Search results for "Mitos"

showing 10 items of 190 documents

Tumor cells can escape DNA-damaging cisplatin through DNA endoreduplication and reversible polyploidy

2008

Cancer chemotherapy can induce tumor regression followed, in many cases, by relapse in the long-term. Thus this study was performed to assess the determinants of such phenomenon using an in vivo cancer model and in vitro approaches. When animals bearing an established tumor are treated by cisplatin, the tumor initially undergoes a dramatic shrinkage and is characterized by giant tumor cells that do not proliferate but maintain DNA synthesis. After several weeks of latency, the tumor resumes its progression and consists of small proliferating cells. Similarly, when tumor cells are exposed in vitro to pharmacological concentrations of cisplatin, mitotic activity stops initially but cells main…

CisplatinCell BiologyGeneral MedicineBiologyMolecular biologyDNA endoreduplicationGiant cellCancer researchmedicineCytotoxic T cellEndoreduplicationClonogenic assayMitosisMitotic catastrophemedicine.drugCell Biology International
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Methylation Reprogramming and Chromosomal Aneuploidy in In Vivo Fertilized and Cloned Rabbit Preimplantation Embryos1

2004

Active demethylation of the paternal genome but not of the maternal genome occurs in fertilized mouse, rat, pig, and bovine zygotes. To study whether this early demethylation wave is important for embryonic development, we have analyzed the global methylation patterns of both in vivo-fertilized and cloned rabbit embryos. Anti-5-methylcytosine immunofluorescence of in vivo-fertilized rabbit embryos revealed that the equally high methylation levels of the paternal and maternal genomes are largely maintained from the zygote up to the 16-cell stage. The lack of detectable methylation changes in rabbit preimplantation embryos suggests that genome-wide demethylation is not an obligatory requireme…

Cloninganimal structuresZygoteEmbryogenesisEmbryoCell BiologyGeneral MedicineMethylationBiologyMolecular biologyCell biologymedicine.anatomical_structureReproductive Medicineembryonic structuresmedicineBlastocystMitosisReprogrammingBiology of Reproduction
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A constitutive 70 kDa heat-shock protein is localized on the fibres of spindles and asters at metaphase in an ATP-dependent manner: A new chaperone r…

2001

In the present study, double immunofluorescence and immunoblot analysis have been used to show that centrosomes, isolated from Paracentrotus lividus sea urchin embryos at the first mitotic metaphase, contain the constitutive chaperone, heat-shock protein (HSP) 70. More specifically, we demonstrate that centrosomes contain only the HSP70-d isoform, which is one of the four isoforms identified in P. lividus . We also provide evidence that p34(cell division control kinase-2) and t complex polypeptide-1 (TCP-1) α, a subunit of the TCP-1 complex, are localized on the centrosomes. Furthermore, inhibition of TCP-1 in vivo, via microinjecting an anti-(TCP-1α) antibody into P. lividus eggs before fe…

Constitutive HSP70Chaperone activityParacentrotus lividus sea urchinCell BiologyMitosiBiochemistryMolecular Biology
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Evidencias psicométricas de una medida breve de resiliencia en adultos mayores peruanos no institucionalizados

2018

Resumen: La resiliencia es comprendida como el dominio de recursos personales y factores contextuales que permiten un afrontamiento exitoso y el logro de una adaptación positiva ante los diferentes estresores que aparecen a lo largo de la vida, siendo así importante dentro del proceso de envejecimiento saludable y exitoso. En la actualidad se han desarrollado instrumentos breves para la medición de la resiliencia como la escala breve de resiliencia (BRCS - Brief Resilient Coping Scale) que evalúa la capacidad de los individuos para hacer frente al estrés de manera adaptativa. En este sentido, el estudio ofrece evidencia de validez y fiabilidad de la BRCS en adultos mayores no institucionali…

Coping (psychology)Social Psychologylcsh:BF1-990ValidityAdultos mayoresFiabilidad050109 social psychology03 medical and health sciences0302 clinical medicineDevelopmental and Educational PsychologyElderly peopleAcoso sexual0501 psychology and cognitive sciences030212 general & internal medicineApplied PsychologySuccessful aging05 social sciencesStressorSpanish versionMean ageAfrontamientoConfirmatory factor analysisMitoslcsh:PsychologySexismoResilienciaValidezPsychologyPercepción socialClinical psychology
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Expression of the kinetochore protein Hec1 during the cell cycle in normal and cancer cells and its regulation by the pRb pathway.

2010

Highly Expressed in Cancer protein 1 (Hec1) is a subunit of the Ndc80 complex, a constituent of the mitotic kinetochore. HEC1 has been shown to be overexpressed in many cancers, suggesting that HEC1 upregulation is involved in the generation and/or maintenance of the tumour phenotype. However, the regulation of Hec1 expression in normal and tumour cells and the molecular alterations promoting accumulation of this protein in cancer cells are still unknown. Here we show that elevated Hec1 protein levels are characteristic of transformed cell lines of different origins and that kinetochore recruitment of this protein is also increased in cancer cell lines in comparison with normal human cells.…

Cyclohexamide CHXRetinoblastoma ProteinCell Line TumorNeoplasmsmedicineHumansGene silencingGene SilencingNuclear proteinKinetochoresMolecular BiologyMitosisHec1biologyCell CycleRetinoblastoma proteinNuclear ProteinsCancerCell BiologyCell cyclemedicine.diseaseCell biologyCytoskeletal ProteinsSettore BIO/18 - GeneticaMitotic exitCancer cellbiology.proteinRNA InterferenceSignal TransductionDevelopmental Biologymicrotubule
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Nuclear and Cytoplasmic Survivin: Molecular Mechanism, Prognostic, and Therapeutic Potential.

