Search results for "Cell cycle"

showing 4 items of 804 documents

Synthesis, antiproliferative activity, and in silico insights of new 3-benzoylamino-benzo[ b ]thiophene derivatives

2014

A new series of 3-benzoylamino-5-imidazol-5-yl-benzo[b]thiophenes and the parent amino derivatives were synthesized and screened as antitumor agents. All tested compounds showed concentration-dependent antiproliferative activity profile against HeLa cell line, exhibiting GI50 values in the low micromolar range. The most active compounds were tested in cell cycle perturbation experiments. A rapid accumulation of cells in the G2/M phase, with a concomitant reduction of cells in both the S and G0/G1 phases, was observed, suggesting that cell exposure to selected derivatives produces mitotic failure. To rationalize the biological results, the 3-benzoylamino-benzo[b]thiophenes were analyzed thro…

thiopheneVLAK protocolStereochemistryIn silicoCellAntineoplastic AgentsMechanism of actionHeLa CellHeLaAntineoplastic AgentStructure-Activity Relationship3-Benzoylamino-5-imidazol-4-yl-benzo[b]Settore BIO/10 - BiochimicaDrug DiscoverymedicineHumansMoietyComputer SimulationMitosisCell ProliferationPharmacologyAntitumor agentsbiologyDose-Response Relationship DrugMolecular StructureChemistryDrug Discovery3003 Pharmaceutical ScienceMedicine (all)Cell CycleOrganic ChemistryAntitumor agentG2/M phaseGeneral MedicineSettore CHIM/06 - Chimica OrganicaHeLa cell linebiology.organism_classificationSettore CHIM/08 - Chimica Farmaceuticamedicine.anatomical_structureCell cultureSettore CHIM/03 - Chimica Generale E InorganicathiophenesAntimitotic AgentTopoisomerase-II InhibitorDrug Screening Assays AntitumorHeLa CellsHuman
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Virus-cell interactions as a pathological mechanism of parvovirus infection

2014

vauriotreplikaatiovuorovaikutusisäntäsolutviruksetCPVpatogeneesimitokondriotapoptosiscanine parvovirussolutuhocell signallinginfektiotmitochondriacell cycle arrestpathologyparvoviruksetapoptoosi
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CVB3 VP1 interacts with MAT1 to inhibit cell proliferation by interfering with Cdk-activating kinase complex activity in CVB3-induced acute pancreati…

2021

Coxsackievirus B3 (CVB3) belongs to the genus Enterovirus of the family Picornaviridae and can cause acute acinar pancreatitis in adults. However, the molecular mechanisms of pathogenesis underlying CVB3-induced acute pancreatitis have remained unclear. In this study, we discovered that CVB3 capsid protein VP1 inhibited pancreatic cell proliferation and exerted strong cytopathic effects on HPAC cells. Through yeast two-hybrid, co-immunoprecipitation, and confocal microscopy, we show that Menage a trois 1 (MAT1), a subunit of the Cdk-Activating Kinase (CAK) complex involved in cell proliferation and transcription, is a novel interaction protein with CVB3 VP1. Moreover, CVB3 VP1 inhibited MAT…

virusesCultured tumor cellsSynthesis PhaseCell Cycle ProteinsBiochemistryCell Cycle and Cell DivisionBiology (General)PhosphorylationPost-Translational ModificationCyclin0303 health sciencesbiologyKinaseChemistry030302 biochemistry & molecular biologyRetinoblastoma proteinvirus diseasesCell DifferentiationTransfectionCyclin-Dependent KinasesCell biologyEnterovirus B HumanCell ProcessesPhosphorylationCell linesBiological culturesResearch ArticleQH301-705.5Protein subunitImmunologyCoxsackievirus InfectionsTransfectionResearch and Analysis MethodsMicrobiology03 medical and health sciencesVirologyCyclinsGeneticsHumansHeLa cellsMolecular Biology TechniquesMolecular Biology030304 developmental biologyCell ProliferationCell growthG1 PhaseBiology and Life SciencesProteinsCell Cycle CheckpointsCell BiologyRC581-607Cell culturesPancreatitisbiology.proteinParasitologyCapsid ProteinsImmunologic diseases. AllergyCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseTranscription FactorsPLoS pathogens
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PTC124-mediated translational readthrough of a nonsense mutation causing Usher syndrome type 1C.

2011

We investigated the therapeutic potential of the premature termination codon (PTC) readthrough-inducing drug PTC124 in treating the retinal phenotype of Usher syndrome, caused by a nonsense mutation in the USH1C gene. Applications in cell culture, organotypic retina cultures, and mice in vivo revealed significant readthrough and the recovery of protein function. In comparison with other readthrough drugs, namely the clinically approved readthrough-inducing aminoglycoside gentamicin, PTC124 exhibits significant better retinal biocompatibility. Its high readthrough efficiency in combination with excellent biocompatibility makes PTC124 a promising therapeutic agent for PTCs in USH1C, as well a…

virusesUsher syndromeGenetic enhancementNonsense mutationGenetic VectorsCell Cycle ProteinsRetina03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivootorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansMolecular BiologyCells Cultured030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesOxadiazolesbusiness.industryfungiAminoglycosideTranslational readthroughmedicine.diseasePhenotype3. Good healthAtalurenMice Inbred C57BLCytoskeletal ProteinsLuminescent ProteinsElectroporationchemistryMicroscopy FluorescenceCodon NonsenseCancer researchMolecular MedicineGentamicinsbusinessUsher Syndromes030217 neurology & neurosurgeryHuman gene therapy
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