Search results for "Suppressor"

showing 10 items of 532 documents

Delayed ageing through damage protection by the Arf/p53 pathway.

2007

The tumour-suppressor pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its potent cancer protection activity. Similar to cancer, ageing also results from the accumulation of damage and, therefore, we have reasoned that Arf/p53 could have anti-ageing activity by alleviating the load of age-associated damage. Here we show that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage. These obser…

Cell signalingAgingTime FactorsTumor suppressor geneLongevityBiologymedicine.disease_causeAntioxidantsTranscriptomeMiceCDKN2ANeoplasmsmedicineAnimalsCells CulturedCyclin-Dependent Kinase Inhibitor p16MultidisciplinaryCell cycleFibroblastsCell biologyOxidative StressAgeingDisease SusceptibilitySignal transductionTumor Suppressor Protein p53Oxidative stressNature
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p53 as the main traffic controller of the cell signaling network

2010

Among different pathological conditions that affect human beings, cancer has received a great deal of attention primarily because it leads to significant morbidity and mortality. This is essentially due to increasing world-wide incidence of this disease and the inability to discover the cause and molecular mechanisms by which normal human cells acquire the characteristics that define cancer cells. Since the discovery of p53 over a quarter of a century ago, it is now recognized that virtually all cell fate pathways of live cells and the decision to die are under the control of p53. Such extensive involvement indicates that p53 protein is acting as a major traffic controller in the cell signa…

Cell signalingSettore MED/06 - Oncologia MedicaApoptosisDiseaseCell fate determinationBiologyNeoplasmsmedicineApoptosis; Cellular Senescence; Gene Expression Regulation Neoplastic; Humans; Mutation; Neoplasms; Polymorphism Genetic; Signal Transduction; Tumor Suppressor Protein p53HumansCellular SenescencePolymorphism GeneticCancerApoptosiCell cyclemedicine.diseaseCell biologyGene Expression Regulation NeoplasticThe Hallmarks of CancerApoptosisCancer cellMutationNeoplasmTumor Suppressor Protein p53HumanSignal Transduction
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Mind-body medicine: stress and its impact on overall health and longevity.

2005

During evolution, DNA viruses have captured a broad array of cellular genes involved in immune recognition and growth control that are nonessential for viral replication. The encoded virokines and viroceptors may act as mimetics or antagonists of their cellular homologues, altering signal transduction and cell communication towards survival of virus-infected cells. Human herpesvirus type 8 (HHV8) is the most recently identified human oncogenic herpesvirus. It is associated with Kaposi's sarcoma and lymphoproliferative diseases, such as pleural effusion lymphomas and multicentric Castleman's disease. HHV8 has captured a unique number of cellular regulatory genes, which redirect gene expressi…

Cell signalingTumor suppressor genemedicine.medical_treatmentLongevityBiologyVirokineGeneral Biochemistry Genetics and Molecular BiologyMind-Body Relations MetaphysicalParacrine signallingHistory and Philosophy of ScienceStress PhysiologicalNeoplasmsmedicineHumansDiseaseAutocrine signallingGeneral Neurosciencevirus diseasesBrainPsychoneuroimmunologyCytokineViral replicationHealthImmunologyCancer researchSignal transductionAnnals of the New York Academy of Sciences
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Cre-mediated cell ablation contests mast cell contribution in models of antibody- and T cell-mediated autoimmunity.

2011

SummaryImmunological functions of mast cells remain poorly understood. Studies in Kit mutant mice suggest key roles for mast cells in certain antibody- and T cell-mediated autoimmune diseases. However, Kit mutations affect multiple cell types of both immune and nonimmune origin. Here, we show that targeted insertion of Cre-recombinase into the mast cell carboxypeptidase A3 locus deleted mast cells in connective and mucosal tissues by a genotoxic Trp53-dependent mechanism. Cre-mediated mast cell eradication (Cre-Master) mice had, with the exception of a lack of mast cells and reduced basophils, a normal immune system. Cre-Master mice were refractory to IgE-mediated anaphylaxis, and this defe…