2007

Abstract Survivin's proposed dual role as an apoptosis inhibitor and a mitotic effector positioned it in the front line of cancer research. Notably, survivin is detected as a cytoplasmic and nuclear protein in cancer patients, which stimulated numerous studies to investigate and to speculate on the functional and prognostic significance of its dynamic localization. Recent evidence shows that the direct interaction of survivin with the nuclear export receptor Crm1 is critically involved in its intracellular localization and cancer-relevant functions. Here, we review our current understanding of the Crm1/survivin interface and discuss its potential prognostic and therapeutic relevance. [Cance…

CytoplasmCancer ResearchPathologymedicine.medical_specialtyApoptosis InhibitorSurvivinActive Transport Cell NucleusMitosisReceptors Cytoplasmic and NuclearKaryopherinsBiologyModels BiologicalInhibitor of Apoptosis ProteinsNeoplasmsSurvivinmedicineHumansNuclear proteinNuclear export signalReceptorMitosisCell NucleusEffectorCancerPrognosismedicine.diseaseNeoplasm ProteinsGene Expression Regulation NeoplasticOncologyCancer researchMicrotubule-Associated ProteinsBiologie
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Transformation of Aspergillus parasiticus using autonomously replicating plasmids from Aspergillus nidulans.

1994

A genetic transformation system for the aflatoxin-producing fungus Aspergillus parasiticus using two autonomously replicating plasmids from A. nidulans (ARp1 and pDHG25) is reported. Transformation frequencies using the plasmid pDHG25 were from 5 x 10(2) to 2.5 x 10(4) transformants per 10(6) viable protoplasts and microgram DNA. The stability of the plasmids in the transformants was also studied. This transformation system offers a new opportunity to clone genes related to aflatoxin production using appropriate aflatoxin-defective mutants.

DNA ReplicationArginine BAutonomously replicating sequenceMitosisLaboratorium voor ErfelijkheidsleerMicrobiologyAspergillus parasiticusAspergillus nidulansMicrobiologyGenetic transformationchemistry.chemical_compoundPlasmidTransformation GeneticAutonomous replicationAspergillus nidulansGeneticsDNA FungalMolecular BiologyGeneGeneticsAspergillus nidulans autonomous replicating plasmidbiologyProtoplastsfood and beveragesProtoplastbiology.organism_classificationAspergillus parasiticusTransformation (genetics)AspergilluschemistryLaboratory of GeneticsDNAPlasmidsFEMS microbiology letters
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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The bacterial cytolethal distending toxin (CDT) triggers a G2 cell cycle checkpoint in mammalian cells without preliminary induction of DNA strand br…

1999

The bacterial cytolethal distending toxin (CDT) was previously shown to arrest the tumor-derived HeLa cell line in the G2-phase of the cell cycle through inactivation of CDK1, a cyclin-dependent kinase whose state of activation determines entry into mitosis. We have analysed the effects induced in HeLa cells by CDT, in comparison to those induced by etoposide, a prototype anti-tumoral agent that triggers a G2 cell cycle checkpoint by inducing DNA damage. Both CDT and etoposide inhibit cell proliferation and induces the formation of enlarged mononucleated cells blocked in G2. In both cases, CDK1 from arrested cells could be re-activated both in vitro by dephosphorylation by recombinant Cdc25…

DNA ReplicationG2 PhaseCancer ResearchCAFFEINECell cycle checkpointCytolethal distending toxinDNA damageRecombinant Fusion Proteins[SDV]Life Sciences [q-bio]Bacterial ToxinsBiologyS Phase03 medical and health sciencesCDC2 Protein KinaseGeneticsHumanscdc25 PhosphatasesCHEK1PhosphorylationMolecular BiologyMitosisEtoposide030304 developmental biology0303 health sciences030306 microbiologyCell growthDNA NeoplasmG2-M DNA damage checkpointCell cycleAntineoplastic Agents PhytogenicNeoplasm Proteins3. Good healthCell biology[SDV] Life Sciences [q-bio]BiochemistryAGENT ANTITUMEURProtein Processing Post-TranslationalCell DivisionDNA DamageHeLa Cells
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Chromosomal instability, reproductive cell death and apoptosis induced by O6-methylguanine in Mex−, Mex+ and methylation-tolerant mismatch repair com…

1998

O6-Methylguanine (O6-MeG) is induced in DNA by methylating environmental carcinogens and various cytostatic drugs. It is repaired by O6-methylguanine-DNA methyltransferase (MGMT). If not repaired prior to replication, the lesion generates gene mutations and leads to cell death, sister chromatid exchanges (SCEs), chromosomal aberrations and malignant transformation. To address the question of how O6-MeG is transformed into genotoxic effects, isogenic Chinese hamster cell lines either not expressing MGMT (phenotypically Mex-), expressing MGMT (Mex+) or exhibiting the tolerance phenotype (Mex-, methylation resistant) were compared as to their clastogenic response. Mex- cells were more sensitiv…

DNA ReplicationMethylnitronitrosoguanidineGuanineDNA RepairDNA damageHealth Toxicology and MutagenesisDrug ResistanceApoptosisCHO CellsGene mutationBiologyChromosomesDNA AdductsO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeChromosome instabilityGeneticsAnimalsSister chromatidsMolecular BiologyMitosisChromosome AberrationsCell DeathModels GeneticMutagenicity TestsDNA replicationDNA MethylationMolecular biologyDNA methylationDNA mismatch repairSister Chromatid ExchangeMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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