Search results for "Mitosis."

showing 10 items of 146 documents

Variability of ecdysteroid-induced cell cycle alterations in Drosophila Kc sublines.

1987

. The cell cycle of two lines isolated from Drosophila Kc cells was followed by flow cytofluorometry and cell counting. The first line is the 8-9K clone which grew in a medium supplemented with 5% serum; the second, named subline Kc0, grew in a serum-free medium. The stationary phase is characterized by a G2 cell accumulation: 73% in the 8-9K clone and 50% in the Kc0 subline. When the medium was supplemented with the steroid moulting hormone 20-hydroxyecdysone, more than 90% of 8-9K cells and 65% of Kc0 cells were progressively arrested in G2. In the continuous presence of 20-hydroxyecdysone, most of the 8-9K cells remain G2-arrested; no massive G2 release into M was observed and only a few…

Programmed cell deathCellClone (cell biology)MitosisCell CountBiologyCell Linechemistry.chemical_compoundmedicineAnimalsInterphaseEcdysteroidCell CycleCell BiologyGeneral MedicineAnatomyDNACell cycleCell countingFlow CytometryMolecular biologyCulture Mediamedicine.anatomical_structureEcdysteronechemistryCell cultureDrosophilaMoultingCell and tissue kinetics
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Synthesis of a new class of pyrrolo[3,4-h]quinazolines with antimitotic activity

2014

Abstract A new series of pyrrolo[3,4- h ]quinazolines was conveniently prepared with a broad substitution pattern. A large number of derivatives was obtained and the cellular cytotoxicity was evaluated in vitro against 5 different human tumor cell lines with GI 50 values reaching the low micromolar level (1.3–19.8 μM). These compounds were able to induce cell death mainly by apoptosis through a mitochondrial dependent pathway. Selected compounds showed antimitotic activity and a reduction of tubulin polymerization in a concentration-dependent manner. Moreover, they showed anti-angiogenic properties since reduced in vitro endothelial cell migration and disrupted HUVEC capillary-like tube net…

Programmed cell deathMitosisAntiproliferative activityCell Line TumorDrug DiscoveryHuman Umbilical Vein Endothelial CellsPiHumansTubulin polymerizationPyrrolesPyrrolo[3Cell-mediated cytotoxicityPyrrolo[34-h]quinazolines Antiproliferative activity Antimitotic activity Tubulin polymerization Vascular disrupting activityTubulin polymerizationVascular disrupting activityPharmacologyMatrigelCell Death4-h]quinazolinesChemistryAntimitotic activityOrganic ChemistryGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaMitochondriaEndothelial stem cellBiochemistryCell cultureApoptosisPyrrolo[3; 4-h]quinazolines; Antiproliferative activity; Antimitotic activity; Tubulin polymerization; Vascular disrupting activityQuinazolinesLysosomes
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Microtubules and the First Cell Cycle in Cultured Mesophyll Protoplasts of Nicotiana

1990

When a protoplast is excised and cultured in vitro, an organized pattern of cell divisions must be reestablished to permit organogenesis, including plant regeneration. However, in a number of species protoplasts have proved to be very recalcitrant with regard to cell division and/or plant regeneration. In an attempt to find means to overcome the regeneration problem in recalcitrant species we are investigating the processes leading to cell division and morphogenesis in mesophyll protoplasts of the model system Nicotiana. Of particular interest are the initiation of the cell cycle and the coordination of progress through the cycles as a prerequisite for subsequent morphogenesis. Mesophyll pr…

ProphaseCell divisionCytoplasmfungiBotanyPreprophase bandBiologyCell cycleMitosisCytokinesisCell biologyPhragmosome
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Three-dimensional structure of the anaphase-promoting complex.

