Search results for "NFATC Transcription Factors"

showing 10 items of 37 documents

NFATc1 releases BCL6-dependent repression of CCR2 agonist expression in peritoneal macrophages fromSaccharomyces cerevisiaeinfected mice

2016

The link between the extensive usage of calcineurin (CN) inhibitors cyclosporin A and tacrolimus (FK506) in transplantation medicine and the increasing rate of opportunistic infections within this segment of patients is alarming. Currently, how peritoneal infections are favored by these drugs, which impair the activity of several signaling pathways including the Ca(++) /CN/NFAT, Ca(++) /CN/cofilin, Ca(++) /CN/BAD, and NF-κB networks, is unknown. Here, we show that Saccharomyces cerevisiae infection of peritoneal resident macrophages triggers the transient nuclear translocation of NFATc1β isoforms, resulting in a coordinated, CN-dependent induction of the Ccl2, Ccl7, and Ccl12 genes, all enc…

0301 basic medicineChemokineReceptors CCR2Calcineurin InhibitorsImmunologySaccharomyces cerevisiaeOpportunistic InfectionsCCL7MonocytesMice03 medical and health sciences0302 clinical medicineCyclosporin aAnimalsProtein IsoformsImmunology and AllergyChemokine CCL7Promoter Regions GeneticCCL12Transcription factorChemokine CCL2NFATC Transcription FactorsbiologyCalcineurinNF-kappa BNFATNFATC Transcription FactorsMonocyte Chemoattractant Proteins3. Good healthCalcineurinProtein Transport030104 developmental biology030220 oncology & carcinogenesisMacrophages PeritonealProto-Oncogene Proteins c-bcl-6biology.proteinCancer researchEuropean Journal of Immunology
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The Amino-Terminal Domain of GRK5 Inhibits Cardiac Hypertrophy through the Regulation of Calcium-Calmodulin Dependent Transcription Factors.

2018

We have recently demonstrated that the amino-terminal domain of G protein coupled receptor kinase (GRK) type 5, (GRK5-NT) inhibits NFκB activity in cardiac cells leading to a significant amelioration of LVH. Since GRK5-NT is known to bind calmodulin, this study aimed to evaluate the functional role of GRK5-NT in the regulation of calcium-calmodulin-dependent transcription factors. We found that the overexpression of GRK5-NT in cardiomyoblasts significantly reduced the activation and the nuclear translocation of NFAT and its cofactor GATA-4 in response to phenylephrine (PE). These results were confirmed in vivo in spontaneously hypertensive rats (SHR), in which intramyocardial adenovirus-med…

0301 basic medicineG-Protein-Coupled Receptor Kinase 5MalecalmodulinMutantWistarPlasma protein binding030204 cardiovascular system & hematologyCatalysilcsh:ChemistryPhenylephrine0302 clinical medicineRats Inbred SHRMyocytes Cardiaclcsh:QH301-705.5SpectroscopybiologyChemistrycardiac hypertrophyNFATComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineLeft VentricularComputer Science ApplicationsCell biologycardiac hypertrophy; transcription factors; calmodulin; GRKGRKHypertrophy Left VentricularCardiacProtein BindingInbred SHRCalmodulinCalmodulin; Cardiac hypertrophy; GRK; Transcription factors; Animals; Binding Sites; Calmodulin; Cell Line; G-Protein-Coupled Receptor Kinase 5; GATA4 Transcription Factor; Hypertrophy Left Ventricular; Male; Myocytes Cardiac; NFATC Transcription Factors; Phenylephrine; Protein Binding; Rats; Rats Inbred SHR; Rats Wistar; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisArticleCell LineInorganic Chemistry03 medical and health sciencesG-Protein-Coupled Receptor Kinase 5transcription factorsAnimalsPhysical and Theoretical ChemistryRats WistarTranscription factorMolecular BiologyG protein-coupled receptor kinaseMyocytesBinding SitesNFATC Transcription FactorsOrganic ChemistryHypertrophyNFATC Transcription FactorsGATA4 Transcription FactorRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinTranscription factorInternational journal of molecular sciences
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Lack of NFATc1 SUMOylation prevents autoimmunity and alloreactivity

2020

A novel transgenic mouse, in which the transcription factor NFATc1 bears lysine-to-arginine mutations that prevent modification by SUMO, develops normally and is healthy. However, SUMO-insensitive NFATc1 transmits strong tolerogenic signals, thus preventing autoimmune and alloimmune T cell responses.

