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. 2018 Feb 5;128(3):1010–1025. doi: 10.1172/JCI95802

Figure 2. Deletion of SAV1 potentiates AKT signaling in PTEN-deficient livers.

Figure 2

(A) Heatmap of differentially expressed genes in the livers of 3-month-old mice as revealed by microarray analysis. (B) GSEA for Pten–/– Sav1–/– (DKO) livers compared with Pten–/– livers. Upregulated gene signatures in DKO mouse livers are depicted using MSigDB (Broad Institute). NES, normalized enrichment score; NOM p-val, nominal P value; FDR q-val, FDR q value. (C) Immunoblot analysis of AKT signaling components and lipogenesis-related proteins in the livers of 3-month-old mice. α-Tubulin was used as a loading control. mSREBP1c, mature form of SREBP1c; pSREBP1c, precursor form of SREBP1c. (D) Immunohistochemical staining of p-AKT (Ser473) and immunofluorescence staining of PIP3 (green fluorescence) in the livers of 3-month-old mice. Scale bars: 50 μm (left) and 100 μm (right). (E–G) qPCR analysis of relative mRNA levels for lipogenesis- or inflammation-related genes in the livers of 3-month-old mice. Data represent the mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001 versus the corresponding value for WT mice; †P < 0.05, ††P < 0.01, and †††P < 0.001 for the indicated comparisons (1-way ANOVA). (A and B) n = 2 mice; (C–G) n = 3 or 5 mice.