Search results for "HeLa Cell"

showing 10 items of 281 documents

Inhibition of Protein Isoprenylation Impairs Rho-Regulated Early Cellular Response to Genotoxic Stress

2000

Activation of c-Jun N-terminal kinases (JNKs) and nuclear factor-kappaB (NF-kappaB) are early cellular responses to genotoxic stress involved in the regulation of gene expression. Pretreatment of cells with the hydroxymethyl glutaryl-CoA reductase inhibitor lovastatin blocked stimulation of JNK1 activity by UV irradiation and by treatment with the alkylating compound methyl methanesulfonate but did not affect activation of extracellular signal-regulated kinase 2 by UV light. Lovastatin also attenuated UV-induced degradation of the NF-kappaB inhibitor IkappaBalpha. The effects of lovastatin on UV-triggered stimulation of JNK1 as well as on IkappaBalpha degradation were reverted by cotreatmen…

rho GTP-Binding ProteinsProtein PrenylationStimulationClostridium difficile toxin BCHO CellsGenotoxic StressBiologychemistry.chemical_compoundCricetinaemedicineAnimalsHumansMitogen-Activated Protein Kinase 8LovastatinPharmacologyMutagenicity TestsKinaseFarnesyltransferase inhibitorNF-kappa BMethyl methanesulfonateCell biologyIκBαchemistryMolecular MedicineLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesHeLa CellsSignal Transductionmedicine.drugMolecular Pharmacology
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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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Variants of human CLDN9 cause mild to profound hearing loss

2021

Hereditary deafness is clinically and genetically heterogeneous. We investigated deafness segregating as a recessive trait in two families. Audiological examinations revealed an asymmetric mild to profound hearing loss with childhood or adolescent onset. Exome sequencing of probands identified a homozygous c.475G>A;p.(Glu159Lys) variant of CLDN9 (NM_020982.4) in one family and a homozygous c.370_372dupATC;p.(Ile124dup) CLDN9 variant in an affected individual of a second family. Claudin 9 (CLDN9) is an integral membrane protein and constituent of epithelial bicellular tight junctions that form semi-permeable, paracellular barriers between inner ear perilymphatic and endolymphatic compartment…

tight junctionsAdolescentclaudin 9In situ hybridizationDeafnessBiologyArticleFrameshift mutationMiceotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansPakistanInner earNonsyndromic deafnessChildClaudinGenetics (clinical)Exome sequencingnonsyndromic deafnessTight junctionGenetic heterogeneityclaudin 9; exome sequencing; Morocco; nonsyndromic deafness; Pakistan; tight junctionsHomozygotemedicine.diseaseMolecular biologyPedigreeMoroccomedicine.anatomical_structureClaudinsMutationexome sequencingHeLa CellsHuman Mutation
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Single-cell analysis of population context advances RNAi screening at multiple levels

2012

Isogenic cells in culture show strong variability, which arises from dynamic adaptations to the microenvironment of individual cells. Here we study the influence of the cell population context, which determines a single cell's microenvironment, in image‐based RNAi screens. We developed a comprehensive computational approach that employs Bayesian and multivariate methods at the single‐cell level. We applied these methods to 45 RNA interference screens of various sizes, including 7 druggable genome and 2 genome‐wide screens, analysing 17 different mammalian virus infections and four related cell physiological processes. Analysing cell‐based screens at this depth reveals widespread RNAi‐induce…

toImage ProcessingDruggabilityGenomeImage analysis0302 clinical medicineComputer-AssistedSX00 SystemsX.ch2604 Applied MathematicsSingle-cell analysisRNA interferenceModels2400 General Immunology and MicrobiologyImage Processing Computer-AssistedViralRNA Small Interfering0303 health scienceseducation.field_of_studyApplied MathematicsSystems BiologyGenomics10124 Institute of Molecular Life SciencesCell biologycell variabilityComputational Theory and MathematicsCellular MicroenvironmentVirus DiseasesVirusesRNA ViralRNA InterferenceSingle-Cell AnalysisGeneral Agricultural and Biological SciencesInformation SystemsSystems biologyVirus infectionPopulationContext (language use)Genomics1100 General Agricultural and Biological SciencesBiologySmall InterferingModels BiologicalGeneral Biochemistry Genetics and Molecular BiologySX08 LipidX03 medical and health sciencesViral ProteinsCell-to-cell variability; Image analysis; Population context; RNAi; Virus infection1300 General Biochemistry Genetics and Molecular BiologyHumansComputer Simulationeducation030304 developmental biologyGeneral Immunology and MicrobiologyCell-to-cell variabilityReproducibility of ResultsBayes TheoremcellBiologicalPopulation contextRNAi570 Life sciences; biologyRNA030217 neurology & neurosurgeryHeLa CellsMolecular Systems Biology
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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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Internalization of novel non-viral vector TAT-streptavidin into human cells

