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Schematic representation of Akt-mediated feedback inhibition. Akt-induced phosphorylation of IRS proteins may lead to their dissociation from PI3K as well as proteasome-dependent degradation. Simultaneously, IRS transcription is inhibited (data not shown), which further reduces IRS levels. Consequently, activation of PI3K is impaired. Loss of signaling via PI3K-dependent but Akt-independent survival pathways can lead to increased injury despite persistent Akt activation.
