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. 2016 Sep 1;30(17):1943–1955. doi: 10.1101/gad.283499.116

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© 2016 Liu et al.; 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://genesdev.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 7. — p-AKT^S473 directly modulates GLI2 protein. (A) Western blots for phospho-(Ser/Thr) AKT substrate after coimmunoprecipitation with IgG or GLI2 antibody in both KS and KCS mouse pancreatic fibroblasts. Quantification is in Supplemental Figure 7. (B) Western blots for phospho-(Ser/Thr) AKT substrate (top panel) or GLI2 (bottom panel) in KS and KCS pancreatic fibroblasts transfected with control vector, Gli2^S320A mutant, or Gli2^WT vectors after coimmunoprecipitation with Flag antibody. (C, top panel) p-AKT^S473 isolated from KS or KCS was incubated with fresh KS lysate followed by immunoprecipitation with GLI2 antibody and immunoblotting for phospho-(Ser/Thr) AKT substrate. The bottom panel shows total GLI2 levels. (D) Western blots for phospho-(Ser/Thr) AKT substrate after immunoprecipitation with GLI2 antibodies in Tet-off myristoylated AKT1 (myr-AKT)-expressing fibroblasts with the indicated doxycycline treatment. (E) Smo deletion leads to activation of the Akt pathway, which phosphorylates and stabilizes GLI2. GLI2 directly binds to the Tgfa promoter and induces its transcription. Secreted TGF-α then triggers ADM events.