Fig. 3: PERK inhibitors activate GCN2 and vice versa.

a Immunoblots of indicated proteins from lysates of HeLa cells treated with indicated concentrations of the PERK inhibitor GSK’414 for 2.5 h. Active (A) and Inactive (I) GCN2 are indicated with arrows. Representative experiment from n = 3, biologically independent experiments. b Newly synthesized proteins labelled for 10 min with ³⁵S-methionine in HeLa cells pre-treated with increasing concentrations of GSK’414 for 2.5 h and a Coomassie-stained gel as control. Representative experiment from n = 2, biologically independent experiments. c Same as panel (b), with HeLa cells treated with 5 μM GSK’414 for the indicated times and a Coomassie-stained gel as control. Representative experiment from n = 2, biologically independent experiments. d Same as panel (a), with increasing concentrations of the PERK inhibitor AMG44 for 2.5 h. Active (A) and Inactive (I) GCN2 are indicated with arrows. Representative experiment from n = 3, biologically independent experiments. e Same as panel (b), with increasing concentrations of AMG44 for 2.5 h. Representative experiment from n = 2, biologically independent experiments. f Same as panel (c), with 20 μM of AMG44 for the indicated times. Representative experiment from n = 2, biologically independent experiments. g Same as panel (a), with increasing concentrations of the GCN2 inhibitor A92 for 5 h. Active (A) and Inactive (I) PERK are indicated with arrows. Representative experiment from n = 3, biologically independent experiments. h Same as panel (b), with increasing concentrations of A92 for 5 h. Representative experiment from n = 2, biologically independent experiments. i Same as panel (c), with 20 μM of A92 for the indicated times. Representative experiment from n = 2, biologically independent experiments. Source data are provided as a Source data file.