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Verfasst von:Aguiló, Juan [VerfasserIn]   i
 Anel, Alberto [VerfasserIn]   i
 Catalán, Elena [VerfasserIn]   i
 Sebastián, Alvaro [VerfasserIn]   i
 Acín-Pérez, Rebeca [VerfasserIn]   i
 Naval, Javier [VerfasserIn]   i
 Wallich, Reinhard [VerfasserIn]   i
 Simon, Markus M. [VerfasserIn]   i
 Pardo, Julián [VerfasserIn]   i
Titel:Granzyme B of cytotoxic T cells induces extramitochondrial reactive oxygen species production via caspase-dependent NADPH oxidase activation
Verf.angabe:Juan I. Aguiló, Alberto Anel, Elena Catalán, Alvaro Sebastián, Rebeca Acín-Pérez, Javier Naval, Reinhard Wallich, Markus M. Simon, Julián Pardo
E-Jahr:2010
Jahr:02 February 2010
Umfang:10 S.
Teil:volume:88
 year:2010
 number:5
 pages:545-554
 extent:10
Fussnoten:Gesehen am 17.05.2021
Titel Quelle:Enthalten in: Immunology & cell biology
Ort Quelle:Hoboken, NJ : Wiley, 1987
Jahr Quelle:2010
Band/Heft Quelle:88(2010), 5, Seite 545-554
ISSN Quelle:1440-1711
Abstract:Induction of reactive oxygen species (ROS) is a hallmark of granzyme B (gzmB)-mediated pro-apoptotic processes and target cell death. However, it is unclear to what extent the generated ROS derive from mitochondrial and/or extra-mitochondrial sources. To clarify this point, we have produced a mutant EL4 cell line, termed EL4-rho(0), which lacks mitochondrial DNA, associated with a decreased mitochondrial membrane potential and a defective ROS production through the electron transport chain of oxidative phosphorylation. When incubated with either recombinant gzmB plus streptolysin or ex vivo gzmB(+) cytotoxic T cells, EL4-rho(0) cells showed phosphatydylserine translocation, caspase 3 activation, Bak conformational change, cytochrome c release and apoptotic morphology comparable to EL4 cells. Moreover, EL4-rho(0) cells produced ROS at levels similar to EL4 under these conditions. GzmB-mediated ROS production was almost totally abolished in both cell lines by the pan-caspase inhibitor, Z-VAD-fmk. However, addition of apocynin, a specific inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, led to a significant reduction of ROS production and cell death only in EL4-rho(0) but not EL4 cells. These data suggest that gzmB-induced cell death is accompanied by a caspase-dependent pathway of extra-mitochondrial ROS production, most probably through activation of NADPH oxidase.
DOI:doi:10.1038/icb.2010.5
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://dx.doi.org/10.1038/icb.2010.5
 Volltext: https://onlinelibrary.wiley.com/doi/epdf/10.1038/icb.2010.5
 DOI: https://doi.org/10.1038/icb.2010.5
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Apoptosis
 Caspases
 Cell Line
 Enzyme Activation
 Granzymes
 Humans
 Immunoblotting
 Mice
 Mice, Inbred C57BL
 Mitochondria
 NADPH Oxidases
 Reactive Oxygen Species
 Reverse Transcriptase Polymerase Chain Reaction
 Signal Transduction
 T-Lymphocytes, Cytotoxic
K10plus-PPN:1757918639
Verknüpfungen:→ Zeitschrift

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