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. Author manuscript; available in PMC: 2021 Jun 23.
Published in final edited form as: Chem Biol Drug Des. 2009 Jul;74(1):57–67. doi: 10.1111/j.1747-0285.2009.00827.x

Figure 2:

Figure 2:

Inhibition of GCN2PKR794G-mediated eIF2α phosphorylation. (A) Indirubin-3′-monoxime, SP600125 and staurosporine block GCN2PKR794G-mediated phosphorylation of eIF2α. Following kinase reactions, the extent of eIF2α phosphorylation was determined by Western blotting using anti-phospho-eIF2α antibodies. Pan-eIF2α antibody was used to control for the sample loadings. The ATP competitive inhibitor, 5′γ-S-ATP, was used as positive control in these reactions. (B) Inhibition of GCN2PKR794G-mediated eIF2α phosphorylation by the SYK inhibitor, SyKI. Kinase reactions were analyzed as described in (A). (C) Schematic diagram of indirubin-3′-monoxime, SP600125, and SyKI.