Search results for "Cell Cycle Protein"

showing 10 items of 131 documents

Centriolar satellites expedite mother centriole remodeling to promote ciliogenesis

2023

Centrosomes are orbited by centriolar satellites, dynamic multiprotein assemblies nucleated by Pericentriolar material 1 (PCM1). To study the requirement for centriolar satellites, we generated mice lacking PCM1, a crucial component of satellites. Pcm1−/− mice display partially penetrant perinatal lethality with survivors exhibiting hydrocephalus, oligospermia, and cerebellar hypoplasia, and variably expressive phenotypes such as hydronephrosis. As many of these phenotypes have been observed in human ciliopathies and satellites are implicated in cilia biology, we investigated whether cilia were affected. PCM1 was dispensable for ciliogenesis in many cell types, whereas Pcm1−/− multiciliated…

Cell Cycle Proteins/geneticsBiologiaGeneral Immunology and MicrobiologyCytoskeletal Proteins/metabolismGeneral NeuroscienceMothersGeneral MedicineGeneral Biochemistry Genetics and Molecular BiologyCentrioles/metabolismCentrosome/metabolismMiceCilia/metabolismAnimalsHumansFemaleeLife
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Role of nuclear glutathione as a key regulator of cell proliferation.

2009

Glutathione (GSH) is essential for survival of eukaryotic but not in prokaryotic cells. Its functions in nucleated cells are far from being known. In fact GSH plays an important role in cell proliferation. The purpose of the present review is to summarize the relationship between glutathione and the important events that take place in the nucleus during the cell cycle. Most GSH co-localizes with nuclear DNA when cells are proliferating. However, when cells were confluent no differences between nucleus and cytoplasm could be seen. A number of relevant nuclear proteins are strictly dependent on nuclear redox status. For instance, we found that telomerase is regulated by shifts in glutathione …

CellsClinical BiochemistryBiochemistryEpigenesis Geneticchemistry.chemical_compoundAnimalsHumansEpigeneticsNuclear proteinCell Cycle ProteinMolecular BiologyTelomeraseCell ProliferationbiologyCell growthGeneral MedicineGlutathioneCell cycleGlutathioneCell biologyOxidative StressHistoneBiochemistrychemistryCytoplasmbiology.proteinMolecular MedicineMolecular aspects of medicine
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Epigenetic Transcriptional Regulation of the Growth Arrest-Specific gene 1 (Gas1) in Hepatic Cell Proliferation at Mononucleosomal Resolution

2011

Background Gas1 (growth arrest-specific 1) gene is known to inhibit cell proliferation in a variety of models, but its possible implication in regulating quiescence in adult tissues has not been examined to date. The knowledge of how Gas1 is regulated in quiescence may contribute to understand the deregulation occurring in neoplastic diseases. Methodology/Principal Findings Gas1 expression has been studied in quiescent murine liver and during the naturally synchronized cell proliferation after partial hepatectomy. Chromatin immunoprecipitation at nucleosomal resolution (Nuc-ChIP) has been used to carry out the study preserving the in vivo conditions. Transcription has been assessed at real …

Chromatin ImmunoprecipitationTranscription GeneticGene Expressionlcsh:MedicineCell Cycle ProteinsRNA polymerase IIBiologyGPI-Linked ProteinsMethylationHistone DeacetylasesChromatin remodelingEpigenesis GeneticS PhaseHistonesMiceMolecular Cell BiologyTranscriptional regulationAnimalsHepatectomyEpigeneticsPromoter Regions Geneticlcsh:ScienceBiologyCell ProliferationHistone AcetyltransferasesRegulation of gene expressionMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionGene Expression Profilinglcsh:RG1 PhaseAcetylationHistone ModificationImmunohistochemistryMolecular biologyChromatinNucleosomesChromatinHistoneGene Expression RegulationLiverbiology.proteinlcsh:QTranscription Initiation SiteChromatin immunoprecipitationProtein BindingResearch ArticlePLoS ONE
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Proliferation state and polo-like kinase1 dependence of tumorigenic colon cancer cells.

