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. 2011 Jan 1;286(10):8338–8348. doi: 10.1074/jbc.M110.204768

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© 2011 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 7. — Proposed mechanism that controls β-cell fate in response to nitric oxide. In response to nitric oxide (supplied exogenously using donor molecules or endogenously following cytokine treatment) there is the loss of Akt-dependent FoxO1 phosphorylation that correlates with FoxO1 nuclear localization. In response to SIRT1 inhibitors, a proapoptotic transcriptional program appears to be activated as indicated by enhanced PUMA mRNA accumulation. If SIRT1 is activated, a FoxO1-dependent DNA repair response is activated as indicated by GADD45 mRNA accumulation.