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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: J Neurochem. 2010 Apr 30;114(3):706–716. doi: 10.1111/j.1471-4159.2010.06791.x

Figure 4.

Figure 4

Figure 4

Figure 4

Western blot of lysates from D2/S100B HEK cells expressing GFP-ataxin-1[82Q] treated as previously described (Fig. 3B) and detected with GFP and phospho-ataxin-1 S776 antibodies. (A) Lanes: Control, 100nM BRC, 60μM FSK, BRC + FSK. (B) Lanes: Control, 10μM H89, 60μM FSK, H89 + FSK. (C) Optical densities of the protein bands were taken using Image J software. FSK increased ataxin-1 S776 phosphorylation compared to control, while BRC and H89 impeded FSK stimulated S776 phosphorylation of ataxin-1. Western blots from the lysates of WT HEK cells expressing GFP-ataxin-1[30Q] (D), [82Q] (E) and GFP alone (F) were used to monitor the effect of drug treatments on the CMV promoter activity. Blots were probed with GFP and β Tubulin antibodies.