Search results for "CDC2 Protein Kinase"

showing 10 items of 17 documents

Molecular analysis of differential antiproliferative activity of resveratrol, epsilon viniferin and labruscol on melanoma cells and normal dermal cel…

2018

IF 3.778 (2016); International audience; Very recently, we have produced new resveratrol derived compounds, especially labruscol by culture of elicited grapevine cell suspensions (Vitis labrusca L.). This new polyphenolic oligomer could function as cancer chemopreventive agent in similar manner of resveratrol. In this study, we have determined the efficiency of resveratrol, ε-viniferin and the labruscol on human melanoma cell with or without metastatic phenotype. Our results show a differential activity of the three compounds where the resveratrol remains the polyphenolic compound with the most effective action compared to other oligomers. These three compounds block cell cycle of melanoma …

0301 basic medicineBioproductsProgrammed cell deathCellCyclin AResveratrolepsilon-ViniferinCell cycleToxicologyS Phase03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line Tumor[SDV.IDA]Life Sciences [q-bio]/Food engineeringCDC2 Protein KinaseCyclin EStilbenesmedicineCytotoxic T cellAnticarcinogenic AgentsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCyclin D1VitisMelanoma cellsMelanomaCyclinBenzofuransCell ProliferationSkinKinaseCyclin-Dependent Kinase 2food and beveragesPolyphenolsGeneral MedicineCell cycleFibroblasts3. Good health030104 developmental biologymedicine.anatomical_structurechemistryResveratrol030220 oncology & carcinogenesis[SDV.TOX]Life Sciences [q-bio]/ToxicologyCancer researchFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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In silico identification of small molecules as new cdc25 inhibitors through the correlation between chemosensitivity and protein expression pattern

2021

The cell division cycle 25 (Cdc25) protein family plays a crucial role in controlling cell proliferation, making it an excellent target for cancer therapy. In this work, a set of small molecules were identified as Cdc25 modulators by applying a mixed ligand-structure-based approach and taking advantage of the correlation between the chemosensitivity of selected structures and the protein expression pattern of the proposed target. In the first step of the in silico protocol, a set of molecules acting as Cdc25 inhibitors were identified through a new ligand-based protocol and the evaluation of a large database of molecular structures. Subsequently, induced-fit docking (IFD) studies allowed us…

0301 basic medicineHepG2Protein familyCdc25In silicoAntiproliferative activityCell cycleLigandsCatalysisArticleInorganic Chemistrylcsh:Chemistry03 medical and health sciencesCdc250302 clinical medicineCDC2 Protein KinaseDrug DiscoveryHumanscdc25 PhosphatasesComputer SimulationMolecular Targeted TherapyPhysical and Theoretical ChemistryPhosphorylationMolecular Biologylcsh:QH301-705.5DRUDITSpectroscopyBinding SitesbiologyCell growthChemistryOrganic ChemistryGeneral MedicineHep G2 CellsCell cycleAntiproliferative activity; Cdc25; Cell cycle; DRUDIT; HepG2; Molecular dockingLigand (biochemistry)Small moleculeComputer Science Applications030104 developmental biologyBiochemistrylcsh:Biology (General)lcsh:QD1-999Docking (molecular)030220 oncology & carcinogenesisMolecular dockingbiology.proteinDrug Screening Assays Antitumor
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Synthesis, antitumor activity and CDK1 inhibiton of new thiazole nortopsentin analogues

2017

A new series of thiazole nortopsentin analogues was conveniently synthesized with fair overall yields. The antiproliferative activity of the new derivatives was tested against different human tumor cell lines of the NCI full panel. Four of them showed good antitumor activity with GI(50) values from micro to nanomolar level. The mechanism of the antiproliferative effect of these derivatives, was pro-apoptotic, being associated with externalization of plasma membrane phosphatidylserine and DNA fragmentation. The most active and selective of the new thiazoles confined viable cells in G2/M phase and markedly inhibited in vitro CDK1 activity. (C) 2017 Elsevier Masson SAS.

