Search results for "cyclin-dependent kinase"

showing 10 items of 164 documents

Escherichia coli cytolethal distending toxin blocks the HeLa cell cycle at the G2/M transition by preventing cdc2 protein kinase dephosphorylation an…

1997

Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized HeLa cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes cell accumulation in G2 and not in M, that it does not slow the progression of cells th…

G2 PhaseCytolethal distending toxinBacterial toxins[SDV]Life Sciences [q-bio]ImmunologyBacterial ToxinsMitosisBiologyMicrobiologyCDTCDC2 Protein KinaseEscherichia coliHumansKinase activityPhosphorylationMitosisCyclin-dependent kinase 1Cell growthCell CycleCell cycleG2-M DNA damage checkpointFlow CytometryMicrobiologie et ParasitologieCell biology[SDV] Life Sciences [q-bio]Enzyme ActivationInfectious DiseasesCytolethal distending toxinsParasitologyCDC2 Protein KinaseHeLa CellsResearch Article
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Type III Secretion-Dependent Cell Cycle Block Caused in HeLa Cells by Enteropathogenic Escherichia coliO103

2001

ABSTRACT Rabbit enteropathogenic Escherichia coli (EPEC) O103 induces in HeLa cells an irreversible cytopathic effect characterized by the recruitment of focal adhesions, formation of stress fibers, and inhibition of cell proliferation. We have characterized the modalities of the proliferation arrest and investigated its underlying mechanisms. We found that HeLa cells that were exposed to the rabbit EPEC O103 strain E22 progressively accumulated at 4C DNA content and did not enter mitosis. A significant proportion of the cells were able to reinitiate DNA synthesis without division, leading to 8C DNA content. This cell cycle inhibition by E22 was abrogated in mutants lacking EspA, -B, and -D…

G2 Phase[SDV]Life Sciences [q-bio]ImmunologyCyclin BMitosisReceptors Cell SurfacePATHOGENICITECyclin BMicrobiology03 medical and health sciencesBacterial ProteinsCDC2 Protein KinaseEscherichia coliHumansCyclin B1PhosphorylationCyclin B1Adhesins BacterialMitosisCytoskeleton030304 developmental biologyIntimin0303 health sciencesCyclin-dependent kinase 1Cellular Microbiology: Pathogen-Host Cell Molecular Interactionsbiology030306 microbiologyCell growthEscherichia coli ProteinsCell CycleREARRANGEMENTCell cycle[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyCell biology[SDV] Life Sciences [q-bio]Infectious Diseasesbiology.proteinTyrosineParasitologyCarrier ProteinsCDC2 Protein KinaseBacterial Outer Membrane ProteinsHeLa Cells
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Role of Gadd45a in Wip1-dependent regulation of intestinal tumorigenesis.

2012

Conversion of intestinal stem cells into tumor-initiating cells is an early step in Apc(Min)-induced polyposis. Wild-type p53-induced phosphatase 1 (Wip1)-dependent activation of a DNA damage response and p53 has a permanent role in suppression of stem cell conversion, and deletion of Wip1 lowers the tumor burden in Apc(Min) mice. Here we show that cyclin-dependent kinase inhibitor 2a, checkpoint kinase 2, and growth arrest and DNA damage gene 45a (Gadd45a) exert critical functions in the tumor-resistant phenotype of Wip1-deficient mice. We further identified Gadd45a as a haploinsufficient gene in the regulation of Wip1-dependent tumor resistance in mice. Gadd45a appears to function through…

Genes APCDNA RepairDNA repairDNA damageApoptosisCell Cycle ProteinsBiologyProtein Serine-Threonine KinasesReceptors G-Protein-CoupledMicePhosphoprotein PhosphatasesGene silencingAnimalsMolecular BiologyCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p16beta CateninMice KnockoutOriginal PaperKinaseIntestinal PolyposisStem CellsJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyCell biologyProtein Phosphatase 2CCheckpoint Kinase 2Cell Transformation NeoplasticCancer researchSignal transductionStem cellTumor Suppressor Protein p53GADD45ASignal TransductionCell death and differentiation
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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GM-CSF restores innate, but not adaptive, immune responses in glucocorticoid-immunosuppressed human blood in vitro.

