Search results for "Kidney"

showing 4 items of 1514 documents

Microtubules and microfilaments in HSV-Infected rabbit-kidney cells.

1981

In rabbit kidney cells infected with strains of Herpes simplex virus producing either cell-rounding or polycaryocytosis. Vinblastine induced paracrystals. This could be shown by phase-contrast- and electron-microscopy. Infections were done under one-step-growth conditions or at low MOI. 90 per cent noninfected cells contained stress fibers as detected by Servablue R250-staining. Shortly after recruitment into polycaryocytes, stress fibres of normal length appearing in criss-cross arrangement can be seen in the periphery of these cells. Later they polymerize to very long fibers and finally they are partially destroyed. The time of destruction depends on the MOI employed. By using Actinomycin…

virusesBiologyCycloheximideMicrofilamentmedicine.disease_causeKidneyVinblastineMicrotubulesCell LineCell Fusionchemistry.chemical_compoundViral ProteinsCytopathogenic Effect ViralVirologymedicineAnimalsSimplexvirusCytoskeletonKidneyCell fusionGeneral MedicineVirologyVinblastinemedicine.anatomical_structureHerpes simplex viruschemistryGiant cellCell cultureDNA ViralRabbitsmedicine.drugArchives of virology
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Single amino acid substitutions in the glycoprotein B carboxy terminus influence the fusion from without property of herpes simplex virus type 1.

1995

Syncytial mutations of herpes simplex virus type 1 (HSV-1) strains ANG, ANG path, HFEM, tsB5 and HSZP cause extensive cell fusion and were mapped to the cytoplasmic domain of glycoprotein B (gB), within the syn 3 locus. These strains are so far the only ones which show the phenotype ‘fusion from without’ (FFWO): 60 min after infection with high m.o.i., cells in a tissue culture are fused without transcription and translation of the viral genome. In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. The transfer of this muta…

virusesMutantRestriction MappingEnzyme-Linked Immunosorbent AssayHerpesvirus 1 HumanBiologymedicine.disease_causeKidneylaw.inventionCell FusionCytopathogenic Effect ViralViral Envelope ProteinslawVirologyCyclosporin aCricetinaeChlorocebus aethiopsmedicineBaby hamster kidney cellAnimalsAmino Acid SequenceAmino AcidsPeptide sequenceVero CellsRecombination GeneticCell fusionAlanineValineVirologyHerpes simplex virusPhenotypeRecombinant DNAVero cellThe Journal of general virology
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Oncolytic targeting of renal cell carcinoma via encephalomyocarditis virus

2010

Apoptosis is a fundamental host defence mechanism against invading microbes. Inactivation of NF-kappaB attenuates encephalomyocarditis virus (EMCV) virulence by triggering rapid apoptosis of infected cells, thereby pre-emptively limiting viral replication. Recent evidence has shown that hypoxia-inducible factor (HIF) increases NF-kappaB-mediated anti-apoptotic response in clear-cell renal cell carcinoma (CCRCC) that commonly exhibit hyperactivation of HIF due to the loss of its principal negative regulator, von Hippel-Lindau (VHL) tumour suppressor protein. Here, we show that EMCV challenge induces a strong NF-kappaB-dependent gene expression profile concomitant with a lack of interferon-me…

virusesTransplantation HeterologousApoptosisMice SCIDBiologyNF-κBMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRNA interferenceCell Line TumorVHLEMCVBasic Helix-Loop-Helix Transcription FactorsAnimalsHIFEncephalomyocarditis virusRNA Small InterferingCarcinoma Renal CellResearch Articles030304 developmental biology0303 health sciencesNF-kappa BNF-κBNFKB1RCCVirologyKidney Neoplasms3. Good healthOncolytic virusOncolytic VirusesViral replicationchemistryVon Hippel-Lindau Tumor Suppressor ProteinApoptosisCell culture030220 oncology & carcinogenesisCancer researchMolecular MedicineRNA InterferenceSignal transductionSignal TransductionEMBO Molecular Medicine
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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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