0301 basic medicineIndolesCell SurvivalStereochemistryMolecular ConformationNortopsentin analogues3-b]pyridinesAntineoplastic AgentsApoptosisMarine alkaloids Nortopsentin analogues Antiproliferative activity Apoptosis CDK1 inhibitors Thiazolyl-1H-pyrrolo[23-b]pyridinesAntiproliferative activity01 natural sciencesStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundMarine alkaloidsCDC2 Protein KinaseDrug DiscoveryHumansThiazoleProtein Kinase InhibitorsCell ProliferationPharmacologyCyclin-dependent kinase 1Dose-Response Relationship DrugMarine alkaloids; Nortopsentin analogues; Antiproliferative activity; Apoptosis; CDK1 inhibitors; Thiazolyl-1H-pyrrolo[2; 3-b]pyridines010405 organic chemistryOrganic ChemistryImidazolesGeneral MedicinePhosphatidylserineThiazolyl-1H-pyrrolo[2Settore CHIM/08 - Chimica FarmaceuticaCyclin-Dependent KinasesIn vitro0104 chemical sciencesCDK1 inhibitors030104 developmental biologyMembranechemistryCell cultureApoptosisMCF-7 CellsDNA fragmentationCaco-2 CellsDrug Screening Assays Antitumor
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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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Resveratrol, a chemopreventive agent, disrupts the cell cycle control of human SW480 colorectal tumor cells

2002

Resveratrol is a natural polyphenolic compound produced by a number of plants and found in high amount in peanuts, seeds, grapes or berries as source of human nutrition. Epidemiological studies strongly suggest that resveratrol may act as a cancer chemopreventive compound. The mechanism by which resveratrol inhibits cell proliferation was studied in human colorectal tumor SW480 cell line. The results show that resveratrol strongly inhibits cell proliferation at the micromolar range in a time- and dose-dependent manner. Resveratrol appears to block the cell cycle at the transition --> G2/M since inhibition of [(3)H]-thymidine incorporation is not observed, while there is an increase of the c…

DNA Replicationendocrine system diseasesCellCyclin AAdenocarcinomaCyclin BProtein Serine-Threonine KinasesResveratrolS Phasechemistry.chemical_compoundCDC2 Protein KinaseStilbenesCDC2-CDC28 KinasesTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansCyclin B1Phosphorylationskin and connective tissue diseasesCyclinCyclin-dependent kinase 1biologyKinaseCell growthorganic chemicalsCell CycleCyclin-Dependent Kinase 2Cyclin-dependent kinase 2food and beveragesGeneral MedicineCell cycleFlow CytometryCyclin-Dependent KinasesGrowth InhibitorsNeoplasm ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureBiochemistrychemistryResveratrolEnzyme Inductionbiology.proteinCancer researchColorectal NeoplasmsProtein Processing Post-TranslationalCell DivisionInternational Journal of Molecular Medicine
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Escherichia coli cytolethal distending toxin blocks the HeLa cell cycle at the G2/M transition by preventing cdc2 protein kinase dephosphorylation an…

1997

Cytolethal distending toxins (CDT) constitute an emerging heterogeneous family of bacterial toxins whose common biological property is to inhibit the proliferation of cells in culture by blocking their cycle at G2/M phase. In this study, we investigated the molecular mechanisms underlying the block caused by CDT from Escherichia coli on synchronized HeLa cell cultures. To this end, we studied specifically the behavior of the two subunits of the complex that determines entry into mitosis, i.e., cyclin B1, the regulatory unit, and cdc2 protein kinase, the catalytic unit. We thus demonstrate that CDT causes cell accumulation in G2 and not in M, that it does not slow the progression of cells th…

G2 PhaseCytolethal distending toxinBacterial toxins[SDV]Life Sciences [q-bio]ImmunologyBacterial ToxinsMitosisBiologyMicrobiologyCDTCDC2 Protein KinaseEscherichia coliHumansKinase activityPhosphorylationMitosisCyclin-dependent kinase 1Cell growthCell CycleCell cycleG2-M DNA damage checkpointFlow CytometryMicrobiologie et ParasitologieCell biology[SDV] Life Sciences [q-bio]Enzyme ActivationInfectious DiseasesCytolethal distending toxinsParasitologyCDC2 Protein KinaseHeLa CellsResearch Article
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Type III Secretion-Dependent Cell Cycle Block Caused in HeLa Cells by Enteropathogenic Escherichia coliO103

