Search results for "EFFECTOR"

showing 10 items of 217 documents

Patchwork Pattern of Transcriptional Reactivation in the Lungs Indicates Sequential Checkpoints in the Transition from Murine Cytomegalovirus Latency…

1999

The lungs are a relevant organ site of primary and recurrent human cytomegalovirus (hCMV) disease (for overviews, see references 21, 22, 31, 34, 39, and 44). Murine CMV (mCMV) can serve us as a model for studying CMV pneumonia in acute infection (6, 27, 33, 37) as well as for studying viral latency, reactivation, and recurrence in the lungs (2, 17, 18, 42, 43). We have shown recently that transcription from the major immediate-early (MIE) transcription unit ie1-ie3 (hereafter referred to as ie1/3), which is driven by a strong MIE promoter-enhancer (MIEPE) (3), occurs during pulmonary latency of mCMV but fails to initiate the productive cycle (17). Notably, the paralogous MIEPE of hCMV can f…

Gene Expression Regulation ViralTranscriptional ActivationHuman cytomegalovirusvirusesImmunologyCytomegalovirusReplicationBiologyMicrobiologyMiceTransactivationTranscription (biology)VirologyGene expressionVirus latencymedicineAnimalsEnhancerGenes Immediate-EarlyLungTranscription factorMice Inbred BALB CEffectormedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsFemaleVirus ActivationTranscription FactorsJournal of Virology
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Alternative Polyadenylation Events Contribute to the Induction of NF-ATc in Effector T Cells

1999

Abstract The transcription factor NF-ATc is synthesized in three prominent isoforms. These differ in the length of their C terminal peptides and mode of synthesis. Due to a switch from the use of a 3′ polyA site to a more proximal polyA site, NF-ATc expression switches from the synthesis of the two longer isoforms in naive T cells to that of short isoform A in T effector cells. The relative low binding affinity of cleavage stimulation factor CstF-64 to the proximal polyA site seems to contribute to its neglect in naive T cells. These alternative polyadenylation events ensure the rapid accumulation of high concentrations of NF-ATc necessary to exceed critical threshold levels of NF-ATc for g…

Gene isoformPolyadenylationImmunologyMolecular Sequence DataGene inductionBiologyLymphocyte ActivationTransfectionT-Lymphocytes RegulatoryJurkat CellsMiceGenes ReporterCritical thresholdTumor Cells CulturedImmunology and AllergyAnimalsHumansAmino Acid SequenceCloning MolecularLuciferasesTranscription factormRNA Cleavage and Polyadenylation FactorsCleavage stimulation factorBase SequenceNFATC Transcription FactorsEffectorNuclear ProteinsRNA-Binding ProteinsMolecular biologyDNA-Binding ProteinsInfectious DiseasesPoly ATranscription FactorsImmunity
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Nfatc1/Αa and Blimp-1 Support the Follicular and Effector Phenotype of Tregs

2021

CD4 + CXCR5 + Foxp3 + T follicular regulatory (T FR ) cells control the germinal center responses. Like follicular helper T-cells, they express high levels of N uclear F actor of A ctivated T -cells c1 , predominantly its short isoform NFATc1/αA. Ablation of NFATc1 in Tregs prevents upregulation of CXCR5 and migration of T FR cells into B-cell follicles. By contrast, constitutive active NFATc1/αA defines the surface density of CXCR5, whose level determines how deep a T FR migrates into the GC and how effectively it controls antibody production. NFATc1/αA is necessary to overcome T FR -expressed B l ymphocyte- i nduced m aturation p rotein (Blimp-1), which can directly repress Cxcr5. Blimp-1…

Gene isoformTransactivationintegumentary systemDownregulation and upregulationChemistryEffectorGerminal centerFOXP3PhenotypeCXCR5Cell biologySSRN Electronic Journal
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Autoregulation of NFATc1/A Expression Facilitates Effector T Cells to Escape from Rapid Apoptosis

