Search results for "cyclin-dependent kinase"

showing 10 items of 164 documents

BRAFV600E Mutation and p27kip1 Expression in Papillary Carcinomas of the Thyroid ≤1 cm and Their Paired Lymph Node Metastases

2007

BACKGROUND. BRAFV600E mutation and p27kip1 expression have been introduced as novel indicators that may predict prognosis in different tumors, as well as in papillary thyroid carcinomas. METHODS. Tissue samples from 214 consecutive patients who underwent total or near-total thyroidectomy with histological diagnosis of papillary thyroid carcinoma (PTC) ≤1 cm were analyzed for BRAFV600E mutation by a real-time, allele-specific amplification and for p27kip1 expression by immunohistochemistry. RESULTS. The BRAFV600E mutation was detected in 88 of the tumors examined, with significant differences between groups with and without lymph node (LN) metastases; the mean age of patients with BRAFV600E …

AdultMaleProto-Oncogene Proteins B-rafCancer ResearchPathologymedicine.medical_specialtymedicine.medical_treatmentDown-RegulationGlutamic AcidSettore MED/08 - Anatomia PatologicaPolymerase Chain ReactionMetastasisSettore MED/13 - EndocrinologiaThyroid carcinomaPredictive Value of TestsCarcinomaBiomarkers TumorMedicineHumansThyroid NeoplasmsLymph nodebusiness.industryThyroidThyroidectomyCancerValineSequence Analysis DNAMiddle Agedmedicine.diseasePrognosispapillary thyroid carcinoma BRAF p27 cell cycle.ImmunohistochemistryCarcinoma PapillaryGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyLymphatic MetastasisMutation (genetic algorithm)MutationFemalebusinessCyclin-Dependent Kinase Inhibitor p27
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Increased expression of p16 in both oral and genital lichen planus.

2018

Background Lichen Planus, LP, is an inflammatory disease of possible autoimmune origin affecting mainly oral and genital mucosa and skin. According to the WHO oral LP is considered a potentially malignant disorders. The p16 tumour suppressor protein can act as an inhibitor of cyclin dependent kinases 4 and 6 and thus down regulate cell cycle progression. Since the discovery of p16 several studies have evaluated its expression in various forms of human cancers. The aim of this study was to evaluate and compare the expression of p16 in oral and genital LP and corresponding healthy mucosa. Material and Methods A total of 76 cases of oral LP (OLP), 34 cases of genital LP (GLP), 12 cases of heal…

AdultMalemedicine.medical_specialtyDisease03 medical and health sciences0302 clinical medicinestomatognathic systemMedicineHumansSex organskin and connective tissue diseasesGeneral DentistryCyclin-Dependent Kinase Inhibitor p16AgedAged 80 and overOral Medicine and Pathologyintegumentary systembusiness.industryResearchLichen Planus030206 dentistryMiddle Aged:CIENCIAS MÉDICAS [UNESCO]Dermatologystomatognathic diseasesOtorhinolaryngology030220 oncology & carcinogenesisUNESCO::CIENCIAS MÉDICASSurgeryFemaleGenital Diseases MalebusinessGenital Diseases FemaleGenital lichen planusLichen Planus OralMedicina oral, patologia oral y cirugia bucal
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Up-Regulation of leucocytes Genes Implicated in Telomere Dysfunction and Cellular Senescence Correlates with Depression and Anxiety Severity Scores

2012

BACKGROUND: Major depressive disorder (MDD) is frequently associated with chronic medical illness responsible of increased disability and mortality. Inflammation and oxidative stress are considered to be the major mediators of the allostatic load, and has been shown to correlate with telomere erosion in the leucocytes of MDD patients, leading to the model of accelerated aging. However, the significance of telomere length as an exclusive biomarker of aging has been questioned on both methodological and biological grounds. Furthermore, telomeres significantly shorten only in patients with long lasting MDD. Sensitive and dynamic functional biomarkers of aging would be clinically useful to eval…

