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Apaf-1 and Caspase-9 in p53-Dependent Apoptosis and Tumor Inhibition
Abstract
The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c- Myc , were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc -expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.
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Metadata
- Authors
- Soengas, M. S., Alarcón, R. M., Yoshida, H., J., A., Giaccia, Hakem, R., Mak, T. W., & Lowe, S. W.
- Venue
- Science
- Published
- 1999-04-02
- Volume
- 284
- Issue
- 5411
- Pages
- 156-159
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2094126824
- Cited by
- 660
- References
- 4
- FWCI
- 22.84
- Type
- journal article
- Language
- en
- Open access
- closed
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