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

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Transformation by polyoma virus middle T-antigen involves the binding and tyrosine phosphorylation of Shc.

Polyoma virus middle T-antigen converts normal fibroblasts to a fully transformed, tumorigenic phenotype. It achieves this, at least in part, by binding and activating one of the non-receptor tyrosine kinases, pp60c-src, pp62c-yes or pp59c-fyn (reviewed in refs 2 and 3). As a result, middle T-antigen itself is phosphorylated on tyrosine residues, one of which ( Tyr 315) acts as a binding site for the SH2 domains of phosphatidylinositol-3'OH kinase 85K subunit. Here we show that another tyrosine phosphorylation site in middle T-antigen ( Tyr 250; refs 4, 5) acts as a binding region for the SH2 domain of the transforming protein Shc. This results in Shc also becoming tyrosine- phosphorylated and binding to the SH2 domain of Grb2 ( ref. 10). This probably stimulates p21ras activity through the mammalian homologue of the Drosophila guanine-nucleotide-exchange factor Sos (reviewed in ref. 11). We suggest that middle T-antigen transforms cells by acting as a functional homologue of an activated tyrosine kinase-associated growth-factor receptor.[1]

References

  1. Transformation by polyoma virus middle T-antigen involves the binding and tyrosine phosphorylation of Shc. Dilworth, S.M., Brewster, C.E., Jones, M.D., Lanfrancone, L., Pelicci, G., Pelicci, P.G. Nature (1994) [Pubmed]
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