Fig 1: ERK1/2 activation ratios. In the hippocampus (a, b) and striatum (c, d) ERK1/2 activation ratios (pERK/ERK total) were calculated (left panels) as well as ERK1/2 total protein expression (right panels) with data normalized to the WT + SAL group. Data were analyzed by two-way ANOVA and pairwise comparisons corrected with FDR. A significant increase in pERK/ERK total ratio was found in the KO + SAL group compared to the WT + SAL group in the hippocampus and striatum (one-tailed) as predicted. The pERK/ERK total ratio increase in the KO + SAL group was also evident when compared to the WT + Acamp group (two-tailed). In both brain regions, chronic treatment with acamprosate (300 mg/kg) reduced pERK/ERK total ratios in the KO mice to a level not distinguishable from WT + SAL mice (one-tailed) as predicted. There were no differences in the amount of ERK1/2 total in either brain region or between any groups. n = 6 per group and brain region; data shown are LS mean ± SEM; *p < 0.05, †p < 0.1; N.S. = not significant
Fig 2: miR-133b overexpression inhibits ERK signaling pathway activity. (A) Western blotting was performed to investigate the protein expression levels of p-ERK1/2 and ERK1/2 in cells treated with the ERK inhibitor U0126, or transfected with miR-133b mimic with or without LM22B-10 (ERK activator) treatment. (B) Semi-quantification of the expression levels. #P<0.05 vs. NC; ^P<0.05 vs. miR-133b; &P<0.05 vs. U0126. miR, microRNA; NC, negative control; p, phosphorylated.
Fig 3: Overexpression of miR-133b induces the apoptosis of 786-O cells and enhances drug sensitivity through inhibiting the ERK signaling pathway. (A) Flow cytometric analysis of apoptosis in cells treated with U0126 or transfected with miR-133b mimic with or without LM22B-10 treatment. (B) Changes in the proliferation rate of 786-O cells treated with DDP, DXT or ADR alone, or in combination with U0126 or miR-133b overexpression with or without LM22B-10 treatment. (C) Western blotting was used to detect the protein expression levels of Bcl-2, Bax, ABCG2 and P-gp in cells treated with U0126 or transfected with miR-133b mimic with or without LM22B-10 treatment. (D) Semi-quantitative analysis of protein expression levels. #P<0.05 vs. NC; ^P<0.05 vs. miR-133b; &P<0.05 vs. U0126; $P<0.05 vs. DDP/DXT/ADR; @P<0.05 vs. miR-133b group + DDP/DXT/ADR; ⋆P<0.05 vs. U0126 + DDP/DXT/ADR. miR, microRNA; DDP, cisplatin; DXT, docetaxel; ADR, doxorubicin; UO126, ERK pathway signal transduction inhibitor; LM22B-10, ERK activator; NC, negative control; PI, propidium iodide; ABCG2, ATP-binding cassette subfamily G2; P-gp, p-glycoprotein; OD, optical density.
Fig 4: Effect of STGPT (20, 40 and 80 mg/kg) on p-p38 MAPKα (A); p-Ikkβ (B); and ERK1/2 (C) in mice with NDEA-induced HCC. Data are presented as the mean ± SD (n = 6). +++ p < 0.001 vs. Control group, ++++ p < 0.0001 vs. Control group, ***p < 0.001 vs. NDEA group, ****p < 0.0001 vs. NDEA group, #### p < 0.0001 vs. STGPT 20 group, @@ p < 0.01 vs. STGPT 40 group, @@@@ p < 0.0001 vs. STGPT 40 group. Control, normal control group received the vehicle; STGPT 80, normal group received sitagliptin (80 mg/kg); NDEA, NDEA-induced HCC group received the vehicle; NDEA + STGPT 20, NDEA-induced HCC group treated with sitagliptin (20 mg/kg); NDEA + STGPT 40, NDEA-induced HCC group treated with sitagliptin (40 mg/kg); NDEA + STGPT 80, NDEA-induced HCC group treated with sitagliptin (80 mg/kg).
Fig 5: Effect of 2 ME and AAC on MAPK signaling pathway. Sham and AAC rats were treated with 2 ME (5 mg/kg/day) in the mini osmotic pump. Then, the MAPKs protein phosphorylation, P-JNK, P-p38 and P-ERK1/2 was determined. The values represent mean ± SEM (n = 6). +p < 0.05 compared to control. *p < 0.05 compared to AAC.
Supplier Page from Abcam for ERK1/2 (pT202/Y204) ELISA Kit