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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

The lymphocytes isolated above were subjected to immunofluorescence staining with Rat FITC, APC, PE (BD Pharmingen, USA), and labeled anti-rat CD3 + , CD4 + , and CD8 + monoclonal antibodies, respectively, reacting at 4C for 30 min in the dark