2012

Abstract Tumor-initiating cells are responsible for tumor maintenance and relapse in solid and hematologic cancers. Although tumor-initiating cells were initially believed to be mainly quiescent, rapidly proliferating tumorigenic cells were found in breast cancer. In colon cancer, the proliferative activity of the tumorigenic population has not been defined, although it represents an essential parameter for the development of more effective therapeutic strategies. Here, we show that tumorigenic colon cancer cells can be found in a rapidly proliferating state in vitro and in vivo, both in human tumors and mouse xenografts. Inhibitors of polo-like kinase1 (Plk1), a mitotic kinase essential fo…

Colorectal cancerCancer stem cellscolorectal cancercell proliferationcell cycle.Cell Cycle ProteinsMice0302 clinical medicineMice Inbred NODAC133 AntigenRNA Small Interfering0303 health scienceseducation.field_of_studyPteridinesCell CycleCell cycleImmunohistochemistry3. Good healthMitochondriaGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColonic NeoplasmsMolecular MedicineFemaleStem cellPopulationTransplantation HeterologousCell Growth ProcessesBiologyProtein Serine-Threonine KinasesPLK103 medical and health sciencesCancer stem cellAntigens CDCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumanseducationProtein Kinase Inhibitors030304 developmental biologyGlycoproteinsSettore MED/04 - Patologia GeneraleCell growthCell Biologymedicine.diseaseTumor progressionImmunologyCancer researchPeptidesDevelopmental BiologyStem cells (Dayton, Ohio)
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Ikaros-1 couples cell cycle arrest of late striatal precursors with neurogenesis of enkephalinergic neurons

2010

et al.

Cyclin-Dependent Kinase Inhibitor p21CalbindinsEnkephalinNeurogenesiseducationCentral nervous systemCell Cycle ProteinsStriatumSubstance PBiologyEfferent PathwaysCalbindinIkaros Transcription FactorMiceS100 Calcium Binding Protein GmedicineAnimalsProgenitor cellTranscription factorhealth care economics and organizationsHomeodomain ProteinsMice KnockoutNeuronsStem CellsGeneral NeuroscienceNeurogenesisCell DifferentiationEnkephalinsCell cycleCorpus StriatumGenes cdcMice Inbred C57BLmedicine.anatomical_structurenervous systemTrans-ActivatorsNeuroscienceTranscription FactorsThe Journal of Comparative Neurology
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A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma.

1995

A mutated cyclin-dependent kinase 4 (CDK4) was identified as a tumor-specific antigen recognized by HLA-A2. 1-restricted autologous cytolytic T lymphocytes (CTLs) in a human melanoma. The mutated CDK4 allele was present in autologous cultured melanoma cells and metastasis tissue, but not in the patient's lymphocytes. The mutation, an arginine-to-cysteine exchange at residue 24, was part of the CDK4 peptide recognized by CTLs and prevented binding of the CDK4 inhibitor p16INK4a, but not of p21 or of p27KIP1. The same mutation was found in one additional melanoma among 28 melanomas analyzed. These results suggest that mutation of CDK4 can create a tumor-specific antigen and can disrupt the ce…

Cyclin-Dependent Kinase Inhibitor p21Tumor suppressor geneMutantMolecular Sequence DataCell Cycle ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeTransfectionPolymerase Chain ReactionMetastasisCell LineAntigenCyclinsProto-Oncogene ProteinsHLA-A2 AntigenmedicineTumor Cells CulturedAnimalsHumansPoint MutationAmino Acid SequenceCloning MolecularneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15MutationMultidisciplinaryintegumentary systemBase SequenceMelanomaTumor Suppressor ProteinsCyclin-Dependent Kinase 4Cell cyclemedicine.diseaseCyclin-Dependent KinasesCytolysisCancer researchCarrier ProteinsMicrotubule-Associated ProteinsCyclin-Dependent Kinase Inhibitor p27T-Lymphocytes CytotoxicScience (New York, N.Y.)
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Regulation of ribonucleotide reductase in response to iron deficiency

2011

Ribonucleotide reductase (RNR) is an essential enzyme required for DNA synthesis and repair. Although iron is necessary for class Ia RNR activity, little is known about the mechanisms that control RNR in response to iron deficiency. In this work, we demonstrate that yeast cells control RNR function during iron deficiency by redistributing the Rnr2–Rnr4 small subunit from the nucleus to the cytoplasm. Our data support a Mec1/Rad53-independent mechanism in which the iron-regulated Cth1/Cth2 mRNA-binding proteins specifically interact with the WTM1 mRNA in response to iron scarcity, and promote its degradation. The resulting decrease in the nuclear-anchoring Wtm1 protein levels leads to the re…