2001

ABSTRACT Rabbit enteropathogenic Escherichia coli (EPEC) O103 induces in HeLa cells an irreversible cytopathic effect characterized by the recruitment of focal adhesions, formation of stress fibers, and inhibition of cell proliferation. We have characterized the modalities of the proliferation arrest and investigated its underlying mechanisms. We found that HeLa cells that were exposed to the rabbit EPEC O103 strain E22 progressively accumulated at 4C DNA content and did not enter mitosis. A significant proportion of the cells were able to reinitiate DNA synthesis without division, leading to 8C DNA content. This cell cycle inhibition by E22 was abrogated in mutants lacking EspA, -B, and -D…

G2 Phase[SDV]Life Sciences [q-bio]ImmunologyCyclin BMitosisReceptors Cell SurfacePATHOGENICITECyclin BMicrobiology03 medical and health sciencesBacterial ProteinsCDC2 Protein KinaseEscherichia coliHumansCyclin B1PhosphorylationCyclin B1Adhesins BacterialMitosisCytoskeleton030304 developmental biologyIntimin0303 health sciencesCyclin-dependent kinase 1Cellular Microbiology: Pathogen-Host Cell Molecular Interactionsbiology030306 microbiologyCell growthEscherichia coli ProteinsCell CycleREARRANGEMENTCell cycle[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyCell biology[SDV] Life Sciences [q-bio]Infectious Diseasesbiology.proteinTyrosineParasitologyCarrier ProteinsCDC2 Protein KinaseBacterial Outer Membrane ProteinsHeLa Cells
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Sequence of lethal events in HeLa cells exposed to the G2 blocking cytolethal distending toxin

2000

The bacterial cytolethal distending toxin (CDT) was previously shown to block the cell cycle of several cell lines at stage G2 through inactivation of the cyclin-dependent kinase Cdkl and without induction of DNA strand breaks. In the present study, we have analyzed, using various methods of analytical cytometry, the progressive transformation and delayed lethal events in the tumor-derived HeLa cell line temporarily exposed to CDT. The cell proliferation arrest induced by CDT was irreversible but, starting about two days after exposure, the G2 block released partially, concomitantly with a decline in the level of Cdkl phosphorylation. This partial release resulted in endoreduplication, lead…

HistologyTime FactorsCytolethal distending toxinCell divisionAntimetabolitesCell Survival[SDV]Life Sciences [q-bio]Bacterial ToxinsMitosisApoptosisKINASE CYCLIQUE DEPENDANTEBiologyCyclin BPathology and Forensic MedicineCDC2 Protein KinaseEndoreduplicationHumansCyclin B1PhosphorylationMitosisCentrosomeCell DeathCell growthCell BiologyGeneral MedicineCell cycleFlow CytometryVirologyMolecular biologyImmunohistochemistry[SDV] Life Sciences [q-bio]BromodeoxyuridineMicroscopy FluorescenceCell cultureApoptosisCell DivisionHeLa Cells
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High-throughput screening with the Eimeria tenella CDC2-related kinase2/cyclin complex EtCRK2/EtCYC3a

2012

The poultry disease coccidiosis, caused by infection with Eimeria spp. apicomplexan parasites, is responsible for enormous economic losses to the global poultry industry. The rapid increase of resistance to therapeutic agents, as well as the expense of vaccination with live attenuated vaccines, requires the development of new effective treatments for coccidiosis. Because of their key regulatory function in the eukaryotic cell cycle, cyclin-dependent kinases (CDKs) are prominent drug targets. The Eimeria tenella CDC2-related kinase 2 (EtCRK2) is a validated drug target that can be activated in vitro by the CDK activator XlRINGO (Xenopus laevis rapid inducer of G2/M progression in oocytes). B…

In silicoPlasmodium falciparumAntiprotozoal AgentsDrug Evaluation PreclinicalProtozoan ProteinsMicrobiologyEimeriaMicrobiology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsparasitic diseasesCDC2 Protein KinaseAnimalsEnzyme Inhibitors030304 developmental biologyCyclin0303 health sciencesCyclin-dependent kinase 1biologyKinaseComputational BiologyPlasmodium falciparumCell cyclebiology.organism_classificationVirologyStandard3. Good healthHigh-Throughput Screening Assays030220 oncology & carcinogenesisCell and Molecular Biology of Microbesbiology.proteinEimeria tenellaMicrobiology
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