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

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Diaz, J.J. et al.

Increase in ribosomal protein S6 phosphorylation is due to v-erbB-transforming activity and not to v-erbA mitogenic activity in avian erythroblastosis virus-infected chicken embryo fibroblasts.

Avian erythroblastosis virus (AEV-ES4), a transforming avian retrovirus, transforms chicken embryo fibroblasts (CEFs) in culture and induces the maintenance of ribosomal protein S6 phosphorylation in the absence of serum. This effect is less pronounced after AEV-ES4 transformation than after transformation by Rous sarcoma virus (PR-RSV A). However, our results indicate that the two viruses induce an activation of the same S6 phosphokinase, as evidenced by the identity of S6 phosphopeptides and phosphoaminoacids in the two cases. Moreover this activation is performed through a protein kinase C-independent pathway. Expression of the v-erbA oncogene alone, which enhances the growth potential of CEFs, is not able to maintain S6 phosphorylation either in the absence of serum or in the presence of low serum concentration (0.5%). Expression of the v-erbB oncogene alone is responsible for all these AEV-ES4-induced effects. Furthermore, the maintenance of S6 phosphorylation in the absence of serum might be correlated with the degree of transformation of AEV-ES4-infected CEFs. These results show that S6 phosphorylation is one of the biochemical mechanisms deregulated by v-erbB expression and is involved in the transformation process.[1]

References

Increase in ribosomal protein S6 phosphorylation is due to v-erbB-transforming activity and not to v-erbA mitogenic activity in avian erythroblastosis virus-infected chicken embryo fibroblasts. Diaz, J.J., Gandrillon, O., Hentzen, D., Leguellec, D., Samarut, J., Madjar, J.J. Oncogene Res. (1989) [Pubmed]

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