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- W78830601 abstract "The phosphoinositide 3-kinase (PI3K)/Akt pathway is central to the control of cell growth, proliferation, and survival, as is the Ras/Raf/Erk pathway. In this study, we used a series of EL4 lymphoma cell lines to test the hypothesis that cross-talk between the Akt and Erk pathways influences Erk activation profiles. Phorbol ester (PMA)-sensitive EL4 cells (e.g., WT2) express RasGRP and show high levels of PMA-induced Erk activation. We have previously shown that RasGRP, a phorbol ester-activated Ras GEF, confers the PMA-sensitive phenotype. However, although both PMA-resistant (e.g., V7) and intermediate (e.g., V3) EL4 cells lack RasGRP, PMA-induced Erk phosphorylation is higher in V3 than that in V7. We found that basal Akt phosphorylation is high in V7, but very low in WT2. Basal phospho-Akt in intermediate cells (V3) is intermediate between WT2 and V7. Akt phosphorylation can be blocked by the PI3K inhibitor, LY294002. PMA-induced Raf and Erk phosphorylations were enhanced by LY294002 in all cell types (WT2, V3 and V7), indicating that PI3K/Akt activation is inhibitory to Erk activation. Despite enhancement by LY294002, PMA-induced Raf/Erk activation in V3 and V7 remained weaker than that seen in WT2. In summary, the results suggest that lack of RasGRP, combined with high basal activity of PI3K/Akt, is responsible for the low level of PMA-induced Raf/Erk activation in PMA-resistant EL4 cells. (NIH CA094144-01)" @default.
- W78830601 created "2016-06-24" @default.
- W78830601 creator A5035766936 @default.
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- W78830601 date "2007-01-01" @default.
- W78830601 modified "2023-10-18" @default.
- W78830601 title "Cross‐talk between the PI3K/Akt and Raf/Erk Pathways in EL4 Cells" @default.
- W78830601 doi "https://doi.org/10.1096/fasebj.21.6.a794-c" @default.
- W78830601 hasPublicationYear "2007" @default.
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