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Apaf-1 and Caspase-9 in p53-Dependent Apoptosis and Tumor Inhibition

Science  02 Apr 1999:
Vol. 284, Issue 5411, pp. 156-159
DOI: 10.1126/science.284.5411.156

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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.

  • * Present address: Department of Immunology, Medical Institute of Bioregulation, Kyushu University, Fukoka, Japan.

  • To whom correspondence should be addressed. E-mail: lowe{at}cshl.org

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