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. 2017 Mar;27(3):427–439. doi: 10.1101/gr.212175.116

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Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — GR increases the number and residence time of CREB1 molecules. (A) Summary of single-molecule tracking data. The percentage of the unbound, fast-bound, and slow-bound fractions as well as each fraction's average residence time is depicted under different treatments: (fsk) forskolin; (dex) dexamethasone. (B) Box plot depicting dwell time distributions of CREB1 molecules under different treatments. (*) Statistical significance (P ≤ 0.05) compared to indicated sample. (n.s.) Not significant. (C) A model for hepatic TF dynamics during fasting. The liver is exposed to glucagon in early fasting, leading to CREB1 activation by phosphorylation. At midterm fasting, GR is activated by increasing levels of corticosterone leading to two trajectories: First, GR assists the loading of CREB1 onto gluconeogenic enhancers resulting in synergized gluconeogenic gene expression and glucose production; and second, GR induces the gene level of PPARA which, as fasting persists, promotes a FAO/ketogenic gene program.