Abstract:
:Apoptosis in response to granzyme B involves activation of caspase-dependent target cell death pathways. Herein, we show that granzyme B initiates caspase processing but cannot fully process procaspase-3 in intact Jurkat T leukemia or NT2 neuronal cells. Rather, the release from mitochondria of proapoptotic mediators cytochrome c, Smac/Diablo, and HtrA2/Omi facilitates full activation of caspases that results from autoprocessing. Bcl-2 overexpression in mitochondria suppresses the release of these proapoptotic molecules, resulting in cell survival despite partial procaspase processing by granzyme B. We propose that binding of inhibitor of apoptosis (IAP) proteins to partially processed procaspases inhibits cell death unless mitochondrial disruption also occurs in response to granzyme B or activated BH3-domain proteins such as truncated Bid.
journal_name
Immunityjournal_title
Immunityauthors
Sutton VR,Wowk ME,Cancilla M,Trapani JAdoi
10.1016/s1074-7613(03)00050-5keywords:
subject
Has Abstractpub_date
2003-03-01 00:00:00pages
319-29issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(03)00050-5journal_volume
18pub_type
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