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. 2015 Sep 7;1:15021. doi: 10.1038/cddiscovery.2015.21

Figure 4.

Figure 4

ERK and AKT signaling pathways are activated in SCs following 10 min EMF exposure. (a) Representative immunoblots showing the variations in phosphorylated ERK 2 (pERK 2), total ERK 2 (tERK 2), both 42 KDa, phosphorylated AKT (pAKT), total AKT (tAKT), both 60 KDa, in SCs at 2 and 6 h following EMF exposure. The β-actin (43 KDa) was used as a housekeeping protein. (b) Quantitative data at 2 h showed that pERK levels significantly increased (***P<0.001), while tERK levels decreased (*P<0.05); the pERK/tERK ratio showed that ERK signaling was activated 2 h following EMF exposure (***P<0.001, white columns). Indeed, pERK levels significantly decreased at 6 h (***P<0.001), while tERK significantly increased at 6 h (***P<0.001); pERK/tERK ratio indicated that this signaling pathway was deactivated within 6 h following EMF exposure (***P<0.001). Experiments were normalized for β-actin, and expressed as percentage versus controls (CONTR, black columns). The values are means±S.D. (N=3). (c) Quantitative data at 2 h showing that pAKT levels significantly increased (***P<0.001), while tAKT levels were unchanged; the pAKT/tAKT ratio showed an activation trend, even not significant. At 6 h, pAKT levels did not change but tAKT levels were significantly rised (***P<0.001); pAKT/tAKT ratio revealed a significant deactivation within 6 h after EMF exposure (***P<0.001, white columns). Experiments were normalized for β-actin, and expressed as percentage versus controls (CONTR, black columns). The values are means±S.D. (N=3). One-way ANOVA using Tukey's post-test was used for all statistical analysis.