Search results for "Replication"

showing 10 items of 489 documents

Loss of surface fibronectin after infection of cultured cells by HSV-1 and 2

1985

Fibronectin is lost from the surface of HSV infected cells during cell rounding. In order to investigate also the fate of fibronectin during the process of HSV-induced cell-fusion, BHK, Vero as well as primary or secondary rabbit kidney cells were infected with HSV-1 strains producing cell-fusion. By immunofluorescence and immunoelectron microscopy a considerable loss of fibronectin after HSV infection could be demonstrated leaving only irregular clumps of fibronectin containing virus particles on the cell surface. Decrease and disarrangement of fibronectin was similar during cell rounding and cell fusion. Loss of Fibronectin was closely connected with the two types of the cytopathic effect…

Cytochalasin BvirusesImmunoelectron microscopyBiologyKidneyVirus ReplicationCell FusionCell membranechemistry.chemical_compoundCricetinaeVirologymedicineAnimalsSimplexvirusProtease InhibitorsCytochalasin BCells CulturedCytopathic effectCell fusionHerpes SimplexGeneral MedicineActin cytoskeletonVirologyFibronectinsFibronectinActin Cytoskeletonmedicine.anatomical_structurechemistryCell culturebiology.proteinRabbitsArchives of Virology
researchProduct

Intracellular route of canine parvovirus entry.

1998

ABSTRACT The present study was designed to investigate the endocytic pathway involved in canine parvovirus (CPV) infection. Reduced temperature (18°C) or the microtubule-depolymerizing drug nocodazole was found to inhibit productive infection of canine A72 cells by CPV and caused CPV to be retained in cytoplasmic vesicles as indicated by immunofluorescence microscopy. Consistent with previously published results, these data indicate that CPV enters a host cell via an endocytic route and further suggest that microtubule-dependent delivery of CPV to late endosomes is required for productive infection. Cytoplasmic microinjection of CPV particles was used to circumvent the endocytosis and membr…

CytoplasmMicroinjectionsParvovirus CanineEndosomeanimal diseasesvirusesImmunologyEndocytic cycleBiologyVirus ReplicationEndocytosisMicrotubulesMicrobiologyCell LineDogsVirologyAnimalsMicroinjectionParvovirusNocodazoleTemperatureCanine parvovirusLipid bilayer fusionbiology.organism_classificationVirologyEndocytosisVirus-Cell InteractionsMicroscopy FluorescenceViral replicationInsect Science
researchProduct

Identification and characterization of amphiphysin II as a novel cellular interaction partner of the hepatitis C virus NS5A protein.

2003

The hepatitis C virus (HCV) NS5A protein is highly phosphorylated by cellular protein kinases. To study how NS5A might be integrated in cellular kinase signalling, we isolated phosphoproteins from HuH-7 hepatoma cells that specifically interacted with recombinant NS5A protein. Subsequent mass spectrometry identified the adaptor protein amphiphysin II as a novel interaction partner of NS5A. Mutational analysis revealed that complex formation is primarily mediated by a proline-rich region in the C-terminal part of NS5A, which interacts with the amphiphysin II Src homology 3 domain. Importantly, we could further demonstrate specific co-precipitation and cellular co-localization of endogenous a…

CytoplasmProlinevirusesImmunoblottingNerve Tissue ProteinsHepacivirusBiologyProtein Serine-Threonine KinasesViral Nonstructural ProteinsVirus ReplicationSH3 domainVirologyTumor Cells CulturedHumansRepliconNS5AFluorescent Antibody Technique IndirectSubgenomic mRNALeucine ZippersKinasevirus diseasesSignal transducing adaptor proteinbiochemical phenomena metabolism and nutritionMAP Kinase Kinase KinasesRNA-Dependent RNA PolymeraseVirologyMolecular biologydigestive system diseasesRecombinant ProteinsViral replicationMutationPhosphorylationRepliconProtein BindingThe Journal of general virology
researchProduct

The DNA-binding subunit p140 of replication factor C is upregulated in cycling cells and associates with G 1 phase cell cycle regulatory proteins

