Apoptosis to necrosis switching downstream of apoptosome formation requires inhibition of both glycolysis and oxidative phosphorylation in a BCL-X-L- and PKB/AKT-independent fashion (Articolo in rivista)

Type
Label
  • Apoptosis to necrosis switching downstream of apoptosome formation requires inhibition of both glycolysis and oxidative phosphorylation in a BCL-X-L- and PKB/AKT-independent fashion (Articolo in rivista) (literal)
Anno
  • 2004-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1038/sj.cdd.4401326 (literal)
Alternative label
  • Gramaglia D.; Gentile A.; Battaglia M.; Ranzato L.; Petronilli V.; Fassetta M.; Bernardi P.; Rasola A. (2004)
    Apoptosis to necrosis switching downstream of apoptosome formation requires inhibition of both glycolysis and oxidative phosphorylation in a BCL-X-L- and PKB/AKT-independent fashion
    in Cell death and differentiation
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Gramaglia D.; Gentile A.; Battaglia M.; Ranzato L.; Petronilli V.; Fassetta M.; Bernardi P.; Rasola A. (literal)
Pagina inizio
  • 342 (literal)
Pagina fine
  • 353 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 11 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
  • PubMe (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Division of Molecular Oncology, Institute for Cancer Research, University of Torino Medical School, Candiolo, Italy; Venetian Institute of Molecular Medicine, University of Padova, Italy; CNR Institute of Neuroscience and Department of Biomedical Sciences, University of Padova, Italy (literal)
Titolo
  • Apoptosis to necrosis switching downstream of apoptosome formation requires inhibition of both glycolysis and oxidative phosphorylation in a BCL-X-L- and PKB/AKT-independent fashion (literal)
Abstract
  • Human T-lymphoma Jurkat cells treated with several intrinsic death stimuli readily undergo a stepwise apoptotic program. Treatment with 1,9-dideoxyforskolin (ddFSK), an inactive analogue of the adenylate cyclase activator forskolin, induces necrotic cell death and switches to necrosis the response to the apoptosis inducers in Jurkat and in other cell models. Yet, in the presence of ddFSK, mitochondrial changes are enhanced and apoptosome formation takes place. We show that ddFSK does not inhibit the catabolic steps of apoptosis, but rather elicits a profound ATP depletion that in turn tunes the mode of cell demise towards necrosis. Treatment with ddFSK impairs both glycolysis and oxidative phosphorylation in a Bcl-X-L- and PKB/Akt-independent fashion, and inhibition of both processes is needed to affect apoptosis progression. Apoptosis is not blocked per se by ATP depletion, as engagement of the Fas receptor directly activates caspases, thus bypassing ddFSK inhibition. (literal)
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