Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition |
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Authors: | Soengas M S Alarcón R M Yoshida H Giaccia A J Hakem R Mak T W Lowe S W |
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Affiliation: | Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA. |
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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. |
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