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. 2020 Jun 26;41:101045. doi: 10.1016/j.molmet.2020.101045

Figure 5.

Figure 5

The activation of SIK1 mediated by phanginin A was LKB1-dependent. (A–B) Primary mouse hepatocytes were pretreated with LKB1 siRNA for 48 h and then treated with 5 μM of phanginin A and then the LKB1 protein and SIK1 phosphorylation levels (A) (n = 4) and gluconeogenesis (B) (n = 5) were examined. (C–D) Primary mouse hepatocytes were pretreated with SIK2 and SIK3 siRNA for 24 h and then treated with or without 5 μM of phanginin A, and the SIK mRNA (C) and gluconeogenesis (D) were tested (n = 5). (E) Primary mouse hepatocytes were pretreated with LKB1 siRNA for 48 h and then treated with 5 μM of phanginin A and then the LKB1 protein and AMPK phosphorylation levels were examined (n = 4). (F–G) Primary mouse hepatocytes were pretreated with AMPK siRNA for 48 h and then treated with or without 5 μM of phanginin A and the AMPK protein level (F) (n = 3) and gluconeogenesis (G) (n = 4) were studied. All of the results are presented as the mean ± SEM. ∗∗P < 0.01 vs individual controls.