Search results for "mitosi"

showing 10 items of 158 documents

Expression of Drosophila Cabut during early embryogenesis, dorsal closure and nervous system development.

2010

cabut (cbt) encodes a transcription factor involved in Drosophila dorsal closure (DC), and it is expressed in embryonic epithelial sheets and yolk cell during this process upon activation of the Jun N-terminal kinase (JNK) signaling pathway. Additional studies suggest that cbt may have a role in multiple developmental processes. To analyze Cbt localization through embryogenesis, we generated a Cbt specific antibody that has allowed detecting new Cbt expression patterns. Immunohistochemical analyses on syncytial embryos and S2 cells reveal that Cbt is localized on the surface of mitotic chromosomes at all mitotic phases. During DC, Cbt is expressed in the yolk cell, in epidermal cells and in…

Nervous systemCentral Nervous SystemRecombinant Fusion ProteinsMitosisBiologybehavioral disciplines and activities03 medical and health sciencesGenes ReporterTubulinmental disordersPeripheral Nervous SystemGeneticsmedicineAnimalsDrosophila ProteinsPromoter Regions GeneticMolecular BiologyMitosis030304 developmental biologyRegulation of gene expressionGeneticsCell Nucleus0303 health sciencesSchneider 2 cells030302 biochemistry & molecular biologyEmbryogenesisGene Expression Regulation DevelopmentalEmbryoEmbryonic stem cellDorsal closureChromatin3. Good healthCell biologyProtein Structure Tertiarymedicine.anatomical_structureEpidermal CellsOrgan SpecificityDrosophilaLamininEpidermisDevelopmental BiologyTranscription FactorsGene expression patterns : GEP
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Triiodothyronine-Induced Shortening of Chromatin Repeat Length in Neurons Cultured in a Chemically Denned Medium

1987

Abstract: At the time of terminal differentiation, mammalian cortical neurons undergo a dramatic change in the structural organization of their chromatin: the nucleosomal repeat length shortens from ∼200 base pairs in fetuses to a value of 165 base pairs after birth. These events occur several days after the end of neuronal proliferation. Previously, we reported that rat cortical neurons cultured in a very selective synthetic medium were not yet programmed to these events at the end of mitotic cycles. Herein, we report that addition of triiodothyronine to neuronal cultures induces a shortening of the chromatin repeat length comparable to the natural one. Copyright © 1987, Wiley Blackwell. A…

Neuronal terminal differentiationTime FactorsCellular differentiationBiologySettore BIO/19 - Microbiologia GeneraleChromatin structureBiochemistryCellular and Molecular NeuroscienceSettore BIO/10 - BiochimicamedicineAnimalsNucleosomeMitosisCells CulturedCerebral CortexNeuronsGeneticsNucleosomal Repeat LengthTriiodothyronineDNAChromatinCulture MediaRatsChromatinCell biologyChemically denned medium)Chemically defined mediummedicine.anatomical_structurenervous systemTriiodothyronineSettore MED/26 - NeurologiaNeuronJournal of Neurochemistry
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A pilot study of vinorelbine on a weekly schedule in recurrent and/or metastatic squamous cell carcinoma of the head and neck.

1993

Vinorelbine (VNR), 5′-nor-anhydrovinblastine, is a new semi-synthetic vinka alkaloid with selective affinity for mitotic microtubules, which has been shown to be active against several non small cell lung cancer lines in vitro [1]. VNR has been reported to yield a 34.7 % and 20 % overall response rate in patients with squamous cell lung carcinoma and bronchial adenocarcinoma respectively [2]. Moreover, VNR has been shown to be active in advanced breast carcinoma where it may induce a 30–50 % response rate depending on the extent of pretreatment [3]. We tested the activity and toxicity of single agent VNR given on a weekly schedule in a series of patients with recurrent and/or metastatic squ…

OncologyMaleCancer Researchmedicine.medical_specialtymedicine.drug_classAntineoplastic AgentsPilot ProjectsVinorelbineVinblastineVinca alkaloidInternal medicineCarcinomamedicineHumansHead and neckLung cancerMitosisbusiness.industryVinorelbineMiddle Agedmedicine.diseaseVinblastineOncologyHead and Neck NeoplasmsToxicityCarcinoma Squamous CellFemalebusinessmedicine.drugEuropean journal of cancer (Oxford, England : 1990)
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Clinicopathologic and DNA Flow Cytometric Analysis of Eighty-three Renal Cell Carcinomas

