To show the involvement of AKT1(E17K) directly in v-Abl-mediated tumorigenesis, we infected bone marrow cells from mice with bicistronic retroviruses encoding v-Abl and either wild-type or the mutant AKT1.
Overall, the evidence indicates that the molecular mechanism underlying E17Koncogenesis is a broadened target lipid selectivity that allows high-affinity binding to PI(4,5)P(2).