Cell typeEncephalomyelitis Autoimmune ExperimentalCarboxypeptidases AT cellT-LymphocytesImmunologyAutoimmunityImmunoglobulin E03 medical and health sciencesMice0302 clinical medicineImmune systemTh2 CellsmedicineImmunology and AllergyAnimalsGenetic Predisposition to DiseaseMast CellsIntestinal MucosaInterleukin 5Anaphylaxis030304 developmental biologyAutoantibodiesMice Knockout0303 health sciencesStem Cell FactorbiologyIntegrasesGene Expression ProfilingImmunoglobulin EMast cellArthritis Experimental3. Good healthInterleukin 33Mice Inbred C57BLDisease Models Animalmedicine.anatomical_structureInfectious DiseasesImmunologyGene Targetingbiology.proteinAntibodyTumor Suppressor Protein p53030215 immunologyImmunity
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Mast Cell–deficient KitW-sh “Sash” Mutant Mice Display Aberrant Myelopoiesis Leading to the Accumulation of Splenocytes That Act as Myeloid-Derived S…

2013

Abstract Mast cell-deficient KitW-sh “sash” mice are widely used to investigate mast cell functions. However, mutations of c-Kit also affect additional cells of hematopoietic and nonimmune origin. In this study, we demonstrate that KitW-sh causes aberrant extramedullary myelopoiesis characterized by the expansion of immature lineage-negative cells, common myeloid progenitors, and granulocyte/macrophage progenitors in the spleen. A consistent feature shared by these cell types is the reduced expression of c-Kit. Populations expressing intermediate and high levels of Ly6G, a component of the myeloid differentiation Ag Gr-1, are also highly expanded in the spleen of sash mice. These cells are …

Cell typeMyeloidT cellImmunologyBiologyImmunophenotypingMice03 medical and health sciences0302 clinical medicineNeoplasmsmedicineAnimalsAntigens LyImmunology and AllergyMyeloid CellsMast CellsProgenitor cell030304 developmental biologyMice KnockoutMyelopoiesis0303 health sciencesCD11b AntigenMast cellAdoptive Transfer3. Good healthCell biologyProto-Oncogene Proteins c-kitHaematopoiesismedicine.anatomical_structureHematopoiesis ExtramedullaryMutationImmunologyMyeloid-derived Suppressor CellFemaleMyelopoiesisNeoplasm TransplantationSpleen030215 immunologyThe Journal of Immunology
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OTUB1 inhibits CNS autoimmunity by preventing IFN-γ-induced hyperactivation of astrocytes.

2019

Astrocytes are critical regulators of neuroinflammation in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Growing evidence indicates that ubiquitination of signaling molecules is an important cell‐intrinsic mechanism governing astrocyte function during MS and EAE. Here, we identified an upregulation of the deubiquitinase OTU domain, ubiquitin aldehyde binding 1 (OTUB1) in astrocytes during MS and EAE. Mice with astrocyte‐specific OTUB1 ablation developed more severe EAE due to increased leukocyte accumulation, proinflammatory gene transcription, and demyelination in the spinal cord as compared to control mice. OTUB1‐deficient astrocytes were hy…

Central Nervous SystemEncephalomyelitis Autoimmune ExperimentalNeuroimmunomodulationmedicine.medical_treatmentexperimental autoimmune encephalomyelitisAutoimmunityBiologymultiple sclerosisubiquitinationGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineastrocytemedicineAnimalsMolecular BiologyCells CulturedNeuroinflammation030304 developmental biologyMice Knockout0303 health sciencesGeneral Immunology and MicrobiologySuppressor of cytokine signaling 1General NeuroscienceExperimental autoimmune encephalomyelitisArticlesmedicine.disease3. Good healthCell biologyMice Inbred C57BLCysteine EndopeptidasesCytokinemedicine.anatomical_structureAnimals NewbornAstrocytesSTAT proteinOTUB1FemaleNeurogenic InflammationJanus kinase030217 neurology & neurosurgeryAstrocyte
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Kif3a interacts with Dynactin subunit p150 Glued to organize centriole subdistal appendages.

2013

Formation of cilia, microtubule-based structures that function in propulsion and sensation, requires Kif3a, a subunit of Kinesin II essential for intraflagellar transport (IFT). We have found that, Kif3a is also required to organize centrioles. In the absence of Kif3a, the subdistal appendages of centrioles are disorganized and lack p150(Glued) and Ninein. Consequently, microtubule anchoring, centriole cohesion and basal foot formation are abrogated by loss of Kif3a. Kif3a localizes to the mother centriole and interacts with the Dynactin subunit p150(Glued) . Depletion of p150(Glued) phenocopies the effects of loss of Kif3a, indicating that Kif3a recruitment of p150(Glued) is critical for s…

