| First Author | Figueroa C | Year | 2003 |
| Journal | Oncogene | Volume | 22 |
| Issue | 36 | Pages | 5554-61 |
| PubMed ID | 12944902 | Mgi Jnum | J:85575 |
| Mgi Id | MGI:2675770 | Doi | 10.1038/sj.onc.1206496 |
| Citation | Figueroa C, et al. (2003) Akt negatively regulates translation of the ternary complex factor Elk-1. Oncogene 22(36):5554-61 |
| abstractText | Cross-talk between signaling pathways plays an important role in regulation of cell growth, differentiation, survival, and death. Here, we show that Akt regulates the Elk-1 transcription factor, independent of its negative regulation of Raf kinases. Using a constitutively active Mek1 to bypass the regulation of Raf by Akt, we find that the Elk-1 and Sap1a proteins are dramatically decreased in the presence of activated Akt. Akt catalytic activity is required. Also, Mek-dependent activation of a TCF (Elk-1/Sap-1a)-dependent c-fos reporter is decreased by activated Akt. Neither the level of Elk-1 mRNA nor the stability of the Elk-1 protein is altered by activated Akt. Instead, the rate of incorporation of labeled methionine into Elk-1 protein is decreased in the presence of Akt. In addition, the level of the Elk-1 protein but not GFP is significantly decreased in the presence of activated Akt, when GFP is expressed from an IRES element in a bicistronic message with Elk-1. We conclude that Akt negatively regulates translation of the Elk-1 mRNA. A coding region determinant that maps within the first 279 nts of the Elk-1 message is necessary and sufficient for Akt-mediated regulation of Elk-1. |