2003

Abstract Infection remains the major complication of immunosuppressive therapy in organ transplantation. Therefore, reconstitution of the innate immunity against infections, without activation of the adaptive immune responses, to prevent graft rejection is a clinically desirable status in transplant recipients. We found that GM-CSF restored TNF mRNA and protein expression without inducing IL-2 production and T cell proliferation in glucocorticoid-immunosuppressed blood from either healthy donors or liver transplant patients. Gene array experiments indicated that GM-CSF selectively restored a variety of dexamethasone-suppressed, LPS-inducible genes relevant for innate immunity. A possible ex…

Graft RejectionLipopolysaccharidesT-LymphocytesCell Cycle ProteinsCell SeparationOrgan transplantationDexamethasoneMiceCDC2-CDC28 KinasesConcanavalin ATumor Cells CulturedImmunology and AllergySkin TransplantationMiddle AgedCyclin-Dependent KinasesUp-RegulationSurvival Ratemedicine.anatomical_structureImmunity ActiveTumor necrosis factor alphaGlucocorticoidCell DivisionCyclin-Dependent Kinase Inhibitor p27Immunosuppressive Agentsmedicine.drugAdultmedicine.medical_specialtyT cellImmunologyDown-RegulationBiologyProtein Serine-Threonine KinasesImmune systemAdjuvants ImmunologicIn vivomedicineAnimalsHumansDexamethasoneAgedSalmonella Infections AnimalInnate immune systemTumor Suppressor ProteinsCyclin-Dependent Kinase 2Granulocyte-Macrophage Colony-Stimulating FactorImmunity InnateGene Expression RegulationImmunologyLeukocytes MononuclearMice Inbred CBAInterleukin-2Interleukin-1Journal of immunology (Baltimore, Md. : 1950)
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The aryl hydrocarbon receptor-dependent deregulation of cell cycle control induced by polycyclic aromatic hydrocarbons in rat liver epithelial cells

2006

Disruption of cell proliferation control by polycyclic aromatic hydrocarbons (PAHs) may contribute to their carcinogenicity. We investigated role of the aryl hydrocarbon receptor (AhR) in disruption of contact inhibition in rat liver epithelial WB-F344 'stem-like' cells, induced by the weakly mutagenic benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF) and by the strongly mutagenic benzo[a]pyrene (BaP). There were significant differences between the effects of BaA and BbF, and those of the strongly genotoxic BaP. Both BaA and BbF increased percentage of cells entering S-phase and cell numbers, associated with an increased expression of Cyclin A and Cyclin A/cdk2 complex activity. Their eff…

Health Toxicology and MutagenesisCyclin AGene ExpressionApoptosisCell Cycle ProteinsCyclin ACell LineBenz(a)AnthracenesBenzo(a)pyreneCytochrome P-450 CYP1A1polycyclic compoundsGeneticsAnimalsRat liver ‘stem-like’ cellsRNA MessengerPolycyclic Aromatic HydrocarbonsRNA Small InterferingMolecular BiologyAryl hydrocarbon receptorCell proliferationCarcinogenCell ProliferationFluorenesBase SequencebiologyChemistryCell growthCell CycleCyclin-Dependent Kinase 2Contact inhibitionEpithelial CellsTransfectionAryl hydrocarbon receptorMolecular biologyPolycyclic aromatic hydrocarbonsPolycyclic Hydrocarbons AromaticRatsReceptors Aryl HydrocarbonBiochemistryApoptosisMultiprotein ComplexesContact inhibitionMutationHepatocytesbiology.proteinCDK inhibitorMutagensMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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p16INK4A (CDKN2A) gene deletion is a frequent genetic event in synovial sarcomas.

2006

We assessed the frequency of genomic deletion of p16 INK4A (CDKN2A) in synovial sarcomas (SSs) and its possible association with immunoexpression of p16 and cyclin D1 and the Ki-67 proliferation index using dualcolor fluorescence in situ hybridization (FISH) on tissue microarray sections of 41 histologically and molecularly confirmed SSs. A heterozygous p16 INK4A gene deletion was identified in 28 (74%) of 38 cases, with 25 (89%) of them showing abnormal p16 protein expression (20 negative and 5 heterogeneous). Of 25 cases, 19 (76%) exhibiting increased cyclin D1 expression also demonstrated heterozygous p16 INK4A deletion. No significant association was observed between p16 INK4A deletion …

HeterozygoteProliferation indexTumor suppressor geneSoft Tissue NeoplasmsBiologySarcoma SynovialCyclin D1CDKN2ACyclin DCyclinsmedicineBiomarkers TumorHumansCDKN2A Gene DeletionCyclin-Dependent Kinase Inhibitor p16In Situ Hybridization FluorescenceCell Nucleusmedicine.diagnostic_testGeneral Medicinemedicine.diseaseImmunohistochemistrySynovial sarcomaKi-67 AntigenTumor progressionTissue Array AnalysisCancer researchGene DeletionFluorescence in situ hybridizationAmerican journal of clinical pathology
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Suppressor activity of anergic T cells induced by IL-10-treated human dendritic cells: association with IL-2- and CTLA-4-dependent G1 arrest of the c…

