expression Regulationbiology.proteinMESH : Mice KnockoutTh17 CellsMESH : AnimalsMESH: 5'-NucleotidaseMESH: DNA-Binding ProteinsMESH : Binding Sites030215 immunologyTranscription FactorsImmunity
researchProduct

Thymidylate synthase gene promoter polymorphisms are associated with TSmRNA expressions but not with microsatellite instability in colorectal cancer

2005

Abstract BACKGROUND: Microsatellite instability (MSI) is a biological characteristic of most tumours, being involved in 85% of hereditary non-polyposis colorectal cancer (HNPCC). It also occurs in 10-15% of sporadic colorectal cancers (CRC). HNPCC appears to be caused by germline mutations in mismatch repair (MMR) genes, which are responsible for repairing single base-pair mismatches. MSI is also associated with a better response of CRC to adjuvant chemotherapy with fluoropyrimidines. We investigated any relationship between the MSI status and the TSmRNA expression, the polymorphisms of 5-Fluorouracil (5-FU cellular target, the enzyme thymidylate synthase (TS) and TS expression evaluated by…

AdultAged 80 and overMalePolymorphism GeneticAntibodies MonoclonalThymidylate SynthaseMiddle AgedSettore MED/08 - Anatomia PatologicaImmunohistochemistryGenomic InstabilityHumansFemaleColorectal cancer thymidylate synthase pharmacogenomic microsatellite instability polymorphism molecular therapeutic.RNA Messenger5' Untranslated RegionsColorectal NeoplasmsPromoter Regions GeneticAgedMicrosatellite Repeats
researchProduct

The transcription factor ZEB1 (deltaEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity.

2007

Epithelial to mesenchymal transition (EMT) is implicated in the progression of primary tumours towards metastasis and is likely caused by a pathological activation of transcription factors regulating EMT in embryonic development. To analyse EMT-causing pathways in tumouri-genesis, we identified transcriptional targets of the E-cadherin repressor ZEB1 in invasive human cancer cells. We show that ZEB1 repressed multiple key determinants of epithelial differentiation and cell–cell adhesion, including the cell polarity genes Crumbs3, HUGL2 and Pals1-associated tight junction protein. ZEB1 associated with their endogenous promoters in vivo, and strongly repressed promotor activities in reporter …

AdultCancer ResearchChromatin ImmunoprecipitationCellular differentiationImmunoblottingDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeEpitheliumArticleCell polarityGeneticsmedicineTumor Cells CulturedHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionCell adhesionPromoter Regions GeneticMolecular BiologyTranscription factorEpithelial polarityAgedOligonucleotide Array Sequence AnalysisHomeodomain ProteinsMembrane GlycoproteinsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell PolarityMembrane ProteinsZinc Finger E-box-Binding Homeobox 1Cell DifferentiationMiddle AgedCadherinsCytoskeletal ProteinsMicroscopy FluorescenceCancer cellColonic NeoplasmsCancer researchDisease ProgressionSnail Family Transcription FactorsCarcinogenesisNucleoside-Phosphate KinaseTranscription FactorsOncogene
researchProduct

Variable maternal methylation overlapping the nc886/vtRNA2-1 locus is locked between hypermethylated repeats and is frequently altered in cancer.

2014

Cancer is as much an epigenetic disease as a genetic one; however, the interplay between these two processes is unclear. Recently, it has been shown that a large proportion of DNA methylation variability can be explained by allele-specific methylation (ASM), either at classical imprinted loci or those regulated by underlying genetic variants. During a recent screen for imprinted differentially methylated regions, we identified the genomic interval overlapping the non-coding nc886 RNA (previously known as vtRNA2-1) as an atypical ASM that shows variable levels of methylation, predominantly on the maternal allele in many tissues. Here we show that the nc886 interval is the first example of a …

AdultCancer ResearchLung NeoplasmsRNA UntranslatedLoss of HeterozygosityLocus (genetics)Breast NeoplasmsBiologyLoss of heterozygosityGenomic ImprintingYoung Adultnc886NeoplasmsHumansEpigeneticsAllelePromoter Regions GeneticMolecular BiologyvtRNA2-1GeneticsDNA methylationMethylationMiddle Agedvault RNAsMolecular biologyDifferentially methylated regionsUrinary Bladder NeoplasmsGenetic LociTandem Repeat SequencesDNA methylationColonic NeoplasmsmiRNAsFemaleimprintingGenomic imprintingResearch PaperEpigenetics
researchProduct

Activity of the antiestrogenic cajanin stilbene acid towards breast cancer

2014

Antiestrogenic therapy is a mainstay for estrogen receptor (ERα)-positive breast cancer. Due to the development of resistance to established antihormones such as tamoxifen, novel compounds are required. The low abundant cajanin stilbene acid (CSA) recently isolated by us from Pigeon Pea (Cajanus cajan) has structural similarities with estrogen. We analyzed the cytotoxic and anticancer activity of CSA in ERα-positive and -negative human breast cancer cells in vitro, in vivo and in silico. CSA exerts anticancer and antiestrogenic activities towards ERα-positive breast cancer, and it showed cytotoxicity towards tamoxifen-resistant MCF-7 cells, implying that CSA may be active against tamoxifen-…