2001

The anaphase-promoting complex (APC) is a cell cycle-regulated ubiquitin-protein ligase, composed of at least 11 subunits, that controls progression through mitosis and G1. Using cryo-electron microscopy and angular reconstitution, we have obtained a three-dimensional model of the human APC at a resolution of 24 A. The APC has a complex asymmetric structure 140 A x 140 A x 135 A in size, in which an outer protein wall surrounds a large inner cavity. We discuss the possibility that this cavity represents a reaction chamber in which ubiquitination reactions take place, analogous to the inner cavities formed by other protein machines such as the 26S proteasome and chaperone complexes. This cag…

Protein subunitUbiquitin-Protein LigasesAnaphase-Promoting Complex-CyclosomeLigasesProtein structureUbiquitinHumansProtein Structure QuaternaryMitosisMolecular Biologychemistry.chemical_classificationDNA ligasebiologyCryoelectron MicroscopyG1 PhaseUbiquitin-Protein Ligase ComplexesCell BiologyPrecipitin TestsCell biologyProtein Structure TertiaryProteasomechemistryChaperone (protein)biology.proteinAnaphase-promoting complexHeLa CellsMolecular cell
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Pterostilbene-induced tumor cytotoxicity: a lysosomal membrane permeabilization-dependent mechanism.

2012

The phenolic phytoalexin resveratrol is well known for its health-promoting and anticancer properties. Its potential benefits are, however, limited due to its low bioavailability. Pterostilbene, a natural dimethoxylated analog of resveratrol, presents higher anticancer activity than resveratrol. The mechanisms by which this polyphenol acts against cancer cells are, however, unclear. Here, we show that pterostilbene effectively inhibits cancer cell growth and stimulates apoptosis and autophagosome accumulation in cancer cells of various origins. However, these mechanisms are not determinant in cell demise. Pterostilbene promotes cancer cell death via a mechanism involving lysosomal membrane …

PterostilbeneCancer Treatmentlcsh:MedicineApoptosisResveratrolBiochemistryLung and Intrathoracic Tumorschemistry.chemical_compoundMolecular cell biologyRNA interferenceNeoplasmsPhagosomesStilbenesDrug DiscoveryBreast TumorsBasic Cancer Researchlcsh:ScienceCytotoxicitySkin TumorsApoptotic Signaling CascadeCellular Stress ResponsesMultidisciplinaryMicroscopy ConfocalCell DeathMalignant MelanomaFlow CytometryCellular StructuresSignaling CascadesCell biologyEukaryotic CellsOncologyCaspasesMedicineCellular TypesCell DivisionResearch ArticleSignal TransductionProgrammed cell deathDrugs and DevicesDrug Research and DevelopmentMitosisAntineoplastic AgentsBiologyPermeabilityCell GrowthInhibitory Concentration 50NecrosisComplementary and Alternative MedicineCell Line TumorGastrointestinal TumorsAutophagyHumansHSP70 Heat-Shock ProteinsBiologyCell ProliferationDose-Response Relationship DrugL-Lactate DehydrogenaseCell growthlcsh:RAutophagyProteinsCancers and NeoplasmsRegulatory ProteinschemistrySubcellular OrganellesApoptosisResveratrolCancer celllcsh:QGene expressionLysosomesCytometryPloS one
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CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death.

2006

KEYWORDS CLASSIFICATION: 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide;Antigens,CD40;Apoptosis;Bronchi;cytology;Caspases;Cell Cycle;Cell Death;Cell Line,Transformed;Cell Survival;Cell Transformation,Viral;Cytoprotection;drug effects;Epithelial Cells;Humans;Italy;mechanisms of carcinogenesis;metabolism;Oxidants;pharmacology;physiology;Research;Simian virus 40;toxicity;Transcription Factor AP-1. CD40 and its ligand regulate pleiotropic biological responses, including cell proliferation, differentiation, and apoptosis. In many inflammatory lung diseases, tissue damage by environmental or endogenous oxidants plays a major role in disease pathogenesis. As the epithelial barrier is a major t…

Pulmonary and Respiratory MedicineNF-BProgrammed cell deathCell SurvivalClinical Biochemistry78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideApoptosisBronchiSimian virus 40Inhibitor of apoptosisAntigens CD40CD40HumansCD40 AntigensMolecular BiologyMitosisCaspaseActivator protein–1Cell Line Transformedoxidant stressbiologyCell DeathCell growthCell CycleEpithelial CellsCell BiologyCell cycleCell Transformation ViralOxidantsapoptosiCell biologyTranscription Factor AP-1activator protein–1ApoptosisCytoprotectionCaspasesbiology.proteinNF- BApoptosis-inducing factorOxidant stress
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p38α deficiency and oxidative stress cause cytokinesis failure in hepatocytes.

