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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Oncogenic function for the Dlg1 mammalian homolog of the Drosophila discs-large tumor suppressor.

The fact that several different human virus oncoproteins, including adenovirus type 9 E4-ORF1, evolved to target the Dlg1 mammalian homolog of the membrane-associated Drosophila discs-large tumor suppressor has implicated this cellular factor in human cancer. Despite a general belief that such interactions function solely to inactivate this suspected human tumor suppressor protein, we demonstrate here that E4-ORF1 specifically requires endogenous Dlg1 to provoke oncogenic activation of phosphatidylinositol 3-kinase (PI3K) in cells. Based on our results, we propose a model wherein E4-ORF1 binding to Dlg1 triggers the resulting complex to translocate to the plasma membrane and, at this site, to promote Ras-mediated PI3K activation. These findings establish the first known function for Dlg1 in virus-mediated cellular transformation and also surprisingly expose a previously unrecognized oncogenic activity encoded by this suspected cellular tumor suppressor gene.[1]

References

  1. Oncogenic function for the Dlg1 mammalian homolog of the Drosophila discs-large tumor suppressor. Frese, K.K., Latorre, I.J., Chung, S.H., Caruana, G., Bernstein, A., Jones, S.N., Donehower, L.A., Justice, M.J., Garner, C.C., Javier, R.T. EMBO J. (2006) [Pubmed]
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