AgingGene Expressionlcsh:MedicineAnxietySocial and Behavioral Sciences0302 clinical medicineBiomarkers of agingMolecular Cell BiologyLeukocytesPathologyPsychologylcsh:ScienceCellular SenescenceDepression (differential diagnoses)Psychiatry0303 health sciencesMultidisciplinaryDepressionChromosome BiologyGenomicsMiddle AgedTelomereAllostatic loadUp-RegulationTelomeresMental HealthMedicineMajor depressive disorderAnxietyBiomarker (medicine)Femalemedicine.symptomResearch ArticleAdultSenescenceClinical PathologyPsychological StressBiologybehavioral disciplines and activitiesMolecular Genetics03 medical and health sciencesDiagnostic Medicinemental disordersGeneticsmedicineHumansBiologyCyclin-Dependent Kinase Inhibitor p16030304 developmental biologyDepressive Disorder Majorlcsh:RComputational BiologyHuman GeneticsDNAmedicine.diseaseTelomereOxygenGene Expression RegulationImmunologyStathminlcsh:QBiomarkers030217 neurology & neurosurgeryDNA DamagePLoS ONE
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Protein kinase activities associated with ribosomes of developing rat brain. Identification of eukaryotic initiation factor 2 kinases.

1986

Protein kinases associated with ribosomes in the brains of suckling (4-10 days) and adult (2 months) rats were extracted from ribosomal fraction with 0.5 M KCl. The different protein kinase activities were characterized by their ability to phosphorylate three exogenous substrates: casein, histone IIs and histone IIIs in the presence of different modulators. Ribosomal salt wash fractions contain a high casein kinase activity which was partially inhibited by heparin and stimulated by calmodulin in the presence of Ca2+, indicating the presence of casein kinase I and II and calcium/calmodulin-dependent kinases. Cyclic AMP and cyclic GMP-dependent kinases and protein kinase C (calcium/phospholip…

AgingbiologyCyclin-dependent kinase 2BrainCaseinsRats Inbred StrainsMitogen-activated protein kinase kinaseRatseIF-2 KinaseDevelopmental NeuroscienceBiochemistryCasein Kinase ICasein kinase 2 alpha 1biology.proteinAnimalsASK1Cyclin-dependent kinase 9Casein kinase 1Casein kinase 2PhosphorylationProtein KinasesRibosomesDevelopmental BiologySubcellular FractionsInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
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Induction of apoptosis in human retinoblastoma cells by topoisomerase inhibitors

1998

PURPOSE:To examine the apoptotic effect induced in human retinoblastoma Y79 cells by camptothecin, etoposide, and amsacrine, to examine the effect of these drugs on the expression of many apoptosis-related modulators, and to test the antiapoptotic effect exerted by insulin-like growth factor-I (IGF-I). METHODS:Morphologic features of apoptosis were demonstrated using acridine orange- ethidium bromide staining and electron microscopy. DNA fragmentation was determined by means of an in situ cell detection procedure (TdT-dUTP terminal nick-end labeling [TUNEL]) or by electrophoresis on agarose gels and was quantified by enzyme-linked immunosorbent assay. The expression of apoptosis-related mod…

AmsacrineCyclin-Dependent Kinase Inhibitor p21topoisomeraseCell SurvivalRetinal NeoplasmsRetinoblastomaApoptosisDNA NeoplasmInsulin-Like Growth Factor Binding Protein 3DNA Topoisomerases Type IProto-Oncogene Proteins c-bcl-2CyclinsProto-Oncogene ProteinsDactinomycinTumor Cells CulturedHumansCamptothecinCycloheximideEnzyme InhibitorsTopoisomerase I InhibitorsTumor Suppressor Protein p53DNA DamageEtoposidebcl-2-Associated X Protein
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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JAK3/STAT5/6 Pathway Alterations Are Associated with Immune Deviation in CD8+ T Cells in Renal Cell Carcinoma Patients

2010

To investigate the molecular mechanisms underlying altered T cell response in renal cell carcinoma (RCC) patients, we compared autologous and allogeneic CD8(+) T cell responses against RCC line from RCC patients and their HLA-matched donors, using mixed lymphocyte/tumor cell cultures (MLTCs). In addition, we analyzed the expression of molecules associated with cell cycle regulation. Autologous MLTC responder CD8(+) T cells showed cytotoxic activity against RCC cell lines; however the analysis of the distribution of CD8(+) T-cell subsets revealed that allogenic counterparts mediate superior antitumor efficacy. In RCC patients, a decreased proliferative response to tumor, associated with defe…

