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M400376200v1
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Papers In Press, published online ahead of print April 22, 2004
J. Biol. Chem, 10.1074/jbc.M400376200
Submitted on January 13, 2004
Revised on April 1, 2004
Accepted on April 22, 2004

The proapoptotic gene Siva is a direct transcriptional target for the tumor suppressors P53 and E2F1

Andre Fortin, Jason G. MacLaurin, Nicole Arbour, Sean P. Cregan, Neena Kushwaha, Steven M. Callaghan, David S. Park, Paul R. Albert, and Ruth S. Slack

Ottawa Health Research Institute, University of Ottawa, Ottawa, ON K1H 8M5

Corresponding Author: rslack{at}uottawa.ca

The p53 tumor suppressor gene is believed to play an important role in neuronal cell death in acute neurological disease and in neurodegeneration. The p53 signaling cascade is complex and that the mechanism by which p53 induces apoptosis is cell type dependent. Using DNA microarray analysis, we have found a striking induction of the proapoptotic gene, SIVA. SIVA is a proapoptotic protein containing a death domain and interacts with members of the TNFR family as well as anti-apoptotic Bcl2 family proteins. SIVA is induced following direct p53 gene delivery; treatment with a DNA damaging agent, camptothecin; and following stroke injury in vivo. SIVA upregulation is sufficient to initiate the apoptotic cascade in neurons. Through isolation and analysis of the SIVA promoter, we have identified response elements for both p53 and E2F1. Like p53, E2F1 is another tumor suppressor gene involved in the regulation of apoptosis including neuronal injury models. We have identified E2F consensus sites in the promoter region while p53 recognition sequences were found in intron1. Sequence analysis has shown that these consensus sites are also conserved between mouse and human SIVA genes. Electrophoretic mobility shift assays reveal that both transcription factors are capable of binding to putative consensus sites, and luciferase reporter assays reveal that E2F1 and p53 can activate transcription from the SIVA promoter. Here, we report that the proapoptotic gene, SIVA, which functions in a broad spectrum of cell types, is a direct transcriptional target for both tumor suppressors, p53 and E2F1.


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