2003

We have previously shown that human IL-10-treated dendritic cells (DC) induce an antigen-specific anergy in CD4+ T lymphocytes. These anergic T cells are characterized by an inhibited proliferation, a reduced production of IL-2, and additionally display antigen-specific suppressor activity. In this study we investigated the mechanisms underlying the anergic state and regulatory function of these T cells. We did not observe enhanced rates of programmed cell death of anergic CD4+ suppressor T cells compared to T cells stimulated with mature DC. Cell cycle analysis by DNA staining and Western blot experiments revealed an arrest of anergic CD4+ T suppressor cells in the G1 phase. High levels of…

ImmunoconjugatesRegulatory T cellT-LymphocytesImmunologyApoptosisCell Cycle ProteinsAbataceptCyclin-dependent kinaseAntigens CDmedicineImmunology and AllergyHumansCTLA-4 AntigenIL-2 receptorClonal AnergybiologyTumor Suppressor ProteinsRetinoblastoma proteinDendritic cellDendritic CellsCell cycleAntigens DifferentiationCell biologyInterleukin-10Interleukin 10medicine.anatomical_structurebiology.proteinInterleukin-2CDK inhibitorCell DivisionCyclin-Dependent Kinase Inhibitor p27European journal of immunology
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High-throughput screening with the Eimeria tenella CDC2-related kinase2/cyclin complex EtCRK2/EtCYC3a

2012

The poultry disease coccidiosis, caused by infection with Eimeria spp. apicomplexan parasites, is responsible for enormous economic losses to the global poultry industry. The rapid increase of resistance to therapeutic agents, as well as the expense of vaccination with live attenuated vaccines, requires the development of new effective treatments for coccidiosis. Because of their key regulatory function in the eukaryotic cell cycle, cyclin-dependent kinases (CDKs) are prominent drug targets. The Eimeria tenella CDC2-related kinase 2 (EtCRK2) is a validated drug target that can be activated in vitro by the CDK activator XlRINGO (Xenopus laevis rapid inducer of G2/M progression in oocytes). B…

In silicoPlasmodium falciparumAntiprotozoal AgentsDrug Evaluation PreclinicalProtozoan ProteinsMicrobiologyEimeriaMicrobiology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsparasitic diseasesCDC2 Protein KinaseAnimalsEnzyme Inhibitors030304 developmental biologyCyclin0303 health sciencesCyclin-dependent kinase 1biologyKinaseComputational BiologyPlasmodium falciparumCell cyclebiology.organism_classificationVirologyStandard3. Good healthHigh-Throughput Screening Assays030220 oncology & carcinogenesisCell and Molecular Biology of Microbesbiology.proteinEimeria tenellaMicrobiology
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Geldanamycin and its derivatives as Hsp90 inhibitors

2012

The Hsp90 molecule, one of the most abundant heat shock proteins in mammalian cells, maintains homeostasis and prevents stress-induced cellular damage. Hsp90 is expressed under normal conditions at a level of about 1-2 Percent of total proteins, while its expression increases 2-10 fold in cancer cells. The two main constitutively expressed isoforms of Hsp90 are known as Hsp90-alpha and Hsp90-beta, and their upregulation is associated with tumor progression, invasion and formation of metastases, as well as development of drug resistance. The Hsp90 is a key target for many newly established, potent anticancer agents containing Hsp90 N-terminal ATP binding inhibitors, such as geldanamycin, and…

IndolesLactams MacrocyclicCyclin-Dependent KinaseAntineoplastic AgentsTanespimycinBenzoquinoneModels BiologicalAntineoplastic Agentchemistry.chemical_compoundDownregulation and upregulationTransforming Growth Factor betaCyclin-dependent kinaseHeat shock proteinBenzoquinonespolycyclic compoundsAnimalsHumansHSP90 Heat-Shock ProteinsbiologyAnimalTriazolesGeldanamycinHsp90Cyclin-Dependent KinasesProto-Oncogene Proteins c-rafHSP90 Heat-Shock Proteinsrc-Family KinaseschemistryTumor progressionMutationCancer cellbiology.proteinCancer researchMacrolidesMacrolideTriazoleTumor Suppressor Protein p53Animals; Antineoplastic Agents; Benzoquinones; Cyclin-Dependent Kinases; HSP90 Heat-Shock Proteins; Humans; Lactams Macrocyclic; Macrolides; Models Biological; Mutation; Novobiocin; Proto-Oncogene Proteins c-raf; Transforming Growth Factor beta; Triazoles; Tumor Suppressor Protein p53; src-Family KinasesNovobiocinHumanFrontiers in Bioscience
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