Article SubjectCell Survivallcsh:Biotechnologylcsh:MedicineEnzyme-Linked Immunosorbent AssayE2F4 Transcription FactorCD8-Positive T-Lymphocytesurologic and male genital diseaseslcsh:TP248.13-248.65Chromium IsotopesSTAT5 Transcription FactorTumor Cells CulturedHumansCarcinoma Renal CellInhibitor of Differentiation Protein 2Microscopy Confocallcsh:RCell CycleIntracellular Signaling Peptides and ProteinsJanus Kinase 3Flow Cytometryfemale genital diseases and pregnancy complicationsKidney NeoplasmsGene Expression Regulation NeoplasticCase-Control StudiesLymphocyte Culture Test MixedSTAT6 Transcription FactorCyclin-Dependent Kinase Inhibitor p27Research ArticleSignal TransductionJournal of Biomedicine and Biotechnology
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Beckwith–Wiedemann syndrome: multiple molecular mechanisms

2006

Beckwith–Wiedemann syndrome (BWS) is a congenital overgrowth condition with an increased risk of developing embryonic tumours, such as Wilms' tumour. The cardinal features are abdominal wall defects, macroglossia and gigantism. BWS is generally sporadic; only 10–15% of cases are familial. A variety of molecular aberrations have been associated with BWS. The only mutations within a gene are loss-of-function mutations in the CDKN1C gene, which codes for an imprinted cell-cycle regulator. CDKN1C mutations appear to be particularly associated with umbilical abnormalities, but not with increased predisposition to Wilms' tumour. In the remaining BWS subgroups, a disturbance of the tight epigeneti…

Beckwith-Wiedemann SyndromeGenotypeTranscription GeneticBeckwith–Wiedemann syndromeBioinformaticsModels BiologicalEpigenesis GeneticGenomic ImprintingGenotypeMacroglossiaAnimalsHumansMedicineEpigeneticsCyclin-Dependent Kinase Inhibitor p57Molecular BiologyModels Geneticbusiness.industryDNA Methylationmedicine.diseasePhenotypeGigantismPhenotypeMutationDNA methylationMolecular Medicinemedicine.symptombusinessGenomic imprintingExpert Reviews in Molecular Medicine
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Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas

2007

AbstractIntegrative genomic and gene-expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored. Array-based comparative genomic hybridization (CGH) and gene-expression microarray analysis of 48 cell lines derived from patients with different B-NHLs delineated 20 homozygous deletions at 7 chromosome areas, all of which contained tumor suppressor gene targets. Further investigation revealed that only a fraction of primary biopsies presented inactivation of these genes by point mutation or intragenic deletion, but instead some of them w…

BiopsyDNA Mutational AnalysisGene DosageVesicular Transport ProteinsApoptosisBiochemistryEpigenesis Geneticimmune system diseaseshemic and lymphatic diseasesChromosomes HumanGenes Tumor SuppressorPromoter Regions GeneticSorting NexinsOligonucleotide Array Sequence AnalysisSequence DeletionBcl-2-Like Protein 11HomozygoteChromosome MappingNuclear ProteinsNucleic Acid HybridizationRNA-Binding ProteinsHematologyDNA NeoplasmBCL10Gene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2DNA methylationLymphoma B-CellTumor suppressor geneImmunologyBiologyGene dosageCell Line TumorProto-Oncogene ProteinsmedicineCyclin-Dependent Kinase Inhibitor p18HumansPoint MutationGene SilencingB cellAdaptor Proteins Signal TransducingHomeodomain ProteinsMembrane ProteinsCell BiologyDNA Methylationmedicine.diseaseMolecular biologyLymphomaCancer researchMantle cell lymphomaApoptosis Regulatory ProteinsCarrier ProteinsDiffuse large B-cell lymphomaTranscription Factors
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TORC1 controls G1–S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway

2015

The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G1–S cell cycle progression, also coined as START, by favouring the expression of G1 cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G1 cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex.…

BioquímicaBiologiaSaccharomyces cerevisiae ProteinsImmunoblottingGeneral Physics and AstronomyCell Cycle ProteinsSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1ArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsImmunoprecipitationProtein Phosphatase 2Cell division control protein 4PhosphorylationProtein kinase ACyclin-Dependent Kinase Inhibitor Proteins030304 developmental biology0303 health sciencesMultidisciplinarybiologyTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesGeneral ChemistryBlotting NorthernFlow CytometryG1 Phase Cell Cycle CheckpointsSic1Cyclin-Dependent KinasesCell biologyBiochemistryMultiprotein Complexes030220 oncology & carcinogenesisUbiquitin ligase complexbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylationTOR Serine-Threonine KinasesMitogen-Activated Protein KinasesPeptidesProtein KinasesCyclin-dependent kinase inhibitor proteinNature Communications
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