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Identification of a caspase 3‐independent role of pro‐apoptotic factor Bak in TNF‐α‐induced apoptosis
Author(s) -
Suyama Eigo,
Kawasaki Hiroaki,
Taira Kazunari
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03193-9
Subject(s) - apoptosis , tumor necrosis factor alpha , hela , microbiology and biotechnology , caspase , caspase 8 , biology , caspase 3 , caspase 9 , caspase 2 , programmed cell death , chemistry , cell culture , immunology , genetics
By using our recently developed gene discovery system, we have identified Bak, a member of the Bcl‐2 family, as a pro‐apoptotic factor in the tumor necrosis factor (TNF)‐α‐induced apoptotic pathway in caspase 3‐deficient cells. Unlike Bcl‐2, Bak stimulates several apoptotic pathways, however the molecular mechanism(s) of its action remains unclear. For example, it is unclear whether Bak induces apoptosis in caspase 3‐deficient cells. In this study, we examined the effects of overexpression of Bak in MCF‐7 cells that lack caspase 3. We found that despite the absence of caspase 3 in MCF‐7 cells, they were more sensitive to the cell death effects of Bak as compared to caspase 3‐expressing HeLa S3 cells. The targeting of Bak function by ribozymes suggests that Bak is required for the TNF‐α‐induced apoptotic pathway in caspase 3‐deficient cells. This study demonstrates the caspase 3‐independent function of Bak in the TNF‐α‐induced apoptotic pathway.