Fig 2: Overexpression of HIP1R633–822 attenuates EGFR downstream signaling. (A) EGFR, Akt and ERK expression and phosphorylation with or without EGF treatment, in DIV 12 neurons. (B) Quantitative analysis of phosphorylated EGFR level. NA, not applicable. (C–E) Quantification of Akt (C), p-Akt (D) level and the p-Akt/Akt ratio (E). Normalized by GAPDH and compared with untreated control. (F–H) Quantification of ERK (F), p-ERK (G) level and the p-ERK/ERK ratio (H). Normalized by GAPDH and compared with untreated control. Mean ± SEM; ns, not significant; *p < 0.05; **p < 0.01; n = 3 independent experiments; unpaired two-tailed t-test.

Fig 3: T. gondii infection significantly reduced host NADPH oxidase(s) level via PI3K/AKT signaling pathway. (A) DC2.4 cells were treated with TgESP and then the expression of NOX family was analyzed by real-time PCR. (B) DC2.4 cells were infected with T. gondii or treated with TgESP for 24 hr. NOX4 levels were measured by western blot and RT-PCR. (C, D) DC2.4 cells were stimulated with GFP-RH or TgESP for 24 hr and treated with PI3K or AKT inhibitor during final 2 hr. NOX4 levels were confirmed by (C) western blot or (D) fluorescence microscopy. Scale bar=10 µm.

Fig 4: Ratio of phosphorylated/total Akt and phosphorylated/total mTOR. For each set of values, the box represents the middle half of the distribution of the data points stretching from the 25th to the 75th percentile. The line across the box represents the median. The lengths of the lines above and below the box are defined by the maximum and minimum data point values, respectively.

Fig 5: Phosphorylation of the insulin-like growth factor (IGF) pathway protein AKT in skeletal muscle.(Top) A representative western blot for phospho-Akt during non-satiation feeding (NSF, -4d), after 4 days of fasting (F, 0d), 90 minutes and 24 hours of satiation feeding (SF). (Bottom) Percentage phosphorylation of Akt, see text for details of normalisation method. Asterisk denotes significant differences between treatments (P<0.05).