2002

AbstractThreshold levels of individual NFAT factors appear to be critical for apoptosis induction in effector T cells. In these cells, the short isoform A of NFATc1 is induced to high levels due to the autoregulation of the NFATc1 promoter P1 by NFATs. P1 is located within a CpG island in front of exon 1, represents a DNase I hypersensitive chromatin site, and harbors several sites for binding of inducible transcription factors, including a tandemly arranged NFAT site. A second promoter, P2, before exon 2, is not controlled by NFATs and directs synthesis of the longer NFATc1/B+C isoforms. Contrary to other NFATs, NFATc1/A is unable to promote apoptosis, suggesting that NFATc1/A enhances eff…

Gene isoformTranscription GeneticMolecular Sequence DataImmunologyApoptosisBiologyT-Lymphocytes RegulatoryJurkat CellsMiceExonAnimalsDeoxyribonuclease IHomeostasisHumansImmunology and AllergyPromoter Regions GeneticTranscription factorMice Inbred BALB CBase SequenceNFATC Transcription Factorsintegumentary systemEffectorNuclear ProteinsNFATDNA MethylationMolecular biologyChromatinDNA-Binding ProteinsAlternative SplicingInfectious DiseasesCpG siteApoptosisElectrophoresis Polyacrylamide GelPoly ATranscription FactorsImmunity
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NF-κB factors control the induction of NFATc1 in B lymphocytes

2014

In peripheral lymphocytes, the transcription factors (TFs) NF-κB, NFAT, and AP-1 are the prime targets of signals that emerge from immune receptors. Upon activation, these TFs induce gene networks that orchestrate the growth, expansion, and effector function of peripheral lymphocytes. NFAT and NF-κB factors share several properties, such as a similar mode of induction and architecture in their DNA-binding domain, and there is a subgroup of κB-like DNA promoter motifs that are bound by both types of TFs. However, unlike NFAT and AP-1 factors that interact and collaborate in binding to DNA, NFAT, and NF-κB seem neither to interact nor to collaborate. We show here that NF-κB1/p50 and c-Rel, th…

Gene isoformintegumentary systemEffectorImmunologybreakpoint cluster regionNFATNF-κBBiologyChromatinCell biologychemistry.chemical_compoundchemistryCancer researchImmunology and AllergyReceptorTranscription factorEuropean Journal of Immunology
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Gene Therapy in Rare Respiratory Diseases: What Have We Learned So Far?

2020

Gene therapy is an alternative therapy in many respiratory diseases with genetic origin and currently without curative treatment. After five decades of progress, many different vectors and gene editing tools for genetic engineering are now available. However, we are still a long way from achieving a safe and efficient approach to gene therapy application in clinical practice. Here, we review three of the most common rare respiratory conditions—cystic fibrosis (CF), alpha-1 antitrypsin deficiency (AATD), and primary ciliary dyskinesia (PCD)—alongside attempts to develop genetic treatment for these diseases. Since the 1990s, gene augmentation therapy has been applied in multiple clinical tria…

Genetic enhancementalpha-1-antitrypsin deficitprimary ciliary dyskinesialcsh:MedicineReviewrare respiratory diseasesBioinformaticsViral vectorcystic fibrosis03 medical and health sciences0302 clinical medicineGenome editingMedicineGene030304 developmental biologyPrimary ciliary dyskinesia0303 health sciencesTranscription activator-like effector nucleaseEffectorbusiness.industrylcsh:RGeneral Medicinemedicine.diseasegene therapyClinical trial030220 oncology & carcinogenesisbusinessJournal of Clinical Medicine
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Playing the Game Together: Coexpression of a Single Chain T Cell Receptor and a T Cell Receptor Constant-Alpha Domain Triggers Tumor Reactivity.

2006

Abstract Grafting T cells by tumor-antigen specific T cell receptors (TCR) could trigger the initiation of effector function and redirect T cell cytotoxicity towards tumors. We utilized various HLA-A2.1 transgenic mice to bypass human MDM2- and p53-specific self-tolerance. In contrast to the use of HuCD8×A2Kb transgenic mice to generate an MDM2-specific CD8-dependent TCR, we generated a high-affinity, CD8-independent p53-specific TCR in single human A2.1 transgenic mice. The efficiency of double chain (dc) TCR modified T cells could be affected by the incorrect TCR α/β chain pairing between endogenous and transgenic TCR constructs to form hybrid TCR potentially leading to autoimmunity. To a…

