Protein kinase inhibitors have become increasingly important therapeutic drugs for the treatment of human diseases; however, resistance and off-target effects can limit their use. In this issue ofCell Chemical Biology,Ross et al. (2017)reveal a novel off-target mechanism where the Src kinase inhibitor SU6656 paradoxically primes AMPK for phosphorylation and activation by the upstream kinase LKB1.

中文翻译：

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假抑制剂：AMPK激活抑制特朗普

蛋白激酶抑制剂已经成为治疗人类疾病的越来越重要的治疗药物。但是，抗性和脱靶效应会限制其使用。在本期《细胞化学生物学》中，罗斯等人。（2017）揭示了一种新型脱靶机制，其中Src激酶抑制剂SU6656自相矛盾地引发AMPK的磷酸化和上游激酶LKB1的激活。