Abstract
Mechanism of Activation of AMPK and Upregulation of OGG1 by Rapamycin in Cancer Cells
Highlights
AMPK is a physiological cellular energy sensor that is activated by phosphorylation at Thr172 in response to changes in cellular ATP levels
Treatment of tuberous sclerosis complex (TSC) patients with rapamycin resulted in reduction in angiomyolipoma volume by nearly 50% [5]. mTOR serves a critical role in the regulation of the translational machinery and, in doing so, affects cellular responses to growth, proliferation, and differentiation, all of which are abnormally manifested in TSC lesions
Rapamycin treatment led to a robust phosphorylation and activation of AMPK and ACC to a degree similar to that observed with AICAR stimulation in TSC2+/− treated with HG further supporting the importance of rapamycin as an activator of AMPK
Summary
AMPK is a physiological cellular energy sensor that is activated by phosphorylation at Thr172 in response to changes in cellular ATP levels. Accumulation of ROS is associated with activation/phosphorylation of Akt at Ser473, inactivation/phosphorylation of tuberin at Thr1462 and activation mTOR/rictor complex II [3]. Akt can be activated through the feedback mechanism of mTOR-rictor complex activation.
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