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Verfasst von:Hentze, Hannes [VerfasserIn]   i
 Krammer, Peter H. [VerfasserIn]   i
Titel:Glutathione dependence of caspase-8 activation at the death-inducing signaling complex
Verf.angabe:Hannes Hentze, Ingo Schmitz, Markus Latta, Andreas Krueger, Peter H. Krammer and Albrecht Wendel
E-Jahr:2002
Jahr:February 15, 2002
Umfang:8 S.
Teil:volume:277
 year:2002
 number:7
 pages:5588-5595
 extent:8
Fussnoten:Gesehen am 15.04.2021
Titel Quelle:Enthalten in: The journal of biological chemistry
Ort Quelle:Bethesda, Md. : Soc., 1905
Jahr Quelle:2002
Band/Heft Quelle:277(2002), 7, Seite 5588-5595
ISSN Quelle:1083-351X
Abstract:<p>Apoptosis triggered by the death receptor CD95 (APO-1 or Fas) is pivotal for the homeostasis of the immune system. We investigated differential effects of glutathione depletion on CD95-triggered apoptosis in T and B cell lines as well as the glutathione dependence of caspase-8 activation. In B lymphoblastoid SKW6.4 cells, CD95-mediated apoptosis was prevented upstream of caspase-8 activation and caspase-3-like activity after acute glutathione depletion by diethyl maleate or<i>cis</i>-chloro-dinitrobenzene. Immunoprecipitation of the death-inducing signaling complex (DISC) revealed that the DISC was still formed in the glutathione-depleted state. The first cleavage step of procaspase-8 activation at the DISC, however, was inhibited. Accordingly, under cell-free conditions, radiolabeled procaspase-8 was processed at the immunoprecipitated DISC only after the addition of exogenous dithiothreitol or reduced glutathione. We also observed suppression of CD95-mediated apoptosis in glutathione-depleted CEM and H9 cells. Notably, Jurkat cells still died upon CD95 engagement under this condition, displaying incomplete nuclear fragmentation and a partial switch to necrosis; this may be explained by reduced cytochrome<i>c</i>/dATP-mediated caspase activation observed in cytosol from glutathione-depleted Jurkat cytosol. Our data indicate that the activation of caspase-8 at the DISC and hence CD95-mediated apoptosis induction shows a cell-specific requirement for intracellular glutathione.</p>
DOI:doi:10.1074/jbc.M110766200
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1074/jbc.M110766200
 Volltext: https://www.jbc.org/article/S0021-9258(19)82601-7/abstract
 DOI: https://doi.org/10.1074/jbc.M110766200
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1755022042
Verknüpfungen:→ Zeitschrift

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