2015

Cytokinesis is the last step in mitosis and it implies re-organization of the actin cytoskeleton. Its failure is one of the major mechanisms of polyploidy and binucleation in mammals. Our aims were 1) to assess the role of redox-sensitive p38α MAPK in cytokinesis by studying the liver of wild type mice or liver-specific p38α knock-out mice; 2) to assess the role of oxidative stress associated with hepatocyte isolation on cytokinesis. When p38α was down-regulated in hepatocytes, MK2 phosphorylation on threonine 334 was completely abrogated. Activation of MNK-1, required for abscission of the intercellular bridge, was diminished. Key proteins of the RhoA pathway (phospho-PRK2, nuclear phospho…

RHOAmacromolecular substancesBiologyCell cycleCofilinActin cytoskeletonBiochemistryCell biologyCytosolPhysiology (medical)biology.proteinMitosisCytokinesisActinFree radical biologymedicine
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Connecting temporal identity to mitosis: the regulation of Hunchback in Drosophila neuroblast lineages.

2006

Both in vertebrates and invertebrates, neural stem cells generate different cell types at different times during development. It has been suggested that this process depends on temporal identity transitions of neural progenitors, but the underlying mechanism has not been resolved, yet. Recently, Drosophila neuroblasts (NBs) have been shown to be an excellent model system to investigate this subject. Here, changes in temporal identity are regulated by sequential and transient expression of transcription factors in the NB, such as Hunchback (Hb) and Kruppel (Kr). The temporal expression profile is maintained in the progeny. Hb is expressed first and thus defines the earliest identity in a giv…

Retinal Ganglion CellsCell typeReceptors SteroidKruppel-Like Transcription FactorsDown-RegulationMitosisNerve Tissue ProteinsBiologyCell fate determinationKrüppelNeuroblastAnimalsDrosophila ProteinsNuclear export signalMolecular BiologyMitosisTranscription factorGeneticsNeuronsModels GeneticNuclear ProteinsCell DifferentiationCell BiologyNeural stem cellDNA-Binding ProteinsProtein BiosynthesisDrosophilaDevelopmental BiologyTranscription FactorsCell cycle (Georgetown, Tex.)
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Functional distinction between Cln1p and Cln2p cyclins in the control of the Saccharomyces cerevisiae mitotic cycle.

2004

Abstract Cln1p and Cln2p are considered as equivalent cyclins on the basis of sequence homology, regulation, and functional studies. Here we describe a functional distinction between the Cln1p and Cln2p cyclins in the control of the G1/S transition. Inactivation of CLN2, but not of CLN1, leads to a larger-than-normal cell size, whereas overexpression of CLN2, but not of CLN1, results in smaller-than-normal cells. Furthermore, mild ectopic expression of CLN2, but not of CLN1, suppresses the lethality of swi4swi6 and cdc28 mutant strains. In the absence of Cln1p, the kinetics of budding, initiation of DNA replication, and activation of the Start-transcription program are not affected; by cont…

Saccharomyces cerevisiae ProteinsMutantSaccharomyces cerevisiaeBlotting WesternMitosisSaccharomyces cerevisiaeBiologyInvestigationsmedicine.disease_causeS PhaseCyclinsGeneticsmedicineImmunoprecipitationFluorescent Antibody Technique IndirectMitosisCyclinCell SizeGeneticsCyclin-dependent kinase 1MutationDNA replicationbiology.organism_classificationBlotting NorthernBridged Bicyclo Compounds HeterocyclicFlow CytometryMolecular biologyThiazolesMutationThiazolidinesEctopic expressionGenetics
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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