Genetically modified mouseSignal peptideEffectorTransgeneImmunologyT-cell receptorCell BiologyHematologyBiologyBiochemistryMolecular biologyCytolysisCell cultureReceptorBlood
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C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

2015

Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mi…

Genetics and Molecular Biology (all)0301 basic medicinePROTEINGeneral Physics and AstronomyMELANOMAApoptosisInbred C57BLBiochemistryDISEASEAnimals; Apoptosis; Cell Line Tumor; Cell Movement; Cell Proliferation; Complement Activation; Complement C1q; Complement C3; Complement C5; Humans; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasms; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Micefluids and secretionsCell Movementimmune system diseasesNeoplasmsIMMUNE-RESPONSEskin and connective tissue diseasesComplement ActivationComplement C1qMice KnockoutComplement component 5TumorMultidisciplinaryQChemistry (all)Complement C5Complement C33. Good healthCell biologyMultidisciplinary SciencesDEFICIENCYmedicine.anatomical_structureScience & Technology - Other TopicsHumanKnockoutSciencechemical and pharmacologic phenomenaBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyTROPHOBLAST INVASIONMECHANISMSCell LinePhysics and Astronomy (all)03 medical and health sciencesClassical complement pathwayImmune systemINFLAMMATIONCell Line TumormedicineAnimalsHumansCell ProliferationScience & TechnologyBiochemistry Genetics and Molecular Biology (all)AnimalCell growthEFFECTOR SYSTEMComplement C1qApoptosiGeneral ChemistryComplement systemMice Inbred C57BL030104 developmental biologyCancer cellNeoplasmBone marrowANTIBODY THERAPYNature Communications
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Drp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic Reprogramming

2018

Summary Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and acc…

Genetics and Molecular Biology (all)0301 basic medicinecell migrationT-LymphocytesCellCell CountMitochondrionLymphocyte ActivationBiochemistryCell MovementHomeostasismetabolic reprogrammingcell migration; cell proliferation; cMyc; Drp1; exhaustion; metabolic reprogramming; mitochondrial dynamics; T cells; thymocytes; tumor immune-surveillance; Biochemistry Genetics and Molecular Biology (all)lcsh:QH301-705.5cMycImmunologic SurveillanceMice KnockoutThymocytesEffectorDrp1; T cells; cMyc; cell migration; cell proliferation; exhaustion; metabolic reprogramming; mitochondrial dynamics; thymocytes; tumor immune-surveillanceCell migrationCell DifferentiationCell biologymedicine.anatomical_structurePhenotypeDynaminsendocrine systemSettore BIO/06Cell SurvivalLymphoid TissueMAP Kinase Signaling SystemT cellT cellsReceptors Antigen T-CellDrp1BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleProto-Oncogene Proteins c-myc03 medical and health sciencestumor immune-surveillancemitochondrial dynamicexhaustionHomeostasimedicineAnimalsCell ProliferationTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)Cell growthAnimalT cellthymocytemitochondrial dynamicsDynamin030104 developmental biologylcsh:Biology (General)T-LymphocyteT cell migration
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Differential expression and glycosylation of proteins in the rat ileal epithelium in response to Echinostoma caproni infection.

2013

Echinostoma caproni (Trematoda: Echinostomatidae) is an intestinal trematode that has been used as experimental model to investigate the factors determining the expulsion of intestinal helminths. We analyze the changes in the protein expression and glycosylation induced by E. caproni in Wistar rat, a host of low compatibility in which the parasites are rapidly rejected. To determine the changes in protein expression, two-dimensional difference gel electrophoresis was employed using protein extracts from the intestine of naïve and infected rats. The patterns of glycosylation were analyzed by lectin blotting. Those spots showing differential expression or glycosylation were analyzed by mass s…

GlycosylationGlycosylationEchinostoma caproniDifference gel electrophoresisBiophysicsIleumBiochemistryMass SpectrometryTwo-Dimensional Difference Gel Electrophoresischemistry.chemical_compoundIleumEchinostomamedicineHelminthsAnimalsIntestinal MucosaRats WistarCytoskeletonEchinostomiasisbiologyEffectorbiology.organism_classificationMolecular biologyRatsmedicine.anatomical_structureBiochemistrychemistryGene Expression RegulationFemaleTrematodaJournal of proteomics
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