Regulation of Death Receptor-Mediated Cell Demise by Glutathione


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HENTZE, Hannes, 2000. Regulation of Death Receptor-Mediated Cell Demise by Glutathione [Dissertation]. Konstanz: University of Konstanz

@phdthesis{Hentze2000Regul-6601, title={Regulation of Death Receptor-Mediated Cell Demise by Glutathione}, year={2000}, author={Hentze, Hannes}, address={Konstanz}, school={Universität Konstanz} }

<rdf:RDF xmlns:dcterms="" xmlns:dc="" xmlns:rdf="" xmlns:bibo="" xmlns:dspace="" xmlns:foaf="" xmlns:void="" xmlns:xsd="" > <rdf:Description rdf:about=""> <dcterms:alternative>Regulation von Todesrezeptor-vermitteltem Zelltod durch Glutathion</dcterms:alternative> <dcterms:title>Regulation of Death Receptor-Mediated Cell Demise by Glutathione</dcterms:title> <dc:language>eng</dc:language> <dspace:isPartOfCollection rdf:resource=""/> <dspace:hasBitstream rdf:resource=""/> <dc:date rdf:datatype="">2011-03-24T17:27:43Z</dc:date> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dcterms:hasPart rdf:resource=""/> <dc:rights>terms-of-use</dc:rights> <dc:creator>Hentze, Hannes</dc:creator> <dcterms:isPartOf rdf:resource=""/> <dcterms:available rdf:datatype="">2011-03-24T17:27:43Z</dcterms:available> <dc:contributor>Hentze, Hannes</dc:contributor> <dcterms:issued>2000</dcterms:issued> <dcterms:rights rdf:resource=""/> <dc:format>application/pdf</dc:format> <dcterms:abstract xml:lang="eng">The activation of the death receptors TNF-receptor-1 (TNF-R1) or CD95, respectively, is a hallmark of inflammatory or viral liver disease. The present thesis investigated the regulation of death receptor-triggered apoptosis by glutathione alterations using different murine in vivo models and an in vitro model of CD95-mediated apoptosis. The findings provide evidence that (i) a depletion of hepatic GSH levels precludes the execution of death receptor-mediated cell death; and that (ii) the molecular target affected by GSH depletion is the activation of caspase-8 at the CD95 DISC (death-inducing signaling complex) and possibly the activation of caspases via the apoptosome. The data suggest that a dysregulation of cell demise at chronically decreased hepatic GSH affects the pathological processes and thus possibly the outcome of liver disease.</dcterms:abstract> <bibo:uri rdf:resource=""/> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> </rdf:Description> </rdf:RDF>

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