0301 basic medicineProtein sumoylationEncephalomyelitis Autoimmune ExperimentalT cellStem Cells & RegenerationImmunologySUMO proteinAutoimmunityBiologyenvironment and public healthT-Lymphocytes RegulatoryArticleMinor Histocompatibility AntigensMice03 medical and health sciences0302 clinical medicineImmune systemNeuroinflammationAldesleukinSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyTranscription factorMice Knockoutintegumentary systemNFATC Transcription FactorsExperimental autoimmune encephalomyelitisSumoylationNFATmedicine.diseaseCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologymedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCytokinesPositive Regulatory Domain I-Binding Factor 1Journal of Experimental Medicine
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The transcription factor NFATc2 controls IL-6–dependent T cell activation in experimental colitis

2008

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell–dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-…

Adjuvants Immunologic; Animals; Humans; Interleukin-13; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mice; Mice Inbred BALB C; Mice Knockout; Mice SCID; Models Biological; NFATC Transcription Factors; Oxazolone; T-LymphocytesT cellT-LymphocytesImmunologyMice SCIDBiologyLymphocyte ActivationInflammatory bowel diseaseModels BiologicalArticleOxazoloneTCIRG1chemistry.chemical_compoundMiceAdjuvants ImmunologicmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansColitisMice KnockoutMice Inbred BALB CInterleukin-13NFATC Transcription FactorsInterleukin-6Interleukin-17OxazoloneArticlesmedicine.diseasemedicine.anatomical_structurechemistryImmunologyInterleukin 13Cancer researchInterleukin 17The Journal of Experimental Medicine
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A genetic basis for IFN-gamma production and T-bet expression in humans.

2005

Abstract Th1 and Th2 cytokines secreted by polarized effector T cells play a pivotal role in the development of autoimmune and allergic diseases. However, the genetic basis of cytokine production by T lymphocytes in humans is poorly understood. In this study, we investigated the genetic contribution to cytokine production and regulation of T cell-specific transcription factors in a prospective twin study. We found a substantial genetic contribution to the production of Th1 cytokines such as IFN-γ and TNF-α with heritabilities of 0.85 (95% confidence intervals, 0.74–0.95) and 0.72 (0.50–0.93), respectively, whereas no genetic influence on production of the Th2 signature cytokine IL-4 was obs…

AdultMaleAdolescentmedicine.medical_treatmentImmunologyGATA3 Transcription FactorBiologyBody Mass IndexInterferon-gammaSex FactorsGenetic variationmedicineImmunology and AllergyHumansProspective StudiesGeneTranscription factorCells CulturedAgedGeneticsNFATC Transcription FactorsEffectorTumor Necrosis Factor-alphaAge FactorsNF-kappa BNFATHeritabilityMiddle AgedTwin studyCytokineImmunologyFemaleInterleukin-4T-Box Domain ProteinsTranscription FactorsJournal of immunology (Baltimore, Md. : 1950)
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NF-ATp plays a prominent role in the transcriptional induction of Th2-type lymphokines

1997

Antigens Differentiation T-LymphocyteCD4-Positive T-LymphocytesTranscription GeneticImmunologyCell CountSpleenDNA-binding proteinMiceTh2 CellsAntigens CDmedicineAnimalsImmunology and AllergyLectins C-TypeLymphocytesL-SelectinNuclear proteinTranscription factorLymphokinesNFATC Transcription FactorsbiologyChemistryLymphokineNuclear ProteinsGene deletionNFATC Transcription FactorsCell biologyDNA-Binding ProteinsHyaluronan Receptorsmedicine.anatomical_structureImmunologybiology.proteinL-selectinGene DeletionSpleenTranscription FactorsImmunology Letters
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Mycobacterial antigen(s) induce anergy by altering TCR- and TCR/CD28-induced signalling events: insights into T-cell unresponsiveness in leprosy.

2009

Present study investigates the role of Mycobacterium leprae (M. leprae) antigens on TCR- and TCR/CD28-induced signalling leading to T-cell activation and further correlates these early biochemical events with T-cell anergy, as prevailed in advanced stages of leprosy. We observed that both whole cell lystae (WCL) and soluble fraction of M. leprae sonicate (MLSA) not only inhibited TCR, thapsigargin and ionomycin induced calcium fluxes by diminishing the opening of calcium channels, but also TCR- or TCR/CD28-induced proximal signalling events like phosphorylation of Zap-70 and protein kinase-C (PKC) activity. Study of TCR- and TCR/CD28-induced downstream signals revealed that M. leprae antige…

Antigens Differentiation T-LymphocyteMAP Kinase Signaling SystemT cellT-LymphocytesImmunologyReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyLymphocyte ActivationJurkat cellsp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundJurkat CellsCD28 AntigensAntigens CDLeprosyCalcium fluxmedicineHumansLectins C-TypeEnzyme InhibitorsPromoter Regions GeneticMolecular BiologyMycobacterium lepraeProtein Kinase CCell ProliferationClonal AnergyAntigens BacterialMitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinaseIonophoresNFATC Transcription FactorsIonomycinT-cell receptorInterleukin-2 Receptor alpha SubunitCD28hemic and immune systemsNFATbiology.organism_classificationCell biologyMycobacterium lepraemedicine.anatomical_structurechemistryGene Expression RegulationIonomycinImmunologyInterleukin-2ThapsigarginCalciumMolecular immunology
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miR-29b negatively regulates human osteoclastic cell differentiation and function: Implications for the treatment of multiple myeloma-related bone di…