CentrioleKnockoutKinesinsBiologycentriole cohesionKif3aMedical and Health SciencesArticleGeneral Biochemistry Genetics and Molecular BiologyMiceMicrotubuleIntraflagellar transportInformation and Computing SciencesAnimalsHumansKIF3AMicrotubule anchoringMolecular BiologyCentriolesMice KnockoutGeneral Immunology and MicrobiologyGeneral NeuroscienceCiliumTumor Suppressor ProteinsNuclear ProteinsKinesinDynactin ComplexBiological SciencesCell biologyCytoskeletal ProteinscentrosomeCentrosomeHela CellsDynactinGeneric health relevanceMicrotubule-Associated Proteinsp150(Glued)HeLa Cellssubdistal appendageDevelopmental Biology
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Mechanisms of ceramide-induced COX-2-dependent apoptosis in human ovarian cancer OVCAR-3 cells partially overlapped with resveratrol.

2013

Ceramide is a member of the sphingolipid family of bioactive molecules demonstrated to have profound, diverse biological activities. Ceramide is a potential chemotherapeutic agent via the induction of apoptosis. Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation. Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide. Induct…

CeramideMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesApoptosisBiologyResveratrolCeramidesBiochemistryp38 Mitogen-Activated Protein KinasesGene Expression Regulation Enzymologicchemistry.chemical_compoundCell Line TumorStilbenesHumansPhosphorylationRNA Small InterferingMolecular BiologyNitrobenzenesCaspase 7Membrane Potential MitochondrialOvarian NeoplasmsSulfonamidesKinaseCaspase 3Anti-Inflammatory Agents Non-SteroidalCell BiologyLipid signalingSphingolipidCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCyclooxygenase 2ResveratrolFemaleSignal transductionTumor Suppressor Protein p53Journal of cellular biochemistry
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p53 is involved in regulation of the DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT) by DNA damaging agents

1998

The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is inducible by genotoxic stress. MGMT induction results from transcriptional activation of the MGMT gene which is a specific response to DNA damage. A possible factor involved in triggering MGMT induction might be p53, because both p53 and MGMT are activated by DNA breaks. To study the effect of p53 on induction of the MGMT gene, we compared the presence of functional wild-type (wt) and mutant p53 with MGMT expression level in various mouse fibroblasts and rat hepatoma cell lines upon genotoxic treatment. Cells which responded to ionizing radiation (IR) by MGMT induction displayed functional p53, whereas in cells not expr…

Chloramphenicol O-AcetyltransferaseCancer ResearchMethyltransferaseDNA RepairDNA damageDNA repairRecombinant Fusion ProteinsBiologyTransfectionDNA methyltransferaseDNA AntisenseGene Expression Regulation EnzymologicMiceO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalGene expressionDNA Repair ProteinTumor Cells CulturedGeneticsAnimalsCancer epigeneticsPromoter Regions GeneticneoplasmsMolecular BiologyCell NucleusMice KnockoutCell Cycle3T3 CellsTransfectionGenes p53Molecular biologydigestive system diseasesRatsCancer researchTumor Suppressor Protein p53DNA DamageOncogene
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p53-Mediated downregulation of H ferritin promoter transcriptional efficiency via NF-Y.

2008

The tumor suppressor protein p53 triggers many of the cellular responses to DNA damage by regulating the transcription of a series of downstream target genes. p53 acts on the promoter of the target genes by interacting with the trimeric transcription factor NF-Y. H ferritin promoter activity is tightly dependent on a multiprotein complex called Bbf; on this complex NF-Y plays a major role. The aim of this work was to study the modulation of H ferritin expression levels by p53. CAT reporter assays indicate that: (i) p53 overexpression strongly downregulates the transcriptional efficiency driven by an H ferritin promoter construct containing only the NF-Y recognition sequence and that the phe…

Chromatin ImmunoprecipitationMultiprotein complexTranscription GeneticDown-RegulationBiologyBiochemistryTranscriptional regulationDownregulation and upregulationTranscription (biology)Transcriptional regulationFerritin geneHumansElectrophoretic mobility shift assayp300-CBP Transcription FactorsPromoter Regions GeneticTranscription factorGeneFerritin gene; Transcriptional regulation; Transcriptional factorCell BiologyHCT116 CellsMolecular biologyGene Expression Regulation NeoplasticCCAAT-Binding FactorDoxorubicinTranscriptional factorApoferritinsTumor Suppressor Protein p53Chromatin immunoprecipitationHeLa CellsProtein Binding
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