期刊
MOLECULAR CELL
卷 8, 期 5, 页码 1005-1016出版社
CELL PRESS
DOI: 10.1016/S1097-2765(01)00380-X
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资金
- NCI NIH HHS [CA73740] Funding Source: Medline
The transcription factor NF-kappaB is essential for survival of many cell types. However, cells can undergo apoptosis despite the concurrent NF-kappaB activation. It is unknown how the protection conveyed by NF-kappaB is overridden during apoptosis. We report here that I kappaB kinase (IKK) beta was specifically proteolyzed by Caspase-3-related caspases at aspartic acid residues 78, 242, 373, and 546 during tumor necrosis factor (TNF)alpha -induced apoptosis. Proteolysis of IKK beta eliminated its enzymatic activity, interfered with IKK activation, and promoted TNF-alpha killing. Point mutations that abrogate IKK beta proteolysis generated a caspase-resistant IKK beta mutant, which suppressed TNF-alpha -induced apoptosis. Thus, our study demonstrates that TNF-alpha -induced apoptosis requires caspase-mediated proteolysis of IKK beta.
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