2013

Skeletal homeostasis relies upon a fine tuning of osteoclast (OCLs)-mediated bone resorption and osteoblast (OBLs)-dependent bone formation. This balance is unsettled by multiple myeloma (MM) cells, which impair OBL function and stimulate OCLs to generate lytic lesions. Emerging experimental evidence is disclosing a key regulatory role of microRNAs (miRNAs) in the regulation of bone homeostasis suggesting the miRNA network as potential novel target for the treatment of MM-related bone disease. Here, we report that miR-29b expression decreases progressively during human OCL differentiation in vitro. We found that lentiviral transduction of miR-29b into OCLs, even in the presence of MM cells,…

Bone diseasePhysiologyCellular differentiationCathepsin KClinical BiochemistryGene ExpressionOsteoclastsOsteolysisMMP9Cathepsin KCells CulturedTartrate-resistant acid phosphataseTumorCulturedReceptor Activator of Nuclear Factor-kappa BGenes fosCell DifferentiationOsteoblastCell biologyIsoenzymesmultiple myelomamedicine.anatomical_structureMatrix Metalloproteinase 9osteoclastMatrix Metalloproteinase 2medicine.medical_specialtyfosCellsAcid PhosphataseBiologyCollagen Type IBone resorptionCell LineOsteoclastCell Line TumorInternal medicinemedicineHumansBone ResorptionOsteoblastsmicroRNA.NFATC Transcription FactorsTartrate-Resistant Acid PhosphatasemiR-29bCell Biologymedicine.diseaseActinsMicroRNAsEndocrinologyGenesAcid Phosphatase; Actins; Bone Resorption; Cathepsin K; Cell Differentiation; Cell Line Tumor; Cells Cultured; Collagen Type I; Gene Expression; Genes fos; Humans; Isoenzymes; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; MicroRNAs; Multiple Myeloma; NFATC Transcription Factors; Osteoblasts; Osteoclasts; Osteolysis; Receptor Activator of Nuclear Factor-kappa BJournal of Cellular Physiology
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A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.

2018

Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas alter…

CD4-Positive T-Lymphocytes0301 basic medicineRegulatory T cellBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciencesNFAT5microRNAImmunogeneticsmedicineAnimalsHumansPI3K/AKT/mTOR pathwaygeographygeography.geographical_feature_categoryNFATC Transcription FactorsAntagomirsFOXP3Forkhead Transcription FactorsGeneral MedicineIsletMice Mutant StrainsMicroRNAsTolerance inductionDiabetes Mellitus Type 1030104 developmental biologymedicine.anatomical_structureCancer researchFemale
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A Key Regulatory Role of the Transcription Factor NFATc2 in Bronchial Adenocarcinoma via CD8+ T Lymphocytes

2009

AbstractThe Ca2+-regulated calcineurin/nuclear factor of activated T cells (NFAT) cascade controls alternative pathways of T-cell activation and peripheral tolerance. Here, we describe reduction of NFATc2 mRNA expression in the lungs of patients with bronchial adenocarcinoma. In a murine model of bronchoalveolar adenocarcinoma, mice lacking NFATc2 developed more and larger solid tumors than wild-type littermates. The extent of central tumor necrosis was decreased in the tumors in NFATc2(−/−) mice, and this finding was associated with reduced tumor necrosis factor-α and interleukin-2 (IL-2) production by CD8+ T cells. Adoptive transfer of CD8+ T cells of NFATc2(−/−) mice induced transforming…

CD4-Positive T-LymphocytesCancer ResearchAdoptive cell transferTranscription GeneticTransplantation HeterologousMice TransgenicReceptors Nerve Growth FactorAdenocarcinomaCD8-Positive T-LymphocytesBiologyReceptors Tumor Necrosis FactorTransforming Growth Factor beta1Interferon-gammaMiceGlucocorticoid-Induced TNFR-Related ProteinAnimalsHumansIL-2 receptorInterleukin-7 receptorMice Inbred BALB CReceptors Interleukin-7NFATC Transcription FactorsTumor Necrosis Factor-alphaBronchial NeoplasmsInterleukin-2 Receptor alpha SubunitPeripheral toleranceForkhead Transcription FactorsNFATCalcineurinDisease Models AnimalOncologyCancer researchInterleukin-2Tumor necrosis factor alphaCD8Cancer Research
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