Subcellular localization of the FLT3-ITD oncogene plays a significant role in the production of NOX- and p22phox-derived reactive oxygen species in acute myeloid leukemia
Tunicamycin and Brefeldin A, induce ER retention of FLT3-ITD. ER retention of FLT3-ITD results in post-translational modification of p22phox and NOX4. NOX-generated ROS contribute to total pro-survival ROS in AML. AKT pathway is vital for FLT3-ITD at the plasma membrane oncogenic effects.