Direct coupling of the cell cycle and cell death machinery by E2F

Nahle, Zaher, Polakoff, Julia, Davuluri, Ramana V., McCurrach, Mila E., Jacobson, Matthew D., Narita, Masashi, Zhang, Michael Q., Lazebnik, Yuri, Bar-Sagi, Dafna, Lowe, Scott W. (2002) Direct coupling of the cell cycle and cell death machinery by E2F. Nature Cell Biology, 4 (11). pp. 859-864. ISSN 1465-7392

DOI: 10.1038/ncb868


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.

Item Type: Paper
Uncontrolled Keywords: Adenovirus E1A Proteins Animals Apoptosis Blotting, Northern Caspases Cell Cycle Cell Cycle Proteins Cell Line, Tumor CpG Islands Cytochromes c DNA-Binding Proteins E2F Transcription Factors E2F1 Transcription Factor Fibroblasts Humans Luciferases Mice Models, Biological Models, Genetic Promoter Regions, Genetic RNA Retinoblastoma Protein Time Factors Transcription Factors Transcription, Genetic Tumor Suppressor Protein p53
CSHL Authors:
Communities: CSHL labs > Labeznik lab
CSHL labs > Lowe lab
Depositing User: Matt Covey
Date: 2002
Date Deposited: 12 Dec 2012 17:30
Last Modified: 12 Dec 2012 17:30
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