Search results for "Cell Cycle Proteins"

showing 10 items of 127 documents

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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Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: Contribution of DNA replication, transcription in…

2007

Cyclophosphamide is one of the most often used anticancer drugs. Although DNA interstrand cross-links are considered responsible for its cytotoxicity, the mechanism of initiation and execution of cell death is largely unknown. Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells. We identified two upstream processes that initiate apoptosis, DNA replication blockage and transcriptional inhibition. In lymphoblastoid cells, wherein DNA replication can be switched off by tetracycline, proliferation is required for induci…

DNA ReplicationProgrammed cell deathTime FactorsTranscription GeneticDNA damageDrug ResistanceAntineoplastic AgentsApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesToxicologyCaspase-Dependent ApoptosisCell Linechemistry.chemical_compoundMafosfamideHumansCHEK1PhosphorylationCyclophosphamideCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyTumor Suppressor ProteinsCell cycleDNA-Binding ProteinsCheckpoint Kinase 2chemistryApoptosisCaspasesCheckpoint Kinase 1Cancer researchbiology.proteinTumor Suppressor Protein p53Protein KinasesSignal TransductionToxicology and Applied Pharmacology
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Class 1 Histone Deacetylases and Ataxia-Telangiectasia Mutated Kinase Control the Survival of Murine Pancreatic Cancer Cells upon dNTP Depletion

2021

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Ent…

DNA Replicationendocrine system diseasesDNA damagereplication stressQH301-705.5RNR Inhibitor COH29Antineoplastic AgentsCell Cycle ProteinsRNRAtaxia Telangiectasia Mutated ProteinsArticle03 medical and health scienceschemistry.chemical_compoundAtaxia TelangiectasiaMice0302 clinical medicineHDACAnimalscancerPDAC cellsRibonucleotide Reductase SubunitEnzyme InhibitorsBiology (General)030304 developmental biology0303 health sciencesbiologyChemistryEntinostatDNA replicationapoptosisGeneral Medicine3. Good healthPancreatic NeoplasmsHistoneRibonucleotide reductase030220 oncology & carcinogenesisATMbiology.proteinCancer researchDNA damageHistone deacetylaseCells
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