1999

The DNA-binding subunit of replication factor C (RFCp140) plays an important role in both DNA replication and DNA repair. The mechanisms regulating activation of RFCp140 thereby controlling replication and cellular proliferation are largely unknown. We analyzed protein expression of RFCp140 during cell cycle progression and investigated the association of RFCp140 with cell cycle regulatory proteins in cell lines of various tissue origin and in primary hematopoietic cells. Western and Northern blot analyses of RFCp140 from synchronized cells showed downregulation of RFCp140 when cells enter a G0-like quiescent state and upregulation of RFCp140 in cycling cells. Translocation from the cytopla…

CytoplasmSaccharomyces cerevisiae ProteinsT-LymphocytesCyclin ACell Cycle ProteinsEukaryotic DNA replicationCell LineMinor Histocompatibility AntigensDNA replication factor CDT1MiceReplication factor CControl of chromosome duplicationDrug DiscoveryAnimalsHumansReplication Protein CGenetics (clinical)Cell NucleusHomeodomain ProteinsbiologyG1 PhaseS-phase-promoting factor3T3 CellsCell cycleMolecular biologyUp-RegulationCell biologyDNA-Binding ProteinsRepressor ProteinsProto-Oncogene Proteins c-bcl-2biology.proteinMolecular MedicineOrigin recognition complexJournal of Molecular Medicine
researchProduct

Type I Interferon Protects Antiviral CD8+ T Cells from NK Cell Cytotoxicity

2014

Summary Despite development of new antiviral drugs, viral infections are still a major health problem. The most potent antiviral defense mechanism is the innate production of type I interferon (IFN-I), which not only limits virus replication but also promotes antiviral T cell immunity through mechanisms, which remain insufficiently studied. Using the murine lymphocytic choriomeningitis virus model system, we show here that IFN-I signaling on T cells prevented their rapid elimination in vivo. Microarray analyses uncovered that IFN-I triggered the expression of selected inhibitory NK-cell-receptor ligands. Consequently, T cell immunity of IFN-I receptor (IFNAR)-deficient T cells could be rest…

Cytotoxicity ImmunologicImmunologyMedizinReceptor Interferon alpha-betaCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisVirus ReplicationLymphocytic choriomeningitisVirusMiceImmunityInterferonmedicineAnimalsLymphocytic choriomeningitis virusImmunology and AllergyCytotoxic T cellCells CulturedMice KnockoutbiologyPerforinNFIL3medicine.diseaseVirologyImmunity InnateKiller Cells NaturalMice Inbred C57BLBasic-Leucine Zipper Transcription FactorsInfectious DiseasesViral replicationPerforinInterferon Type IImmunologybiology.proteinSignal Transductionmedicine.drugImmunity
researchProduct

Harmonization of Neuroticism and Extraversion phenotypes across inventories and cohorts in the Genetics of Personality Consortium:an application of I…

2014

Mega- or meta-analytic studies (e.g. genome-wide association studies) are increasingly used in behavior genetics. An issue in such studies is that phenotypes are often measured by different instruments across study cohorts, requiring harmonization of measures so that more powerful fixed effect meta-analyses can be employed. Within the Genetics of Personality Consortium, we demonstrate for two clinically relevant personality traits, Neuroticism and Extraversion, how Item-Response Theory (IRT) can be applied to map item data from different inventories to the same underlying constructs. Personality item data were analyzed in >160,000 individuals from 23 cohorts across Europe, USA and Australia…

DIMENSIONSDISORDERS515 PsychologyeducationPersonality AssessmentGenome-wide association studiesExtraversion PsychologicalNEO-PI5-FACTOR MODELGeneticsHumansGenetics(clinical)Ecology Evolution Behavior and SystematicsOriginal ResearchNeuroticismMeasurementNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Models StatisticalOther Research Radboud Institute for Health Sciences [Radboudumc 0]GENOME-WIDE METAANALYSISTEMPERAMENTASSOCIATIONAnxiety Disorders3142 Public health care science environmental and occupational healthMeta-analysisPhenotypeMEASUREMENT INVARIANCECLONINGERSUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]REPLICATIONDevelopmental PsychopathologyItem-Response TheoryConsortiumGenome-Wide Association StudyPersonality
researchProduct

Oxidative stress triggers the preferential assembly of base excision repair complexes on open chromatin regions