CytoplasmSaccharomyces cerevisiae ProteinsDeoxyribonucleoside triphosphateRibonucleoside Diphosphate ReductaseRNA StabilityProtein subunitSaccharomyces cerevisiaeCell Cycle ProteinsSaccharomyces cerevisiaeProtein Serine-Threonine KinasesBiologyResponse ElementsArticleTristetraprolinGene Expression Regulation FungalRibonucleotide ReductasesHumansRNA MessengerMolecular BiologyTranscription factorCell NucleusDNA synthesisIntracellular Signaling Peptides and ProteinsFungal geneticsRNA-Binding ProteinsRNA FungalIron DeficienciesCell Biologybiology.organism_classificationDNA-Binding ProteinsRepressor ProteinsCheckpoint Kinase 2Protein SubunitsProtein TransportRibonucleotide reductaseBiochemistryCytoplasmTranscription Factors
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The DNA-binding subunit p140 of replication factor C is upregulated in cycling cells and associates with G 1 phase cell cycle regulatory proteins

1999

The DNA-binding subunit of replication factor C (RFCp140) plays an important role in both DNA replication and DNA repair. The mechanisms regulating activation of RFCp140 thereby controlling replication and cellular proliferation are largely unknown. We analyzed protein expression of RFCp140 during cell cycle progression and investigated the association of RFCp140 with cell cycle regulatory proteins in cell lines of various tissue origin and in primary hematopoietic cells. Western and Northern blot analyses of RFCp140 from synchronized cells showed downregulation of RFCp140 when cells enter a G0-like quiescent state and upregulation of RFCp140 in cycling cells. Translocation from the cytopla…

CytoplasmSaccharomyces cerevisiae ProteinsT-LymphocytesCyclin ACell Cycle ProteinsEukaryotic DNA replicationCell LineMinor Histocompatibility AntigensDNA replication factor CDT1MiceReplication factor CControl of chromosome duplicationDrug DiscoveryAnimalsHumansReplication Protein CGenetics (clinical)Cell NucleusHomeodomain ProteinsbiologyG1 PhaseS-phase-promoting factor3T3 CellsCell cycleMolecular biologyUp-RegulationCell biologyDNA-Binding ProteinsRepressor ProteinsProto-Oncogene Proteins c-bcl-2biology.proteinMolecular MedicineOrigin recognition complexJournal of Molecular Medicine
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Circadian rhythms and chemical carcinogenesis: Potential link. An overview.

2009

Circadian rhythm is an integral and not replaceable part of the organism's homeostasis. Its signalling is multidimensional, overlooking global networks such as chromatin remodelling, cell cycle, DNA damage and repair as well as nuclear receptors function. Understanding its global networking will allow us to follow up not only organism dysfunction and pathology (including chemical carcinogenesis) but well-being in general having in mind that time is not always on our side. The authors thank ECNIS (Environmental Cancer, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5: Food Quality and Safety (Contract no. …

DNA RepairDNA repairDNA damageHealth Toxicology and MutagenesisCell Cycle ProteinsBiologymedicine.disease_causeNeoplasmsGeneticsmedicineHomeostasisHumansAnimalsCircadian rhythmOrganismCell CyclePeriod Circadian ProteinsDNACell biologyCircadian RhythmCLOCKNuclear receptorCarcinogensPeriod Circadian ProteinsCarcinogenesisDNA Damage
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The APC/C cofactor Cdh1 prevents replicative stress and p53-dependent cell death in neural progenitors

2013

The E3-ubiquitin ligase APC/C-Cdh1 is essential for endoreduplication but its relevance in the mammalian mitotic cell cycle is still unclear. Here we show that genetic ablation of Cdh1 in the developing nervous system results in hypoplastic brain and hydrocephalus. These defects correlate with enhanced levels of Cdh1 substrates and increased entry into the S phase in neural progenitors. However, cell division is prevented in the absence of Cdh1 due to hyperactivation of cyclin-dependent kinases, replicative stress, induction of p53, G2 arrest and apoptotic death of these progenitor cells. Concomitant ablation of p53 rescues apoptosis but not replicative stress, resulting in the presence of …

DNA ReplicationMaleProgrammed cell deathCell divisionNeurogenesisGeneral Physics and AstronomyApoptosisCell Cycle ProteinsBiologyAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsProgenitor cell030304 developmental biologyProgenitorMice KnockoutNeuronschemistry.chemical_classification0303 health sciencesDNA ligaseMultidisciplinaryCell CycleNeurogenesisBrainOrgan SizeGeneral ChemistryCell cycle3. Good healthCell biologyMice Inbred C57BLchemistrySynaptic plasticityFemaleTumor Suppressor Protein p53Cell Division030217 neurology & neurosurgeryNature Communications
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