2007

BMC Biotechnology, 7 (1)

virusesEndocytic cyclePROTEINS + POLYPEPTIDES (BIOCHEMISTRY)02 engineering and technologyei-virusperäinen vektoriProtein EngineeringgeeniterapiaPost Transductionchemistry.chemical_compoundTHERAPIES + THERAPEUTICS (MEDICINE)Drug Delivery SystemsLääketieteen bioteknologia - Medical biotechnologyInternalizationmedia_commoninfo:eu-repo/classification/ddc/5700303 health sciencesPinocytosisNocodazoleVEKTOREN (GENETISCHE TECHNIKEN)021001 nanoscience & nanotechnologyLife sciencesCell biologyEndosomal EscapeBiotinylationGene Products tatVirusesVECTORS (GENETIC TECHNIQUES)VEKTOREN (GENETISCHE TECHNIKEN); THERAPIEN + THERAPEUTIK (MEDIZIN); PROTEINE + POLYPEPTIDE (BIOCHEMIE); VECTORS (GENETIC TECHNIQUES); THERAPIES + THERAPEUTICS (MEDICINE); PROTEINS + POLYPEPTIDES (BIOCHEMISTRY)0210 nano-technologyTHERAPIEN + THERAPEUTIK (MEDIZIN)BiotechnologyResearch ArticleStreptavidinEndosomeImmunoelectron microscopymedia_common.quotation_subjectRecombinant Fusion Proteinslcsh:BiotechnologyGenetic VectorsBiologyEndocytosis03 medical and health sciencesstreptavidiiniddc:570lcsh:TP248.13-248.65HumansEndosomal Marker030304 developmental biologyMolecular biologyEndocytic VesiclechemistryStreptavidinTATPROTEINE + POLYPEPTIDE (BIOCHEMIE)HeLa CellsBMC Biotechnology
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The Nasal Epithelium as a Factory for Systemic Protein Delivery

2002

We have previously shown that recombinant Sendai virus (SeV) produces efficient in vivo airway epithelial gene transfer. The ability to produce therapeutic levels of circulating proteins following noninvasive gene transfer would have widespread clinical application. Here, we compared nose, lung, and skeletal muscle for the ability to produce circulating levels of the secreted mouse antiinflammatory cytokine interleukin-10 (IL10) following SeV-mediated gene transfer. High levels of serum IL10 were obtained from each site with a potency order of lung > nose > muscle for a given viral titer. Serum levels from each site were within the likely required range for anti-inflammatory effects. The co…

virusesGenetic enhancementmedicine.medical_treatmentMucous membrane of noseSendai virus03 medical and health sciences0302 clinical medicineIn vivoDrug DiscoverymedicineGeneticsAnimalsHumansMuscle SkeletalLungMolecular BiologyNose030304 developmental biologyPharmacology0303 health sciencesLungbiologyGene Transfer TechniquesSkeletal musclerespiratory systembiology.organism_classificationSendai virus3. Good healthInterleukin-10Nasal Mucosamedicine.anatomical_structureCytokine030220 oncology & carcinogenesisImmunologyCOS CellsMolecular MedicineHeLa CellsMolecular Therapy
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Human Papillomavirus Types 16, 18, and 31 Share Similar Endocytic Requirements for Entry

