Energy Requirement for Caspase Activation and Neuronal Cell Death

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NICOTERA, Pierluigi, Marcel LEIST, Eugenio FAVA, Laura BERLIOCCHI, Christiane VOLBRACHT, 2000. Energy Requirement for Caspase Activation and Neuronal Cell Death. In: Brain Pathology. 10(2), pp. 276-282. ISSN 1015-6305. eISSN 1750-3639

@article{Nicotera2000Energ-8313, title={Energy Requirement for Caspase Activation and Neuronal Cell Death}, year={2000}, number={2}, volume={10}, issn={1015-6305}, journal={Brain Pathology}, pages={276--282}, author={Nicotera, Pierluigi and Leist, Marcel and Fava, Eugenio and Berliocchi, Laura and Volbracht, Christiane} }

<rdf:RDF xmlns:dcterms="" xmlns:dc="" xmlns:rdf="" xmlns:bibo="" xmlns:dspace="" xmlns:foaf="" xmlns:void="" xmlns:xsd="" > <rdf:Description rdf:about=""> <bibo:uri rdf:resource=""/> <dcterms:issued>2000</dcterms:issued> <dc:rights>terms-of-use</dc:rights> <dspace:isPartOfCollection rdf:resource=""/> <dc:date rdf:datatype="">2011-03-24T17:42:36Z</dc:date> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> <dc:contributor>Leist, Marcel</dc:contributor> <dcterms:available rdf:datatype="">2011-03-24T17:42:36Z</dcterms:available> <dcterms:title>Energy Requirement for Caspase Activation and Neuronal Cell Death</dcterms:title> <dcterms:hasPart rdf:resource=""/> <dc:format>application/pdf</dc:format> <dc:creator>Fava, Eugenio</dc:creator> <dc:contributor>Fava, Eugenio</dc:contributor> <dc:contributor>Nicotera, Pierluigi</dc:contributor> <dcterms:rights rdf:resource=""/> <dcterms:abstract xml:lang="eng">Recent work has shown that execution of the apoptotic program involves a relatively limited number of pathways. According to a general view, these would converge to activate the caspase family of proteases. However, there is increasing evidence that apoptotic-like features can be found also when cells are treated with inhibitors of caspases as the cell permeable tripeptide, Z-Val-Ala-Asp-fluoromethyl-ketone (Z-VAD-fmk), or analogous compounds. This has posed the question as to whether apoptosis may occur in a caspase independent way, and whether caspase inhibitors may then be used to treat diseases characterised by an excess apoptosis. It is also becoming clear, that ATP depletion during the early phases of apoptosis can preclude caspase activation, and consequently switch execution of cell death towards necrosis. In vivo, a block or partial inhibition of the typical apoptotic demise may have profound implications, as persistence of damaged but "undead" cells within the nervous system, followed by delayed lysis may favour neuroinflammatory reactions. In this review, we discuss some recent findings, which suggest that cells may use diverging execution pathways, with different implications in neuropathology and therapy.</dcterms:abstract> <dcterms:isPartOf rdf:resource=""/> <dc:contributor>Volbracht, Christiane</dc:contributor> <dc:creator>Nicotera, Pierluigi</dc:creator> <dcterms:bibliographicCitation>First publ. in: Brain Pathology 10 (2000), 2, pp. 276-282</dcterms:bibliographicCitation> <dspace:hasBitstream rdf:resource=""/> <dc:contributor>Berliocchi, Laura</dc:contributor> <dc:language>eng</dc:language> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dc:creator>Volbracht, Christiane</dc:creator> <dc:creator>Leist, Marcel</dc:creator> <dc:creator>Berliocchi, Laura</dc:creator> </rdf:Description> </rdf:RDF>

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