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Anticancer drugs induce caspase-8/FLICE activation and apoptosis in the absence of CD95 receptor/ligand interaction
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- Wesselborg, Sebastian (författare)
- Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany.
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- Engels, I. H. (författare)
- Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany
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- Rossmann, E. (författare)
- Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany
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- Los, Marek Jan (författare)
- Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany
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- Schulze-Osthoff, Klaus (författare)
- Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany
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Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany Department of Internal Medicine I, Eberhard-Karls-University, Tübingen, Germany (creator_code:org_t)
- American Society of Hematology, 1999
- 1999
- Engelska.
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Ingår i: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 93:9, s. 3053-3063
- Relaterad länk:
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http://bloodjournal....
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https://liu.diva-por... (primary) (Raw object)
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Abstract
Ämnesord
Stäng
- Proteases of the caspase family are the critical executioners of apoptosis. Their activation has been mainly studied upon triggering of death receptors, such as CD95 (Fas/APO-1) and tumor necrosis factor-R1, which recruit caspase-8/FLICE as the most proximal effector to the receptor complex. Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C. In Jurkat leukemic T cells, all drugs induced apoptosis and the cleavage of procaspase-8 to its active p18 subunit. However, cells resistant to CD95 were equally susceptible to anticancer drugs and activated caspase-8 with a similar kinetic and dose response as CD95-sensitive cells. The broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone prevented apoptosis and caspase-8 activation in response to CD95 and drug treatment, whereas a neutralizing CD95 decoy as well as a dominant-negative FADD construct selectively abrogated CD95, but not drug-induced effects. A potent activation of caspase-8 was also induced by cycloheximide, indicating that it was independent of protein synthesis. Our data, therefore, show that (1) anticancer drug-induced apoptosis does not require de novo synthesis of death ligands or CD95 interaction, and (2) that caspase-8 can be activated in the absence of a death receptor signaling. (C) 1999 by The American Society of Hematology.
Ämnesord
- NATURVETENSKAP -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)
Nyckelord
- cancer-chemotherapy
- cell-death
- chemotherapy-induced apoptosis
- confer immune privilege
- cytochrome-c
- domain-containing receptor
- fadd-dependent apoptosis
- nf-kappa-b
- poly(adp-ribose) polymerase
- signaling complex disc
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- art (ämneskategori)
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