AI Article Synopsis
- - In hamster fibroblasts transformed by Rous sarcoma virus (RSV), the PI-3K/Akt pathway is activated, leading to increased protein synthesis through the initiation factor eIF2B.
- - Inhibition of PI-3K with wortmannin reduces the phosphorylation of p70 S6k and ribosomal protein S6 in non-transformed cells, indicating its role in normal cells.
- - However, in RSV-transformed cells, PI-3K does not regulate p70 S6k, suggesting that RSV transformation alters the signaling pathway involved in protein synthesis.
Article Abstract
Our data show that in hamster fibroblasts transformed by Rous sarcoma virus (RSV), the phosphoinositide 3'-kinase (PI-3K)/Akt/glycogen synthase kinase 3 antiapoptotic pathway is upregulated and involved in increased protein synthesis through activation of initiation factor eIF2B. Upon inhibition of PI-3K by wortmannin, phosphorylation of 70-kDa ribosomal protein S6 kinase (p70 S6k) and its physiological substrate, ribosomal protein S6, decreased in the non-transformed cells but not in RSV-transformed cells. Thus PI-3K, which is thought to be involved in regulation of p70 S6k, signals to p70 S6k in normal fibroblasts, but it does not appear to be an upstream effector of p70 S6k in fibroblasts transformed by v-src oncogene, suggesting that changes in the PI-3K signalling pathway upstream of p70 S6k are induced by RSV transformation.
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| http://dx.doi.org/10.1016/s0014-5793(03)00415-0 | DOI Listing |
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