| Abstract No.: | C-B3072 |
| Country: | China |
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| Title: | IGF-1 STIMULATES THE PHOSPHORYLATION OF PRAS40 IN CULTURED HIPPOCAMPAL NEURONS VIA THE PI3/AKT PATHWAY |
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| Authors/Affiliations: | 3 Z.W. Zeng*; 3 X.H. Zhou; 2 Q. Wen; 2 X.L. Duan; 2 L.M. Yao; 2 C.M Sun; 2 Q.S. Zhang; 1 Y. Dumont; 1 R. Quiron;
1 Douglas Mental Health University Institute, Dept. of Psychiatry, McGill University, Montreal, QC, Canada; 2 Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China; 3 School of Pharmaceutical Sciences, Sun Yat-Sen University, China
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| Content: | Insulin-like growth factor-1 (IGF-1) is a polypeptide growth factor with a variety of functions in both neuronal and non-neuronal cells. Previously we have shown that IGF-1 promotes the survival of cultured hippocampal neurons via the PI3/Akt pathway (Zheng et al., JBC 2002). In the present study, we investigated the effects of IGF-1 on the phosphorylation of PRAS40{a 40 kilodaltons proline-rich protein identified as a substrate of Akt and a mammalian target of rapamycin (mTOR) complex 1 (mTORC1)} and their underlying mechanisms in cultured hippocampal neurons and PC12 cells. Our data show that IGF-1 stimulates the phosphorylation of PRAS40 at T246 residue in cultured hippocampal neurons and PC12 cells. The phosphorylation of PRAS40 induced by IGF-1 is time (0-40 min)- and concentration (1-100nM)-dependent and is mediated by the PI3K/Akt pathway as the PI3K inhibitor LY290002 blocked the phosphorylation of PRAS40 induced by IGF-1. These data suggest that PRAS40 is a downstream target of PI3K/Akt in IGF-1 receptor signalling in neuronal cells. Supported by National Natural Science Fund of China (No:30670652 and 30711120) and in part by the Canadian Institutes of Health Research. |
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