Search results for "Deubiquitinating enzyme"

showing 5 items of 15 documents

Hematopoietic stem cell quiescence and function are controlled by the CYLD–TRAF2–p38MAPK pathway

2015

Tesio at al. identify a novel pathway controlled by the tumor suppressor and deubiquitinase cylindromatosis (CYLD), which is involved in the regulation of hematopoietic stem cell quiescence and repopulation potential.

TRAF2Tumor suppressor geneMAP Kinase Signaling SystemImmunologyRegulatorBiologyp38 Mitogen-Activated Protein KinasesArticleMicemedicineAnimalsImmunology and AllergyMice KnockoutRegulation of gene expressionNF-kappa BHematopoietic stem cellCell BiologyHematopoietic Stem CellsTNF Receptor-Associated Factor 2PhenotypeDeubiquitinating Enzyme CYLDCell biologyCysteine EndopeptidasesHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutationStem cellJournal of Experimental Medicine
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The tumor suppressor CYLD controls the function of murine regulatory T cells.

2012

Abstract CYLD was originally identified as a tumor suppressor gene mutated in familial cylindromatosis, an autosomal dominant predisposition to multiple benign neoplasms of the skin known as cylindromas. The CYLD protein is a deubiquitinating enzyme that acts as a negative regulator of NF-κB and JNK signaling through its interaction with NEMO and TNFR-associated factor 2. We have previously described a novel mouse strain that expresses solely and excessively a naturally occurring splice variant of CYLD (CYLDex7/8). In this study, we demonstrate that CYLD plays a critical role in Treg development and function. T cells of CYLDex7/8 mice had a hyperactive phenotype manifested by increased prod…

Tumor suppressor geneT cellImmunologyBiologyT-Lymphocytes RegulatoryDeubiquitinating Enzyme CYLDlaw.inventionProinflammatory cytokineMicelawmedicineImmunology and AllergyAnimalsCTLA-4 AntigenIL-2 receptorTumor Suppressor ProteinsInterleukin-2 Receptor alpha SubunitIntracellular Signaling Peptides and ProteinsNF-kappa BFOXP3PhenotypeMice Mutant StrainsCell biologyDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structureGene Expression RegulationImmunologySuppressorJournal of immunology (Baltimore, Md. : 1950)
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Naturally occurring short splice variant of CYLD positively regulates dendritic cell function

2009

Abstract Deubiquitination of NF-κB members by CYLD is crucial in controlling the magnitude and nature of cell activation. The role of the naturally occurring CYLD splice variant in dendritic cell (DC) function was analyzed using CYLDex7/8 mice, which lack the full-length CYLD (flCYLD) transcript and overexpress the short splice variant (sCYLD). Bone marrow–derived DCs from CYLDex7/8 mice display a hyperactive phenotype in vitro and in vivo and have a defect in establishing tolerance with the use of DEC-205–mediated antigen targeting to resting DCs. The combination of sCYLD overexpression and lack of flCYLD in CYLDex7/8 DCs leads to enhanced NF-κB activity accompanied by an increased nuclear…

Tumor suppressor geneTransgeneImmunologyRegulatorMice TransgenicBiologyBiochemistryDeubiquitinating Enzyme CYLDMiceAnimalsAntigen-presenting cellNF-kappa BDendritic CellsCell BiologyHematologyDendritic cellDeubiquitinating Enzyme CYLDCell biologyMice Inbred C57BLAlternative SplicingCysteine EndopeptidasesPhenotypeImmunologySignal transductionCell activationSignal TransductionBlood
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The deubiquitinating enzyme CYLD regulates the differentiation and maturation of thymic medullary epithelial cells.

2014

The cross talk between thymocytes and the thymic epithelium is critical for T-cell development and the establishment of central tolerance. Medullary thymic epithelial cells (mTECs) are located in the thymic medulla and mediate the elimination of self-reactive thymocytes, thereby preventing the onset of autoimmunity. Previous studies identified the deubiquitinating enzyme CYLD as a critical regulator of T-cell development by activating proximal T-cell receptor signaling during the transition of double-positive to single-positive thymocytes. Here we evaluated the impact of the naturally occurring short-splice variant of the cyld gene (sCYLD) on the development and maturation of mTECs. We foun…

medicine.medical_specialtyMedullary cavityImmunologyReceptors Antigen T-CellCell CountThymus GlandBiologyDeubiquitinating Enzyme CYLDImmunophenotypingMiceInternal medicinemedicineImmunology and AllergyAnimalsMice KnockoutThymocytesUbiquitinationCell DifferentiationEpithelial CellsCell BiologyCell biologyDeubiquitinating Enzyme CYLDCysteine EndopeptidasesEndocrinologyPhenotypeAntigens SurfaceMutationFemaleSignal TransductionImmunology and cell biology
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Liver specific deletion of CYLDexon7/8 induces severe biliary damage, fibrosis and increases hepatocarcinogenesis in mice

2012

Background & Aims CYLD is a tumor suppressor gene that is mutated in familial cylindromatosis, an autosomal dominant predisposition to tumors of skin appendages. Reduced CYLD expression has been observed in other tumor entities, including hepatocellular carcinoma. In the present study, we analyzed the role of CYLD in liver homeostasis and hepatocarcinogenesis in vivo . Methods Mice with liver-specific deletion of CYLDexon7/8 ( CYLD FF xAlbCre ) were generated. Liver tissues were histologically analyzed and oval cell activation was investigated. Hepatocarcinogenesis was induced by diethylnitrosamine/phenobarbital (DEN/PB). Microarray expression profiling of livers was performed in untreated …

medicine.medical_specialtyTumor suppressor geneBiliary Tract DiseasesIn Vitro TechniquesBiologymedicine.disease_causeDimethylnitrosamineDeubiquitinating Enzyme CYLDMiceRisk FactorsFibrosisInternal medicinemedicineAnimalsHomeostasisGenetic Predisposition to DiseaseHepatologyLiver NeoplasmsExonsTransforming growth factor betamedicine.diseaseFibrosisMice Mutant StrainsDeubiquitinating Enzyme CYLDMice Inbred C57BLGene expression profilingCysteine EndopeptidasesDisease Models AnimalPhenotypeEndocrinologyLiverPhenobarbitalHepatocellular carcinomaCancer researchbiology.proteinCell activationCarcinogenesisGene DeletionJournal of Hepatology
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