Skip to main content
. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: J Neurochem. 2015 Aug 11;135(3):508–521. doi: 10.1111/jnc.13252

Fig. 3.

Fig. 3

Ethanol activates ALK signaling in IMR-32 cells. (a) Representative Western blots showing increased pALK 220 and 140, pERK, and pSTAT3, but not pAKT within 5 min of 100 mM ethanol treatment. Total ALK, ERK, STAT3, and AKT Western blots are shown below each phosphorylated protein blot for comparison. The effect of ethanol on phosphorylation was blocked by pre-treatment with the ALK inhibitor TAE684 (+, lanes 2, 4, 6 and 8) compared to the DMSO control (-, lanes 1, 3, 5 and 7). (b–e) Quantification of Western blots using ImageJ. Significant increases in pALK (b), pERK (c), and pSTAT3 (d), but not pAKT (e) were observed within 5 min of ethanol treatment, effects that were blocked by TAE684. Data are presented as mean ± S.D. *p < 0.05, **p < 0.01 compared to 0 minute time point within DMSO controls. #Significant difference when comparing DMSO control vs. TAE684 treatment within each time point.