Search results for "OSiS"

showing 10 items of 15931 documents

The effect of PLC-inhibitor on echovirus 1 internalization probed with fluorescently labeled echovirus 1

2014

Echovirus 1 (EV1) kuuluu Pikornavirusperheeseen ja tarkemmin luokiteltuna Enterovirusten sukuun. EV1 on pieni ja vaipaton RNA-virus, jonka proteiinikuori koostuu neljästä proteiinista VP1-VP4. Infektion on osoitettu alkavan, kun EV1 tarttuu α2β1-integriiniin solun pinnalla, jonka jälkeen virus otetaan solun sisään kaveoliinivälitteistä endosytoosia sekä makropinosytoosia muistuttavalla mekanismilla. Toisaalta sitä, kuinka virus avautuu sekä vapauttaa RNA:nsa, ei vielä tarkalleen tiedetä. Tässä tutkimuksessa EV1 puhdistettiin ensin sakkaroosigradientilla, jonka jälkeen virus leimattiin fluoresoivalla amiinireaktiivisella värillä. Tulokset osoittivat, että leimauksen onnistumiseksi tarvitaan …

viruksetfluoresenssifluorescent labelingECHO-viruksetEchovirus 1uncoatingendocytosis inhibitorendosytoosiinhibiittorit
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Iron and virulence in the zoonotic pathogen Vibrio vulnificus

2014

Vibrio vulnificus es un patógeno humano emergente que es autóctono de ecosistemas acuáticos salobres de climas templados, tropicales y subtropicales. La especie se subdivide en 3 biotipos (Bt), de los cuales el Bt2 contiene un grupo de cepas que, además de poder infectar al hombre, pueden causar infecciones en peces. Este grupo es un complejo clonal serológicamente homogéneo que denominamos serovar E o serovar zoonótica (VvBt2SerE). Como patógeno humano, VvBt2SerE causa casos esporádicos de infecciones graves en heridas que pueden derivar en septicemia secundaria en pacientes inmunocomprometidos y como patógeno de peces, brotes o epizootias de una septicemia hemorrágica conocida como vibrio…

virulenciahierroUNESCO::CIENCIAS DE LA VIDA::Biología molecular:CIENCIAS DE LA VIDA::Microbiología [UNESCO]toxinavulnificuszoonosisvibriomicroarrayUNESCO::CIENCIAS DE LA VIDA::Microbiología:CIENCIAS DE LA VIDA::Biología molecular [UNESCO]
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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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Binding and internalization of human papillomavirus type 33 virus-like particles by eukaryotic cells

1995

Infection of cells by human papillomaviruses (HPVs) associated with malignant genital lesions has not been studied because of the lack of an in vitro system and the unavailability of virions. We have now used virus-like particles (VLPs) of HPV type 33 to analyze the initial events in the interaction of the HPV capsid with cell lines. Binding of VLPs to HeLa cells was observed in biochemical assays and by immunofluorescence. VLP binding was inhibited by antisera raised against VLPs but not by monoclonal antibodies recognizing either L1 or L2 epitopes accessible on VLPs. Under saturating conditions, approximately 2 x 10(4) VLPs were bound per cell, with a dissociation constant of about 100 pM…

virusesImmunoelectron microscopyImmunologyBiologyAntibodies ViralMembrane Fusioncomplex mixturesMicrobiologyVirusEpitopeCell LineMiceVirologyAnimalsHumansMicroscopy ImmunoelectronPapillomaviridaeCapsomereVirionMembrane Proteinsvirus diseasesLipid bilayer fusionbiochemical phenomena metabolism and nutritionMolecular biologyEndocytosisEndocytic vesicleCapsidCell cultureInsect ScienceResearch ArticleJournal of Virology
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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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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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Enhancement by TNF-alpha of reactivation and replication of latent herpes simplex virus from trigeminal ganglia of mice.

1995

The influence of tumor-necrosis-factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukine-1 (IL-1) and IL-3 on the in vitro reactivation frequency and replication rate of trigeminal ganglia of mice latently infected with herpes simplex virus (HSV) strain KOS was studied. It could be demonstrated that TNF-alpha and possibility GM-CSF, but not IL-1 and IL-3, enhanced the reactivation frequency and replication of HSV. Interferon alpha/beta (IFN alpha/beta) prevented reactivation and replication.

virusesmedicine.medical_treatmentHerpesvirus 1 HumanBiologymedicine.disease_causeVirus ReplicationVirusHerpesviridaeMiceInterferonVirologyAlphaherpesvirinaeChlorocebus aethiopsmedicineAnimalsHumansVero CellsMice Inbred BALB CTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorInterferon-alphaGeneral MedicineInterferon-betabiology.organism_classificationVirologyIn vitroVirus LatencyCytokineHerpes simplex virusViral replicationTrigeminal GanglionInterleukin-3Virus Activationmedicine.drugInterleukin-1Archives of virology
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Replay

2010

vitamin D FIBROSIS HCV
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Reply

2010

vitamin d HCV FIBROSIS SVR
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