1995

The clinical and anatomopathologic features as well as DNA content of 83 renal cell carcinomas were analyzed. The possible interrelationship and prognostic value of these factors were also considered. The DNA study has been performed by flow cytometry using paraffin-embedded tissues. In each case an internal control with nonneoplastic renal tissue obtained in the same nefrectomy was also done in order to calculate the DNA index. Differences in patient age, nuclear grade, and mitotic activity were related with outcome; however, this relationship was not confirmed by the Cox test. Stage (P = .005), cell type (P = .002), and metastatic disease (P = .001) had independent prognostic values. Ren…

Pathologymedicine.medical_specialtyCell typemedicine.diagnostic_testbusiness.industryCellmedicine.diseasePathology and Forensic MedicineFlow cytometrychemistry.chemical_compoundmedicine.anatomical_structurechemistryRenal cell carcinomamedicineSurgeryAnatomyStage (cooking)businessNuclear gradeMitosisDNAInternational Journal of Surgical Pathology
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Mitotic figure counts are significantly overestimated in resection specimens of invasive breast carcinomas.

2013

Several authors have demonstrated an increased number of mitotic figures in breast cancer resection specimen when compared with biopsy material. This has been ascribed to a sampling artifact where biopsies are (i) either too small to allow formal mitotic figure counting or (ii) not necessarily taken form the proliferating tumor periphery. Herein, we propose a different explanation for this phenomenon. Biopsy and resection material of 52 invasive ductal carcinomas was studied. We counted mitotic figures in 10 representative high power fields and quantified MIB-1 immunohistochemistry by visual estimation, counting and image analysis. We found that mitotic figures were elevated by more than th…

Pathologymedicine.medical_specialtyMitotic indexTime FactorsTissue FixationBiopsyMitosisBreast NeoplasmsBiologyPathology and Forensic MedicineBreast cancerPredictive Value of TestsBiopsyCarcinomamedicineMitotic IndexHumansNeoplasm InvasivenessMetaphaseMitosisMastectomyCell Proliferationmedicine.diagnostic_testCarcinoma Ductal BreastReproducibility of ResultsCell cyclemedicine.diseaseImmunohistochemistryKi-67 AntigenMitotic FigureLinear ModelsFemaleNeoplasm GradingModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
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Hemmung der Adenosintriphosphatase durch Colchicin

1951

The ATPase activity is inhibited by Colchicin in concentrations of 10−3 m and 10−4 m at a rate of 40 to 20 %, but in no way in the range of 10−7 m and 10−8 m, where Colchicin exerts its typical spindle-blocking action on the mitotic cell division. It is therefore no evidence, that Colchicin acts by influence on the energy yielding ATP-ATPase system, which was proposed to be responsible for the spindle contraction.

PharmacologyCellular and Molecular NeuroscienceContraction (grammar)PhosphataseMolecular MedicineAtpase activityCell BiologyBiologyMolecular BiologyMitosisMolecular biologyCell biologyExperientia
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Über die Hemmung von Desoxyribonucleotide spaltenden Fermenten durch Colchicin

1949

The authors raise the question, if enzymatic processes possibly linked with the mitotic cell division may be influenced by mitotic poisons. The presented date show an inhibition of the dephosphorylation of desoxyribonucleotides at a rate of about 50% and of the deamination of about 40% by colchicine (final concentration 1·2·10−2M).