AdultEndocrinology Diabetes and MetabolismClinical BiochemistryMice NudeEstrogen receptorBreast NeoplasmsPharmacologyBiochemistryBreast cancerCell Line TumorAntineoplastic Combined Chemotherapy ProtocolsStilbenesAnimalsHumansMedicineCytotoxic T cellPromoter Regions Geneticskin and connective tissue diseasesCytotoxicityMolecular BiologyNutrition and Dieteticsbusiness.industryEstrogen AntagonistsEstrogen Receptor alphaCancerMiddle Agedmedicine.diseaseXenograft Model Antitumor AssaysSalicylatesGene Expression Regulation NeoplasticTamoxifenReceptors EstrogenCancer cellMCF-7 CellsFemalebusinessEstrogen receptor alphaTamoxifenmedicine.drugThe Journal of Nutritional Biochemistry
researchProduct

The microcephaly ASPM gene and schizophrenia: A preliminary study

2006

AdultGeneticsMicrocephalyGenotypeSchizophrenia (object-oriented programming)HaplotypeGene ExpressionNerve Tissue ProteinsBiologymedicine.diseasePolymorphism Single NucleotideASPMPsychiatry and Mental healthGene FrequencyHaplotypesGenotypeGene expressionMicrocephalySchizophreniamedicineHumansPromoter Regions GeneticGeneAllele frequencyBiological PsychiatrySchizophrenia Research
researchProduct

Cytokine genotyping (TNF and IL-10) in patients with celiac disease and selective IgA deficiency

2003

Selective IgA deficiency (IgAD) and celiac disease (CD) are frequently associated and share the ancestral haplotype human leukocyte antigen (HLA)-8.1, which is characterized by a peculiar cytokine profile. The aim of this study was to evaluate the role of tumor necrosis factor (TNF) and interleukin (IL)-10 alleles in CD and CD-IgAD.The distribution of some biallelic polymorphisms of both cytokine promoters (-308G--A and -863C--A at TNF promoter sequence and -1082G--A, -819C--A, and -592C--T at IL-10 promoter) were typed using biotilinated specific probes in 32 celiac patients, in 34 CD-IgAD patients, and in 96 healthy controls.In CD and CD-IgAD, the -308A allele was significantly more frequ…

AdultGenotypemedicine.medical_treatmentDiseaseSelective IgA deficiencyCoeliac diseaseGene FrequencyImmunopathologyHumansMedicineChildPromoter Regions GeneticGenotypingPolymorphism GeneticHepatologyTumor Necrosis Factor-alphabusiness.industryIgA DeficiencyGastroenterologynutritional and metabolic diseasesmedicine.diseasedigestive system diseasesInterleukin-10Celiac DiseaseInterleukin 10Cross-Sectional StudiesCytokineImmunologyCytokinesTumor necrosis factor alphabusinessSequence AnalysisThe American Journal of Gastroenterology
researchProduct

Molecular analysis of sequence variants in the Fcepsilon receptor I beta gene and IL-4 gene promoter in Italian atopic families

2004

The genetic variants in the Fcepsilon receptor I beta gene (Glu237Gly) and the T allele of the (C590T) polymorphism of interleukin (IL)-4 gene promoter were reported to be associated with atopy. But the data of the studies in different populations are contrasting with one another.

AdultHypersensitivity ImmediateMalePolymorphism GeneticGenotypeAdolescentReceptors IgEGenetic Variation; Gene Frequency; Polymorphism Genetic; Humans; Child; Receptors IgE; Genotype; Promoter Regions Genetic; Immunoglobulin E; Adult; Interleukin-4; Hypersensitivity Immediate; Middle Aged; Adolescent; Male; Amino Acid Substitution; FemaleGenetic VariationImmunoglobulin EMiddle AgedGene FrequencyAmino Acid SubstitutionFemaleInterleukin-4ChildPromoter Regions GeneticHuman
researchProduct

Lack of TERT promoter mutations in melanomas with extensive regression

2015

AdultMale0301 basic medicineTelomeraseSkin NeoplasmsDermatologyTert promoter030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicinemedicineHumansPromoter Regions GeneticMelanomaTelomeraseAgedbusiness.industryMelanomaCase-control studyMiddle Agedmedicine.diseaseRegressionNeoplasm regression030104 developmental biologyNeoplasm Regression SpontaneousCase-Control StudiesMutationMutation (genetic algorithm)Cancer researchFemalebusinessJournal of the American Academy of Dermatology
researchProduct

Urea cycle dysregulation in non-alcoholic fatty liver disease.

2018

Background & Aims: In non-alcoholic steatohepatitis (NASH), the function of urea cycle enzymes (UCEs) may be affected, resulting in hyperammonemia and the risk of disease progression. We aimed to determine whether the expression and function of UCEs are altered in an animal model of NASH and in patients with non-alcoholic fatty liver disease (NAFLD), and whether this process is reversible. Methods: Rats were first fed a high-fat, high-cholesterol diet for 10 months to induce NASH, before being switched onto a normal chow diet to recover. In humans, we obtained liver biopsies from 20 patients with steatosis and 15 with NASH. Primary rat hepatocytes were isolated and cultured with free fatty …

AdultMale0301 basic medicinemedicine.medical_specialtyCarbamoyl-Phosphate Synthase (Ammonia)Ornithine transcarbamylase03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAmmoniaGlutamate-Ammonia LigaseNon-alcoholic Fatty Liver DiseaseInternal medicineGene expressionmedicineAnimalsHumansUreaRats WistarPromoter Regions GeneticCells CulturedOrnithine CarbamoyltransferaseAgedHepatologyChemistryFatty liverHyperammonemiaDNA MethylationMiddle Agedmedicine.diseaseRats030104 developmental biologyEndocrinologyLiverUrea cycleHepatocytesUreaFemale030211 gastroenterology & hepatologySteatohepatitisSteatosis
researchProduct