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Higdon J

In summary, our data demonstrate that increased radioresistance of cancer cells expressing the clinically relevant activation-associated AKT mutant protein AKT-E17K involves multiple metabolic mechanisms: On the one hand, AKT-E17K promoted increased glycolytic activity at basal state and improved the capability of the cells for activating compensatory glycolysis upon irradiation

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The group of Chavkin showed that rKOR is phosphorylated in vivo at S369 by GRK3 upon U50,488 exposure (Mclaughlin et al., 2004) and in vitro by GRK2 (Mclaughlin et al., 2003)