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. 2011 Feb;336(2):344–355. doi: 10.1124/jpet.110.174805

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Fig. 4. — Effects of EET administration on the epidermal growth factor signaling pathway in human leukemia cells. A, cellular proliferation was stimulated by 11,12-EETs (1 μM) and decreased by inhibitors of JNK (SP600125), mitogen-activated protein kinase (apigenin), EGFR (AG1478), AMPK (Compound C), Akt (Akt inhibitor), and PI3K (LY294002), but not by inhibitors of PKC (539560), eNOS (l-N^G-nitroarginine methyl ester; l-NAME), and PPARγ (GW9662). B, increased phosphorylation of EGFR in K562 cells after 11,12-EET (1 μM) treatment is reversed by C26 (10 μM). C, increased phosphorylation of AMPK in K562 cells after 11,12-EET (1 μM) treatment is reversed by C26 (10 μM). D, increased expression of PI3K and p-Akt in K562 cells after 11,12-EET (1 μM) treatment is reversed by C26 (10 μM). E, increased phosphorylation of JNK in K562 cells after 11,12-EET (1 μM) treatment is reversed by C26 (10 μM). Results shown are mean ± S.E. (n = 5); *, p < 0.05 versus control; #, p < 0.05 versus EET.