Search results for "Cell Differentiation"

showing 10 items of 907 documents

Cutting Edge: TGF-β Signaling Is Required for the In Vivo Expansion and Immunosuppressive Capacity of Regulatory CD4+CD25+ T Cells

2004

Abstract Data regarding the role of TGF-β for the in vivo function of regulatory CD4+CD25+ T cells (Treg) are controversial. A transgenic mouse model with impaired TGF-β signaling specifically in T cells was used to assess the role of endogenous TGF-β for the in vivo function of CD4+CD25+ Treg in a murine model of colitis induced by dextran sulfate. Transfer of wild-type, but not transgenic CD4+CD25+ Treg was found to suppress colitis in wild-type mice. In addition, by transferring CFSE-labeled CD4+CD25+ Treg we could demonstrate that endogenous TGF-β promotes the expansion of CD4+CD25+ Treg in vivo. Transgenic mice themselves developed reduced numbers of peripheral CD4+CD25+ Treg and were …

Genetically modified mouseAdoptive cell transferTransgeneImmunologychemical and pharmacologic phenomenaEndogenyBiologyT-Lymphocytes RegulatoryMiceTransforming Growth Factor betaIn vivomedicineAnimalsHumansImmunology and AllergyGenetic Predisposition to DiseaseLymphocyte CountIL-2 receptorColitisReceptorCell DifferentiationReceptors Interleukin-2hemic and immune systemsColitismedicine.diseaseAdoptive TransferCell biologyImmunologySignal TransductionThe Journal of Immunology
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A Cre-inducible diphtheria toxin receptor mediates cell lineage ablation after toxin administration.

2004

A new system for lineage ablation is based on transgenic expression of a diphtheria toxin receptor (DTR) in mouse cells and application of diphtheria toxin (DT). To streamline this approach, we generated Cre-inducible DTR transgenic mice (iDTR) in which Cre-mediated excision of a STOP cassette renders cells sensitive to DT. We tested the iDTR strain by crossing to the T cell- and B cell-specific CD4-Cre and CD19-Cre strains, respectively, and observed efficient ablation of T and B cells after exposure to DT. In MOGi-Cre/iDTR double transgenic mice expressing Cre recombinase in oligodendrocytes, we observed myelin loss after intraperitoneal DT injections. Thus, DT crosses the blood-brain bar…

Genetically modified mouseCell SurvivalTransgeneT cellT-LymphocytesCellCre recombinaseApoptosisMice TransgenicReceptors Cell SurfaceBiologyBiochemistryCell LineMicemedicineAnimalsCell LineageDiphtheria ToxinReceptorMolecular BiologyDiphtheria toxinIntegrasesCell DifferentiationCell BiologyMolecular biologyRecombinant ProteinsOligodendrogliamedicine.anatomical_structureCell cultureIntercellular Signaling Peptides and ProteinsBiotechnologyHeparin-binding EGF-like Growth FactorNature methods
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GSK3β overexpression induces neuronal death and a depletion of the neurogenic niches in the dentate gyrus

2010

Overexpression of GSK3β in transgenic mice induces learning deficits and some features associated with Alzheimer's disease (AD), including dentate gyrus (DG) atrophy. Here, we assessed whether these mice also recapitulate DG atrophy as well as impaired neurogenesis reported in AD. Ultrastructural analysis revealed that there were fewer and more disorganized neurogenic niches in these animals, coupled with an increase in the proportion of immature neurons. Indeed, the maturation of granule cells is delayed as witnessed by the alterations to the length and patterning of their dendritic trees and to the mossy fiber terminals. Together with an increase in neuronal death, these phenomena lead to…

Genetically modified mouseProgrammed cell deathOverexpressionNeurogenesisproliferationCognitive NeuroscienceCellular differentiationeducationProliferationMice TransgenicBiologyGlycogen Synthase Kinase 3MiceAtrophyAlzheimer DiseaseMaturationmedicineAnimalsHumanshippocampal stem cellsGSK3Bhealth care economics and organizationsCell ProliferationGlycogen Synthase Kinase 3 betaCell DeathMicrogliamaturationDentate gyrusNeurogenesisGSK3 betaCell DifferentiationAlzheimer's diseasemedicine.diseaseMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureHippocampal stem cellsDentate GyrusGSK3bMicrogliaAlzheimer’s diseaseNeuroscienceoverexpressionHippocampus
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Mutated cylindromatosis gene affects the functional state of dendritic cells

2010

Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating enzyme, which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling. Here, we report that DC derived from transgenic mice, which solely express a naturally occurring CYLD isoform (CYLD(ex7/8)), display a higher content of nuclear RelB and express elevated levels of NF-κB family members as well as of known NF-κB-target genes comprising costimulatory molecules and pro-inflammatory cytokines, as compared with WT DC. Accordingly, unstimulated CYLD(ex7/8) DC exhibited a significantly higher primary allogenic T-cell stimulatory capacity than WT DC and exerted no tolerogenic activity. Tr…

Genetically modified mouseTransgeneBlotting WesternImmunologyMice TransgenicBiologyDexamethasoneDeubiquitinating enzymeSmall hairpin RNAMiceImmune ToleranceAnimalsImmunology and AllergyGlucocorticoidsMice KnockoutReverse Transcriptase Polymerase Chain ReactionTumor Suppressor ProteinsRELBTranscription Factor RelBNF-kappa BPeripheral toleranceCell DifferentiationDendritic CellsFlow CytometrySpecific Pathogen-Free OrganismsCell biologyIsoenzymesTranscription Factor AP-1MutationKnockout mouseImmunologybiology.proteinRNAFemaleSignal transductionSignal TransductionEuropean Journal of Immunology
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Cdc42 in osterix-expressing cells alters osteoblast behavior and myeloid lineage commitment

