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- W2104855680 endingPage "e1000990" @default.
- W2104855680 startingPage "e1000990" @default.
- W2104855680 abstract "Akt represents a nodal point between the Insulin receptor and TOR signaling, and its activation by phosphorylation controls cell proliferation, cell size, and metabolism. The activity of Akt must be carefully balanced, as increased Akt signaling is frequently associated with cancer and as insufficient Akt signaling is linked to metabolic disease and diabetes mellitus. Using a genome-wide RNAi screen in Drosophila cells in culture, and in vivo analyses in the third instar wing imaginal disc, we studied the regulatory circuitries that define dAkt activation. We provide evidence that negative feedback regulation of dAkt occurs during normal Drosophila development in vivo. Whereas in cell culture dAkt is regulated by S6 Kinase (S6K)-dependent negative feedback, this feedback inhibition only plays a minor role in vivo. In contrast, dAkt activation under wild-type conditions is defined by feedback inhibition that depends on TOR Complex 1 (TORC1), but is S6K-independent. This feedback inhibition is switched from TORC1 to S6K only in the context of enhanced TORC1 activity, as triggered by mutations in tsc2. These results illustrate how the Akt-TOR pathway dynamically adapts the routing of negative feedback in response to the activity load of its signaling circuit in vivo." @default.
- W2104855680 created "2016-06-24" @default.
- W2104855680 creator A5002156552 @default.
- W2104855680 creator A5027285428 @default.
- W2104855680 creator A5060571905 @default.
- W2104855680 creator A5071083794 @default.
- W2104855680 creator A5083708653 @default.
- W2104855680 creator A5087921962 @default.
- W2104855680 date "2010-06-17" @default.
- W2104855680 modified "2023-09-26" @default.
- W2104855680 title "Dynamic Switch of Negative Feedback Regulation in Drosophila Akt–TOR Signaling" @default.
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