期刊
IMMUNITY
卷 12, 期 6, 页码 621-632出版社
CELL PRESS
DOI: 10.1016/S1074-7613(00)80213-7
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资金
- NHLBI NIH HHS [T32HL07088] Funding Source: Medline
- NIDDK NIH HHS [DK49786] Funding Source: Medline
- NIGMS NIH HHS [GMR01-55942] Funding Source: Medline
Granzyme B (GzmB) is a component of cytotoxic lymphocyte granules that can rapidly initiate apoptosis in target cells. While several procaspases are cleaved and activated by GzmB, the absolute requirement of caspase activation for GzmB-induced apoptosis is controversial. In this report, we demonstrate that GzmB can initiate apoptosis in the absence of caspase-3 activity by directly cleaving DFF45/ICAD to liberate activated DFF40/CAD. DFF45/ICAD cleavage occurs less efficiently in cells that lack caspase-3 activity, suggesting that the caspases normally amplify the GzmB death signal. DFF45/ICAD-deficient mouse embryo fibroblasts are partially resistant to GzmB-induced death, demonstrating the biological importance of DFF45/ICAD for GzmB-mediated apoptosis.
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