2013

ABSTRACT Human papillomavirus type 18 (HPV18), one of the HPVs with malignant potential, enters cells by an unknown endocytic mechanism. The key cellular requirements for HPV18 endocytosis were tested in comparison to those for HPV16 and -31 endocytoses. HPV18 (like HPV16 and -31) entry was independent of clathrin, caveolin, dynamin, and lipid rafts but required actin polymerization and tetraspanin CD151, and the viruses were routed to the same LAMP-1-positive compartment. Hence, the viruses shared similar cellular requirements for endocytic entry.

virusesImmunologyEndocytic cycleTetraspanin 24EndocytosisMicrobiologyClathrinDynamin IIPolymerizationDynamin IIMembrane MicrodomainsTetraspaninVirologyCaveolinHumansHuman papillomavirus 31Lipid raftDynaminHuman papillomavirus 16Microscopy ConfocalHuman papillomavirus 18biologyvirus diseasesLysosome-Associated Membrane GlycoproteinsVirus InternalizationVirologyActinsEndocytosisVirus-Cell InteractionsCell biologyMicroscopy ElectronMicroscopy FluorescenceInsect Sciencebiology.proteinElectrophoresis Polyacrylamide GelHeLa CellsJournal of Virology
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In vitro studies on the activation of the hepatitis C virus NS3 proteinase by the NS4A cofactor.

1996

AbstractProteolytic processing of the nonstructural proteins of the hepatitis C virus (HCV) is mediated by two viral proteinases: the NS2-3 proteinase cleaving at the NS2/3 junction and the NS3 serine-type proteinase responsible for processing at the NS3/4A, NS4A/B, NS4B/5A, and NS5A/B sites. Activity of the NS3 proteinase is modulated by NS4A. In the absence of this cofactor processing at the NS3-dependent sites does not occur or, in the case of the NS5A/B junction, is poor but increased when NS4A is present. Although recent studies demonstrated that proteinase activation requires direct interaction between NS3 and NS4A, the mechanism by which NS4A exerts the activation function is not kno…

virusesMolecular Sequence DataHepacivirusBiologyViral Nonstructural ProteinsCell LineEnzyme activatorProteinase 3VirologyCricetinaeMicrosomesAnimalsHumansAmino Acid SequenceBinding siteNS5APeptide sequenceSequence Deletionchemistry.chemical_classificationNS3Binding SitesBase Sequencevirus diseasesIntracellular Membranesbiochemical phenomena metabolism and nutritionMolecular biologyIn vitrodigestive system diseasesAmino acidEnzyme ActivationBiochemistrychemistryDNA ViralPeptidesHeLa CellsVirology
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Clathrin- and Caveolin-Independent Entry of Human Papillomavirus Type 16—Involvement of Tetraspanin-Enriched Microdomains (TEMs)

2008

BACKGROUND: Infectious entry of human papillomaviruses into their host cells is an important step in the viral life cycle. For cell binding these viruses use proteoglycans as initial attachment sites. Subsequent transfer to a secondary receptor molecule seems to be involved in virus uptake. Depending on the papillomavirus subtype, it has been reported that entry occurs by clathrin- or caveolin-mediated mechanisms. Regarding human papillomavirus type 16 (HPV16), the primary etiologic agent for development of cervical cancer, clathrin-mediated endocytosis was described as infectious entry pathway. METHODOLOGY/PRINCIPAL FINDINGS: Using immunofluorescence and infection studies we show in contra…

viruseslcsh:MedicinePlatelet Membrane GlycoproteinsTetraspanin 24CaveolaeKidneyEndocytosisClathrinVirusCell LineMembrane MicrodomainsViral life cycleTetraspaninAntigens CDCaveolaeInfectious Diseases/Viral InfectionsCaveolinInfectious Diseases/Sexually Transmitted DiseasesHumanslcsh:ScienceHuman papillomavirus 16MultidisciplinarybiologyTetraspanin 30lcsh:RVirionMembrane Proteinsvirus diseasesCell BiologyVirus InternalizationVirology/Host Invasion and Cell EntryVirologyClathrinEndocytosisCell biologyCell culturebiology.proteinFemalelcsh:QMicrobiology/Cellular Microbiology and PathogenesisHeLa CellsResearch ArticlePLoS ONE
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