Fig 2: Total and phosphorylated nephrin and Akt expression in mice fed diet of 20% ISP. (A & B) Immunoblots of glomerular whole cell lysates from individual male (A) and female (B) mice fed casein or ISP as an exclusive source of protein (n = 3 shown). ß-actin was used as a loading control. (C & D) Densitometry of immunoblots in A and B (C & D, respectively), normalized to casein controls.Note. Data are presented as mean ± standard error of the mean. Statistical significance compared to casein control mice was determined using Student’s t test and is marked by an asterisk. ISP = isolated soy protein; ns = no significance.*P < .05.

Fig 3: Model explaining the relationship among PI3K, AKT1, miR-196a, FoxO1, p27 and HOXA9

Fig 4: The reduced Akt2 expression and the verification of Akt2 siRNAs efficacy (related to Fig 1) AqRT–PCR analysis for the mRNA expression of Akt1 (n = 3), Akt2 (n = 3), Akt3 (n = 4) in the different tissues of at least three different WT C57BL/6 mice.B, CThe mRNA expression of Akt1, Akt2, or Akt3 in the liver, spleen, or lung from WT mice after the VSV infection for 6 h (1 × 106 PFU/g, i.v.) were detected by qRT–PCR. Akt1 in liver, n = 5; Akt2 in liver, n = 7; Akt3 in liver, n = 5; Akt2 in spleen, n = 7; Akt2 in lung, n = 7.DqRT–PCR analysis for the mRNA expression of AKT2 in the liver tissue of the normal individuals (n = 3) or HBV-infected different HCC patients (n = 8).EImmunoblot analysis of p-AKT2 (Ser473), AKT2, p-TBK1 (Ser172), TBK1, p-IRF3 (Ser396), IRF3 and GAPDH in the VSV-stimulated PEMs at indicated time points.FThe mRNA expression of Ifnb1 and Cxcl10 were measured by qRT–PCR in the WT and Ifnar1 KO PEMs stimulated with VSV and lipo-ISD for 6 h. n = 3, respectively.GqRT–PCR analysis for the mRNA expression of Ifnb1 (n = 3, left panel) and then, the mRNA change of Akt2 (n = 3, right panel) were further calculated by compared with “siNC mock” in the PEMs with Socs1 or Socs3 knockdown followed by stimulation of VSV for 6 h.HThe mRNA level (left panel, by qRT–PCR) and protein expression (right panel, by immunoblot) of AKT2, AKT1, AKT3 in WT PEMs transfected with siNC, siAkt2-1, or siAkt2-2 for 48 h. Data information: *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001; using unpaired t-test (B–D), or two-way ANOVA test (G). Data are pooled from at least three independent experiments (B, C, F, G) or representative of three independent biological replicates (A, E, H). Error bars (A-D, H, mean ± SD; F and G, mean ± SEM). Source data are available online for this figure.

Fig 5: miR-192-5p inhibited TRIP13 expression in HCC cells. a-c qRT-PCR and western blot analysis of TRIP13 mRNA in HCC cells transfected with miR-192-5p mimics or miR-192-5p inhibitor. d The putative miR-192-5p binding sequence in the 3'-UTR of TRIP13 (left penal). Luciferase activity of 293 T cells co-transfected with WT or MUT luciferase reporter plasmids and miR-192-5p mimics or negative control (right penal). e-f Cell migration and invasion were measured in HCC cells transfected with miR-192-5p mimics or negative control. g A model depicting the major molecular mechanisms of the miR-192-5p–TRIP13–ACTN4–AKT/mTOR axis in HCC. *P < 0.05, **P < 0.01, ***P < 0.001