Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Usher syndrome: molecular links of pathogenesis, proteins and pathways.

2006

Contains fulltext : 50437.pdf (Publisher’s version ) (Closed access) Usher syndrome is the most common form of deaf-blindness. The syndrome is both clinically and genetically heterogeneous, and to date, eight causative genes have been identified. The proteins encoded by these genes are part of a dynamic protein complex that is present in hair cells of the inner ear and in photoreceptor cells of the retina. The localization of the Usher proteins and the phenotype in animal models indicate that the Usher protein complex is essential in the morphogenesis of the stereocilia bundle in hair cells and in the calycal processes of photoreceptor cells. In addition, the Usher proteins are important in…

Genetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeCell Cycle ProteinsNerve Tissue ProteinsBiologyRetinaAdherens junctionMiceHair Cells AuditoryCell polarityGeneticsmedicineotorhinolaryngologic diseasesNeurosensory disorders [UMCN 3.3]AnimalsHumansProtein IsoformsCell Cycle ProteinMolecular BiologyGenetics (clinical)Renal disorder [IGMD 9]Adaptor Proteins Signal TransducingStereociliumMembrane ProteinsSignal transducing adaptor proteinGeneral MedicineActin cytoskeletonmedicine.diseaseeye diseasesCell biologyCytoskeletal ProteinsGenetic defects of metabolism [UMCN 5.1]Ear InnerMultiprotein ComplexesCateninSynapsessense organsUsher SyndromesPhotoreceptor Cells Vertebrate
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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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Mutations in KIAA0586 Cause Lethal Ciliopathies Ranging from a Hydrolethalus Phenotype to Short-Rib Polydactyly Syndrome

2015

KIAA0586, the human ortholog of chicken TALPID3, is a centrosomal protein that is essential for primary ciliogenesis. Its disruption in animal models causes defects attributed to abnormal hedgehog signaling; these defects include polydactyly and abnormal dorsoventral patterning of the neural tube. Here, we report homozygous mutations of KIAA0586 in four families affected by lethal ciliopathies ranging from a hydrolethalus phenotype to short-rib polydactyly. We show defective ciliogenesis, as well as abnormal response to SHH-signaling activation in cells derived from affected individuals, consistent with a role of KIAA0586 in primary cilia biogenesis. Whereas centriolar maturation seemed una…

Heart Defects CongenitalMolecular Sequence DataCell Cycle ProteinsBiologyShort Rib-Polydactyly SyndromeCiliopathies03 medical and health sciencesFatal OutcomeCiliogenesisReportGLI3GeneticsmedicineHumansGenetics(clinical)Europe EasternGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesLikelihood FunctionsShort rib – polydactyly syndromePolydactylyBase SequenceCilium030305 genetics & hereditySequence Analysis DNAmedicine.diseasePhenotypeHuman geneticsHedgehog signaling pathwayFounder EffectPedigreePhenotypeCodon NonsenseCentriolar satelliteErratumHand Deformities CongenitalCiliary Motility DisordersHydrocephalus
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Polo-like kinase 1 as a target for human cytomegalovirus pp65 lower matrix protein

1999

ABSTRACT Human cytomegalovirus (HCMV) pp65 protein is the major constituent of viral dense bodies but is dispensable for viral growth in vitro. pp65 copurifies with a S/T kinase activity and has been implicated in phosphorylation of HCMV IE1 immediate-early protein and its escape from major histocompatibility complex 1 presentation. Furthermore, the presence of pp65 correlates with a virion-associated kinase activity. To clarify the role of pp65, yeast two-hybrid system (THS) screening was performed to identify pp65 cellular partners. A total of 18 out of 48 yeast clones harboring cDNAs for putative pp65 binding proteins encoded the Polo-like kinase 1 (Plk1) C-terminal domain. Plk1 behaved …

Human cytomegalovirusvirusesRecombinant Fusion ProteinsImmunologyCytomegalovirusCell Cycle ProteinsPolo-like kinaseBiologyProtein Serine-Threonine KinasesMicrobiologyDNA-binding proteinPLK1Cell LineViral Matrix ProteinsVirologyProto-Oncogene ProteinsmedicineAnimalsHumansKinase activityViral matrix proteinKinasevirus diseasesmedicine.diseasePhosphoproteinsMolecular biologyVirus-Cell Interactionssurgical procedures operativeInsect ScienceCOS CellsPhosphorylationProtein KinasesHeLa Cells
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Ubiquitin-independent function of optineurin in autophagic clearance of protein aggregates.

2013

Summary Aggregation of misfolded proteins and the associated loss of neurons are considered a hallmark of numerous neurodegenerative diseases. Optineurin is present in protein inclusions observed in various neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Huntington's disease, Alzheimer's disease, Parkinson's disease, Creutzfeld-Jacob disease and Pick's disease. Optineurin deletion mutations have also been described in ALS patients. However, the role of optineurin in mechanisms of protein aggregation remains unclear. In this report, we demonstrate that optineurin recognizes various protein aggregates via its C-terminal coiled-coil domain in a ubiquitin-independent m…

HuntingtinSOD1AggrephagyCell Cycle ProteinsMice TransgenicProtein aggregationBiologyArticle03 medical and health sciencesMice0302 clinical medicineTANK-binding kinase 1UbiquitinTranscription Factor TFIIIAAutophagyAnimalsHumansPhosphorylationZebrafishZebrafish030304 developmental biologyOptineurin0303 health sciencesUbiquitinamyotrophic lateral sclerosis; Huntington disease; Huntingtin; optineurin; phosphorylation; SOD1; TBK1; ubiquitinMembrane Transport ProteinsNeurodegenerative DiseasesCell Biologybiology.organism_classification3. Good healthMice Inbred C57BLDisease Models AnimalCancer researchbiology.protein030217 neurology & neurosurgeryHeLa CellsProtein BindingJournal of cell science
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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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Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Yeast Dun1 Kinase Regulates Ribonucleotide Reductase Inhibitor Sml1 in Response to Iron Deficiency

2014

Iron is an essential micronutrient for all eukaryotic organisms because it participates as a redox-active cofactor in many biological processes, including DNA replication and repair. Eukaryotic ribonucleotide reductases (RNRs) are Fe-dependent enzymes that catalyze deoxyribonucleoside diphosphate (dNDP) synthesis. We show here that the levels of the Sml1 protein, a yeast RNR large-subunit inhibitor, specifically decrease in response to both nutritional and genetic Fe deficiencies in a Dun1-dependent but Mec1/Rad53- and Aft1-independent manner. The decline of Sml1 protein levels upon Fe starvation depends on Dun1 forkhead-associated and kinase domains, the 26S proteasome, and the vacuolar pr…

Iron-Sulfur ProteinsProteasome Endopeptidase ComplexSaccharomyces cerevisiae ProteinsDeoxyribonucleoside triphosphateRibonucleotideIronDeoxyribonucleotidesGenes FungalSaccharomyces cerevisiaeCell Cycle ProteinsSaccharomyces cerevisiaeRibonucleotide reductase inhibitorProtein Serine-Threonine KinasesBiologyProtein degradationchemistry.chemical_compoundTristetraprolinRibonucleotide ReductasesAspartic Acid EndopeptidasesPhosphorylationMolecular BiologyCheckpoint Kinase 2Binding SitesKinaseIntracellular Signaling Peptides and ProteinsArticlesCell Biologybiology.organism_classificationDNA-Binding ProteinsDeoxyribonucleosideCheckpoint Kinase 2chemistryBiochemistryProteolysisGene DeletionTranscription FactorsMolecular and Cellular Biology
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