2010

How DNA repair machineries detect and access, within the context of chromatin, lesions inducing little or no distortion of the DNA structure is a poorly understood process. Removal of oxidized bases is initiated by a DNA glycosylase that recognises and excises the damaged base, initiating the base excision repair (BER) pathway. We show that upon induction of 8-oxoguanine, a mutagenic product of guanine oxidation, the mammalian 8-oxoguanine DNA glycosylase OGG1 is recruited together with other proteins involved in BER to euchromatin regions rich in RNA and RNA polymerase II and completely excluded from heterochromatin. The underlying mechanism does not require direct interaction of the prote…

DNA RepairHMG-boxDNA damageDNA repairGenome Integrity Repair and ReplicationCell LineDNA GlycosylasesEuchromatinDNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansGuanosinebiologyBromatesBase excision repairChromatinProliferating cell nuclear antigenChromatinDNA-Binding ProteinsOxidative StressX-ray Repair Cross Complementing Protein 1BiochemistryDNA glycosylasebiology.proteinDNA DamageNucleotide excision repairNucleic Acids Research
researchProduct

Nucleotide excision repair of abasic DNA lesions

2019

AbstractApurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, w…

DNA RepairTranscription GeneticDNA damageDNA repairGenome Integrity Repair and ReplicationGene Knockout Techniques03 medical and health sciencesEndonucleasechemistry.chemical_compoundTranscription (biology)CRISPR-Associated Protein 9DNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansAP siteCell Line TransformedSkin030304 developmental biologyGene Editing0303 health sciencesBase SequencebiologyGenome Human030302 biochemistry & molecular biologyDNABase excision repairFibroblastsMolecular biologyXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinschemistryMutationbiology.proteinCRISPR-Cas SystemsDNADNA DamageProtein BindingNucleotide excision repairNucleic Acids Research
researchProduct

Cell proliferation and DNA breaks are involved in ultraviolet light-induced apoptosis in nucleotide excision repair-deficient Chinese hamster cells.

2002

UV light targets both membrane receptors and nuclear DNA, thus evoking signals triggering apoptosis. Although receptor-mediated apoptosis has been extensively investigated, the role of DNA damage in apoptosis is less clear. To analyze the importance of DNA damage induced by UV-C light in apoptosis, we compared nucleotide excision repair (NER)-deficient Chinese hamster ovary cells (lines 27-1 and 43-3B mutated for the repair genes ERCC3 and ERCC1, respectively) with the corresponding DNA repair-proficient fibroblasts (CHO-9 and ERCC1 complemented 43-3B cells). NER-deficient cells were hypersensitive as to the induction of apoptosis, indicating that apoptosis induced by UV-C light is due to u…

DNA RepairTranscription GeneticDNA repairDNA damageCell SurvivalUltraviolet RaysApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsRadiation ToleranceArticleMiceCricetinaeUltraviolet lightAnimalsMolecular BiologyChromosome AberrationsIntrinsic apoptosisCell CycleDNA replicationCell BiologyFibroblastsMolecular biologyCaspase InhibitorsChromatinCell biologyKineticsUVB-induced apoptosisProto-Oncogene Proteins c-bcl-2ApoptosisMutationTumor Suppressor Protein p53Cell DivisionNucleotide excision repairDNA DamageMolecular biology of the cell
researchProduct

Heterochromatin Networks: Topology, Dynamics, and Function (a Working Hypothesis)

2021

Open systems can only exist by self-organization as pulsing structures exchanging matter and energy with the outer world. This review is an attempt to reveal the organizational principles of the heterochromatin supra-intra-chromosomal network in terms of nonlinear thermodynamics. The accessibility of the linear information of the genetic code is regulated by constitutive heterochromatin (CHR) creating the positional information in a system of coordinates. These features include scale-free splitting-fusing of CHR with the boundary constraints of the nucleolus and nuclear envelope. The analysis of both the literature and our own data suggests a radial-concentric network as the main structural…

DNA Replication TimingQH301-705.5HeterochromatinEmbryonic DevelopmentReviewtranscriptional pulsingTopologyModels Biologicalpositional informationphysics of lifeCell Line TumorAnimalsHumansConstitutive heterochromatinNucleosomeEpigeneticsBiology (General)PhysicsReplication timingheterochromatincytoskeletonActomyosinGeneral MedicineGenetic codenucleolar boundaryRatsChromatinGene Expression RegulationOrgan SpecificitynetworksRNA splicingscale-free oscillationsChickensCell Nucleoluschromatin organizationCells
researchProduct