2021

Osteoblasts are not only responsible for bone formation. They also support hematopoiesis. This requires responding to cues originating from several signaling pathways, a task performed by Rho GTPases. We therefore examined several transgenic mouse models and used inhibitors of Cdc42 in vitro. Deletion of Cdc42 in vivo using the Osterix promoter suppressed osteoblast function, while its deletion in differentiating osteoblasts using the Collagen-a1(I) promoter decreased osteoblast numbers. In both cases, bone mineral density diminished confirming the importance of Cdc42. Evaluation of hematopoiesis revealed that deletion of Cdc42 using the Osterix, but not the Collagen-a1(I) promoter increase…

Genetically modified mousemusculoskeletal diseasesOsteoblastsHistologyMyeloidStromal cellPhysiologyChemistryEndocrinology Diabetes and MetabolismCell DifferentiationOsteoblastmacromolecular substancesBone and BonesCell biologyMiceHaematopoiesismedicine.anatomical_structureOsteogenesismedicineAnimalsCell LineageMyelopoiesisBone marrowSignal transduction
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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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MicroRNAs and cellular phenotypy.

2010

This Essay explores the notion that specialized cells have unique vulnerabilities to environmental contingencies that microRNAs help to counteract. Given the ease with which new microRNAs evolve, they may serve as ideal facilitators for the emergence of new cell types.

GeneticsCognitive scienceMicroRNAsPhenotypeGene Expression RegulationBiochemistry Genetics and Molecular Biology(all)Gene Expression ProfilingmicroRNAAnimalsHumansCell DifferentiationBiologyGeneral Biochemistry Genetics and Molecular BiologyCell
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Complementation among developmental mutants in Aspergillus nidulans.

1973

In heterokaryons between pairs of aconidial mutants of Aspergillus nidulans one of the component strains usually shows a striking prevalance in the contribution to the conidial crop. By assuming that the prevailing strain is blocked earlier and the succumbent one later in the process of differentiation, a series of mutations can be arranged in a consistent order. Some mutant strains do not fit the scheme exactly but show a general tendency to be succumbent to “early” mutants and prevalent over the “late” ones. A criterion for arraying genes involved in differentiation according to the order of their physiological action is proposed.

GeneticsHeterokaryonCell NucleusbiologyStrain (chemistry)GenotypeUltraviolet RaysfungiMutantGenetic Complementation TestCell Differentiationbiology.organism_classificationAspergillus nidulansComplementationAspergillus nidulansMutationGeneticsRadiation GeneticsMolecular BiologyGeneMoleculargeneral genetics : MGG
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Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype

2007

Abstract Background Genetic instability is a hallmark of tumours and preneoplastic lesions. The predominant form of genome instability in human cancer is chromosome instability (CIN). CIN is characterized by chromosomal aberrations, gains or losses of whole chromosomes (aneuploidy), and it is often associated with centrosome amplification. Centrosomes control cell division by forming a bipolar mitotic spindle and play an essential role in the maintenance of chromosomal stability. However, whether centrosome amplification could directly cause aneuploidy is not fully established. Also, alterations in genes required for mitotic progression could be involved in CIN. A major candidate is represe…

Genome instabilityCancer ResearchCellular differentiationAneuploidyApoptosisCell CommunicationSpindle ApparatusBiologyProtein Serine-Threonine Kinaseslcsh:RC254-282Aurora KinasesChromosome instabilityChromosomal InstabilitymedicineTumor Cells CulturedGeneticsHumansRNA Small InterferingMitosisIn Situ Hybridization FluorescenceAurora Kinase ACentrosomePloidiesReverse Transcriptase Polymerase Chain ReactionAurora-A centrosomes amplification aneuploidyCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAneuploidyCell biologySpindle apparatusUp-RegulationSettore BIO/18 - GeneticaCell Transformation NeoplasticPhenotypeMicroscopy FluorescenceOncologyCentrosomeColonic NeoplasmsEctopic expressionMicrosatellite InstabilityResearch ArticleBMC Cancer
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Neuronal Cell Nuclear Factor. A Nuclear Receptor Possibly Involved in the Control of Neurogenesis and Neuronal Differentiation

1997

We have cloned from a cDNA library of neuronal derivatives of retinoic-acid-induced embryonic carcinoma cells a nuclear receptor that may be involved in the control of late neurogenesis and early neuronal differentiation. The receptor which is practically identical in sequence with germ cell nuclear factor, has been designated neuronal cell nuclear factor (NCNF). NCNF is exclusively expressed in the neuronal derivatives of PCC7-Mz1 cells, with the expression beginning within hours of exposure to retinoic acid. In the developing mouse brain, NCNF is expressed in the marginal zones of the neuroepithelium which are known to contain young postmitotic neurons. NCNF binds to the DRO sequence ther…

Germ cell nuclear factorRetinoic acidReceptors Cytoplasmic and NuclearTretinoinBiologyLigandsBiochemistryMicechemistry.chemical_compoundNuclear Receptor Subfamily 6 Group A Member 1Tumor Cells CulturedAnimalsCloning MolecularReceptorIn Situ HybridizationNuclear receptor co-repressor 1NeuronsNeurogenesisBrainGene Expression Regulation DevelopmentalCell DifferentiationDNABlotting NorthernMolecular biologyDNA-Binding ProteinsRepressor ProteinsNeuroepithelial cellNuclear receptor coactivator 1Blotting SouthernOligodeoxyribonucleotidesnervous systemchemistryNuclear receptorEuropean Journal of Biochemistry
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