期刊
NATURE CELL BIOLOGY
卷 4, 期 11, 页码 859-864出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb868
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- NCI NIH HHS [P30 CA008748, CA13106] Funding Source: Medline
- NHGRI NIH HHS [HG01696] Funding Source: Medline
Unrestrained E2F activity forces S phase entry and promotes apoptosis through p53-dependent and -independent mechanisms. Here, we show that deregulation of E2F by adenovirus E1A, loss of Rb or enforced E2F-1 expression results in the accumulation of caspase proenzymes through a direct transcriptional mechanism. Increased caspase levels seem to potentiate cell death in the presence of p53-generated signals that trigger caspase activation. Our results demonstrate that mitogenic oncogenes engage a tumour suppressor network that functions at multiple levels to efficiently induce cell death. The data also underscore how cell cycle progression can be coupled to the apoptotic machinery.
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