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Imatinib and Nilotinib inhibit Bcr–Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox
In this study, using the K562 CML cell line we showed that inhibition of Bcr–Abl signalling, by either Imatinib or Nilotinib, led to a significant reduction in ROS levels which was concurrent with the GSK-3β dependent, post-translational down-regulation of the small membrane-bound protein p22phox, an essential component of the Nox complex. Furthermore, siRNA knockdown of p22phox in these cells established its importance in ROS production and proliferation. Taken together we believe our results provide a possible link between Bcr–Abl signalling and ROS production through Nox activity and demonstrate a novel mechanism o...
Source: Leukemia Research - December 5, 2012 Category: Hematology Authors: William D. Landry, John F. Woolley, Thomas G. Cotter Tags: Laboratory Studies Source Type: research