Model for nutrient-dependent regulation of FOXA2 stability via SIRT1-mediated deacetylation.

<p>Graphical representation of the interaction and deacetylation of FOXA2 by SIRT1 depending on available nutrient levels. In times of nutrient excess (left panel) SIRT1 interacts with FOXA2 in the nucleus, resulting in FOXA2 deacetylation and subsequent proteasomal degradation. When nutrients are limited (right panel), FOXA2 is required to exert its transcriptional program in the nucleus. The interaction of FOXA2 with SIRT1 is diminished, resulting in enhanced acetylation and stability of FOXA2.