Pharmacologychemistry.chemical_classificationDeaminationCell BiologyBiologyDephosphorylationCellular and Molecular Neurosciencechemistry.chemical_compoundEnzymechemistryBiochemistryMolecular MedicineColchicineNucleotideMolecular BiologyMitosisExperientia
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Cell Cycle in Potentially Dedifferentiating Cereal Mesophyll Protoplasts Cultured in vitro II. Behaviour of the Cytoskeleton

1993

Summary Following up on the recent finding that mesophyll protoplasts of wheat and oats were able to reenter the cell cycle when cultured in vitro , the behaviour of the cytoskeleton was studied. The aim was to elucidate whether changes in the cytoskeletal patterns correlate with the abnormal progression through the cycle observed previously. Protoplasts freshly isolated from mature mesophyll tissue (type B) exhibited very few, fragmented microtubules, whereas mesophyll protoplasts isolated from immature leaf tissue (type A) showed an abundant network fo microtubules. Type B protoplasts of wheat, which were able to reenter but recalcitrant to complete S-phase, failed to reestablish a microt…

PhysiologyPreprophasefungifood and beveragesPlant ScienceCell platebiochemical phenomena metabolism and nutritionBiologyPhragmoplastMicrofilamentPhragmosomeCell biologyCytoskeletonAgronomy and Crop ScienceMitosisCytokinesisJournal of Plant Physiology
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“Mitotic Slippage” and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres

2020

Mitotic slippage (MS), the incomplete mitosis that results in a doubled genome in interphase, is a typical response of TP53-mutant tumors resistant to genotoxic therapy. These polyploidized cells display premature senescence and sort the damaged DNA into the cytoplasm. In this study, we explored MS in the MDA-MB-231 cell line treated with doxorubicin (DOX). We found selective release into the cytoplasm of telomere fragments enriched in telomerase reverse transcriptase (hTERT), telomere capping protein TRF2, and DNA double-strand breaks marked by γH2AX, in association with ubiquitin-binding protein SQSTM1/p62. This occurs along with the alternative lengthening of telomeres (ALT) and DNA repa…

PolyploidizationALTSQSTM1/p62lcsh:ChemistryNeoplasmsSequestosome-1 Proteincellular senescenceTelomeric Repeat Binding Protein 2mtTP53 cancerTelomeraseAmoeboid conversionlcsh:QH301-705.5Telomere ShorteningSpectroscopyAntibiotics AntineoplasticGeneral MedicineTelomereComputer Science ApplicationsCell biologyinverted meiosisExtranuclear DNA<i>mtTP53</i> cancerSpo11DNA repairTelomere CappingMitosisBudding of mitotic progenygenotoxic treatmentamoeboid conversionInverted meiosisBiologyCellular senescenceArticleCatalysisInorganic ChemistryMeiosisCell Line Tumorextranuclear DNAHumansTelomerase reverse transcriptasePhysical and Theoretical ChemistryMolecular BiologyMitosisCell ProliferationGenotoxic treatmentOrganic ChemistryRecombinational DNA RepairCell Cycle CheckpointsDNA<i>SQSTM1/p62</i>polyploidizationTelomerelcsh:Biology (General)lcsh:QD1-999DoxorubicinDrug Resistance Neoplasmbiology.proteinHomologous recombinationbudding of mitotic progenyDNA DamageInternational Journal of Molecular Sciences
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Poriferan survivin exhibits a conserved regulatory role in the interconnected pathways of cell cycle and apoptosis

2010

Survivin orchestrates intracellular pathways during cell division and apoptosis. Its central function as mitotic regulator and inhibitor of cell death has major implications for tumor cell proliferation. Analyses in early-branching Metazoa so far propose an exclusive role of survivin as a chromosomal passenger protein, whereas only later during evolution a complementary antiapoptotic function might have arisen, concurrent with increased organismal complexity. To lift the veil on the ancestral function(s) of this key regulator, a survivin-like protein (SURVL) of one of the earliest-branching metazoan taxa was identified and functionally characterized. SURVL of the sponge Suberites domuncula …

Programmed cell deathCell divisionRecombinant Fusion ProteinsMolecular Sequence DataApoptosisTransfectionCell LineInhibitor of Apoptosis ProteinsLipopeptidesSurvivinAnimalsHumansAmino Acid SequenceMolecular BiologyMitosisGeneticsOriginal PaperBase SequencebiologyCell CycleCell BiologyCell cyclebiology.organism_classificationCell biologySuberites domunculaCell cultureCaspasesSuberitesSequence AlignmentCell DivisionIntracellularCadmiumCell Death &amp; Differentiation
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