Search results for " Up-Regulation"

showing 4 items of 24 documents

TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

2007

The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HN…

Transcriptional ActivationTGFβFAK; MT; Src; TGFβ; Animals; Biomarkers Tumor; Cadherins; Cell Line; Cell Transformation Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell BiologyCell LineMesodermFocal adhesionMiceTransforming Growth Factor betaBiomarkers TumorAnimalsHepatocyteNeoplasm InvasivenessNeoplasm InvasiveneEpithelial CellFocal Adhesion Protein-Tyrosine KinaseFAKbiologyAnimalCadherinLiver NeoplasmsMesenchymal stem cellEpithelial CellsCell BiologyTransforming growth factor betaTgf beta; fak; srcCadherinsUp-RegulationCell biologyEnzyme ActivationCell Transformation Neoplasticsrc-Family KinasesHepatocyte nuclear factor 4Liver NeoplasmTumor progressionMTFocal Adhesion Protein-Tyrosine KinasesCadherinHepatocytesCancer researchbiology.proteinsrc-Family KinaseSignal transductionSrcSignal TransductionProto-oncogene tyrosine-protein kinase SrcExperimental Cell Research
researchProduct

Smad7 controls resistance of colitogenic T cells to regulatory T cell-mediated suppression.

2008

Background & Aims Foxp3-expressing regulatory T cells (Tregs) play a key role in the maintenance of the gut immune homeostasis, and an intact transforming growth factor (TGF)-β signaling is required for their function. In inflammatory bowel disease (IBD), the TGF-β signaling is impaired because of high expression of the inhibitory molecule Smad7. Although no intrinsic defects in Tregs function have been shown in IBD, it is still unknown whether colitogenic T cells are susceptible to Treg-mediated suppression. In this study, we have investigated whether IBD mucosal CD4+ T cells are resistant to Tregs and whether Smad7 is involved in this process. Methods IBD lamina propria mononuclear cells …

antisense oligonucleotideCD4-Positive T-LymphocytesAdoptive cell transferT-Lymphocytesanimal cellCell CommunicationInbred C57BLT-Lymphocytes RegulatoryTransgenicMiceregulatory T lymphocyteCrohn DiseaseTransforming Growth Factor betamononuclear cellRAG1 proteinIntestinal MucosaenteritisCells CulturedMice KnockoutSettore MED/12 - GastroenterologiaCulturedintegumentary systemmedicine.diagnostic_testarticleGastroenterologyInterleukinhemic and immune systemsT helper cellColitisRegulatoryUp-Regulationmedicine.anatomical_structurepriority journalgamma interferonSignal TransductionRegulatory T cellColonCellsKnockoutanimal experimentinterleukin 6chemical and pharmacologic phenomenaMice TransgenicBiologyinterleukin 2Recombination-activating geneFlow cytometryProinflammatory cytokineSmad7 ProteinmedicineAnimalsHumanscontrolled studyhumanlamina propriamouseCell ProliferationHomeodomain ProteinsCD4+ T lymphocytenonhumanHepatologyAnimalflow cytometryhuman cellanimal cell culturetransgenic mouseMice Inbred C57BLDisease Models Animalantisense oligonucleotide; gamma interferon; interleukin 17; interleukin 2; interleukin 6; RAG1 protein; Smad7 protein; animal cell; animal cell culture; animal experiment; article; CD4+ T lymphocyte; cell proliferation; colitis; controlled study; enteritis; flow cytometry; human; human cell; knockout mouse; lamina propria; mononuclear cell; mouse; nonhuman; priority journal; regulatory T lymphocyte; transgenic mouse; Animals; CD4-Positive T-Lymphocytes; Cell Communication; Cell Proliferation; Cells Cultured; Colitis; Colon; Crohn Disease; Disease Models Animal; Homeodomain Proteins; Humans; Intestinal Mucosa; Mice; Mice Inbred C57BL; Mice Knockout; Mice Transgenic; Signal Transduction; Smad7 Protein; T-Lymphocytes Regulatory; Transforming Growth Factor beta; Up-RegulationDisease ModelsImmunologyinterleukin 17knockout mouseTransforming growth factorGastroenterology
researchProduct

The increase in maternal expression of axin1 and axin2 contribute to the zebrafish mutant ichabod ventralized phenotype.

2014

β-Catenin is a central effector of the Wnt pathway and one of the players in Ca(+)-dependent cell-cell adhesion. While many wnts are present and expressed in vertebrates, only one β-catenin exists in the majority of the organisms. One intriguing exception is zebrafish that carries two genes for β-catenin. The maternal recessive mutation ichabod presents very low levels of β-catenin2 that in turn affects dorsal axis formation, suggesting that β-catenin1 is incapable to compensate for β-catenin2 loss and raising the question of whether these two β-catenins may have differential roles during early axis specification. Here we identify a specific antibody that can discriminate selectively for β-…

axin1axin2zebrafish mutant ichabodMessengerEmbryonic DevelopmentBiochemistryBETA-CATENINAxin2-RGS DOMAINAxin ProteinAntibody SpecificitySettore BIO/10 - BiochimicaAnimalsAxin2-RGS DOMAIN; AXIS FORMATION; BETA-CATENIN; Wnt signaling; ZEBRAFISH; Animals; Antibody Specificity; Axin Protein; Blastula; Cell Nucleus; Embryonic Development; Female; Gene Expression Regulation Developmental; Genes Dominant; Immunohistochemistry; Lithium Chloride; Mutation; Phenotype; Protein Stability; Protein Transport; RNA Messenger; Signal Transduction; Up-Regulation; Zebrafish; Zebrafish Proteins; beta Catenin; Biochemistry; Cell Biology; Molecular BiologyDevelopmentalDominantRNA MessengerMolecular BiologyZebrafishbeta CateninGenes DominantAXIS FORMATIONCell NucleusProtein StabilityGene Expression Regulation DevelopmentalCell BiologyBlastulaZebrafish ProteinsWnt signalingImmunohistochemistryUp-RegulationProtein TransportPhenotypeGene Expression RegulationGenesMutationRNAFemaleLithium ChlorideSignal Transduction
researchProduct

The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid…

2009

Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as…

musculoskeletal diseasesAdultMalemedicine.medical_specialtyComplement systemEndotheliumNeutrophilsArthritisInflammationComplement Membrane Attack ComplexArthritis RheumatoidEndothelium; Osteoprotegerin; Inflammation; Complement systemRheumatologyOsteoprotegerinInternal medicineCell AdhesionMedicineHumansPharmacology (medical)EndotheliumCells CulturedAgedInflammationEndothelial CellDose-Response Relationship Drugbusiness.industryNeutrophilSynovial MembraneOsteoprotegerinEndothelial CellsMiddle Agedmedicine.diseaseIn vitroComplement systemUp-RegulationEndothelial stem cellEndocrinologymedicine.anatomical_structureNeutrophil InfiltrationFemaleComplement system; Endothelium; Inflammation; Osteoprotegerin; Adult; Aged; Arthritis Rheumatoid; Cell Adhesion; Cells Cultured; Complement Membrane Attack Complex; Dose-Response Relationship Drug; Endothelial Cells; Endothelium Vascular; Female; Humans; Male; Middle Aged; Neutrophil Infiltration; Neutrophils; Osteoprotegerin; Synovial Membrane; Up-Regulation; Rheumatology; Pharmacology (medical)Endothelium Vascularmedicine.symptombusinessComplement membrane attack complexHuman
researchProduct