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BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak
Open accessAbstract
The BH3-only proteins Bim and Bad bind to the antiapoptotic Bcl-2 proteins and induce apoptosis in wild-type cells and cells from either bax−/− or bak−/− animals. In contrast, constitutively active forms of Bim and Bad failed to induce apoptosis in bax−/−bak−/− cells. Expression of Bax restored susceptibility of the cells to Bim and Bad. In addition, Bax but not Bim or Bad sensitized the bax−/−bak−/− cells to a wide variety of cell death stimuli including UV irradiation, chemotherapeutic agents, and ER stress. These results suggest that neither activation of BH3-only proteins nor suppression of pro-survival Bcl-2 proteins is sufficient to kill cells in the absence of both Bax and Bak. Furthermore, whereas mouse embryo fibroblasts (MEF) expressing only Bax or Bak displayed resistance to transformation,bax−/−bak−/− MEF were nearly as prone to oncogenic transformation as p53−/− MEF. Thus, the function of either Bax or Bak appears required to initiate most forms of apoptosis and to suppress oncogenic transformation.
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Metadata
- Authors
- Zong, W.-X., Lindsten, T., Ross, A. J., MacGregor, G. R., & Thompson, C. B.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2001-06-15
- Volume
- 15
- Issue
- 12
- Pages
- 1481-1486
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2166601968
- Cited by
- 808
- References
- 2
- Type
- posted content
- Language
- en
- Open access
- diamond
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