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. 2018 Jan 19;114(5):737–746. doi: 10.1093/cvr/cvy011

Figure 4.

Figure 4

Activation of JNK2 but not JNK1 contributes to the increase in CaMKIIδ protein expression in cultured HL-1 myocytes. (A) Co-infection of constitutively activated JNK upstream regulator MKK7D and JNK2, but not JNK1, increases the level of CaMKIIδ. (B) Treatment of HL-1 myocytes with anisomycin (JNK activator) for 24 h increases CaMKIIδ protein, which is prevented in the presence of JNK2-specific inhibitor JNK2I-IX. The lower panel shows phospho-JNK is increased by anisomycin. immunoblotting images and summarized data showing that overexpression of inactivated dominant negative JNK2 (JNK2dn) completely reverses anisomycin-induced upregulation of CaMKIIδ (C). As control, adenovirus expressing LacZ has no effect on anisomycin action. In contrast, overexpressing dominant negative JNK1 (JNK1dn) does not affect the expression of CaMKIIδ (D).