ERK1/2 Antibody

Application: WB Species:rat; Sample:rat

Fig. 4. FGFR- ERK signaling pathway is involved in FGF2-induced EAAC1 expression. (A) C6 cells were incubated with FGF2 (10 ng/mL) for different durations. (B, C) Before incubation with FGF2 (10 ng/mL) for 15 min (B) or 24 h (C), cells were pretreated with the FGFR kinase inhibitor SU5402 (SU; 25 lM, 5 min) or the ERK inhibitor U0126 (U0; 10 lM, 1 h). Phosphorylation of FRS2a or ERK1/2 (A and B, respectively), and EAAC1 expression (C) were analyzed by Western blots. Data are shown as mean ± SEM from three independent experiments. * p < 0.05; **p < 0.01 versus the control group. # p < 0.05; ##p < 0.01 versus the FGF2 alone group.

Application: WB Species:human; Sample:Not available

Figure 4: Induction of miR-370 over-expression reduces EGFR and HIF-1α expression and inhibits the ERK and AKT phosphorylation in XWLC-05 and H157 cells. XWLC-05 and H157 cells were transfected with miR-370 mimics, miR-370 inhibitor or corresponding controls for 24 h. The relative levels of EGFR, HIF-1α, ERK, AKT expression, ERK and AKT phosphorylation were determined by Western blot assays. Data are representative images or expressed as the means ± SEM of each group of cells from three separate experiments. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Application: WB Species:pig; Sample:jejunum

Figure 6: Effect of OEO on the levels of p-Akt, p-ERK, p-p38, p-JNK, and NF-

Application: WB Species:rat; Sample:C6 Cells

Fig. 3 OBHS and RAL increase Akt and ERK phosphorylation through GPER1. a Akt and ERK inhibitors attenuated the pro-survival effects of OBHS and RAL against Aβ toxicity. Cells were pretreated with specific inhibitors LY294002 (LY, 20 μM), U0126 (U,10 μM) for one hour and then incubated with OBHS (1 μM) or RAL (1 μM) for 45 min, after Aβ treatment for an additional 24 h. Cell viability was measured by MTT method. b,c C6 cells were preincubated with PI3K/Akt inhibitor LY (b) or ERK inhibitor U (c) for one hour, followed by OBHS (1 μM) or RAL (1 μM) treatment for 15 min. d GPER1 antagonist G15 (10 μM) was added to the media for 24 h, before OBHS (1 μM) or RAL (1 μM) treatment for 15 min of C6 cells. The proteins were analyzed by the western blot method. The data were shown as the mean±SD from three independent experiments.

Application: WB Species:mouse; Sample:Not available

Figure 4: MiR-377 promotes inflammation and insulin-resistance in mature 3T3-L1 cells. After transfection with 100 nM miR-377 mimics or inhibitor for 24 h, differentiated 3T3-L1 adipocytes were treated with 10 ng/ml TNFα for 24 h and then stimulated with 100 nM insulin for 15 min. Cells were then harvested for real-time PCR and immunoblotting analyses. (A) The effect of miR-377 overexpression on inflammation-related gene expression. *P < 0.05, **P < 0.01 vs. NC 0.1% BSA; ##P < 0.01 vs. NC 10 ng/ml TNFα; ns, not signifcant (n = 3). (B) The effect of miR-377 inhibition on inflammation-related gene expression under conditions of TNFα-induced insulin-resistance. ##P < 0.01 vs. NC 10 ng/ml TNFα(n = 3). (C) The effect of miR-377 overexpression on JNK phosphorylation under conditions of TNFα-induced insulin-resistance. *P < 0.05 vs. NC without insulin; #P < 0.05 vs. NC with insulin (n = 3). (D and E) The effect of miR-377 overexpression on AKT and ERK phosphorylation. *P < 0.05 vs. NC with 0.1% BSA and insulin; #P < 0.05 vs. NC with 10 ng/ml TNFα and insulin (n = 3). (F) The effect of miR-377 inhibition on JNK phosphorylation under conditions of TNFα-induced insulin-resistance. *P < 0.05 vs. NC without insulin; #P < 0.05 vs. NC with insulin (n = 3). (G and H) The effect of miR-377 inhibition on AKT and ERK phosphorylation. *P < 0.05 vs. NC with 0.1% BSA and insulin; #P < 0.05 vs. NC with 10 ng/ml TNFα and insulin (n = 3).

Application: WB Species:human; Sample:MCF-7

Figure 5: Effect of miR-29a on the insulin signaling pathways. (A) IGF-1R, CDC42, p85α, p-ERK and ERK mRNA levels were determined by qPCR in ER-positive cells transfected with a miR-29a mimic or miR-29a inhibitor. (B, C) Western blotting analysis was performed to monitor IGF-1R, CDC42, p85α, p-ERK and ERK expression in ER-positive cells transfected with a miR-29a mimic or miR-29a inhibitor. The results showed that ERK, CDC42 and p85α are the target genes of miR-29a; however, miR-29a promotes breast cancer cell growth and proliferation mainly by activating ERK phosphorylation.