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. 2012 Mar 19;196(6):727–742. doi: 10.1083/jcb.201107096

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© 2012 Ryan et al.

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Figure 5. — Maintaining Ac–α-tubulin status permits flux through the secretory pathway after dystonin depletion. (A) Western blot analysis of 293T cell lysate shows that TSA treatment maintains Ac–α-tubulin after depletion of dystonin-a2. (B) TSA promotes VSVG trafficking to the Golgi and PM after dystonin-a2 depletion relative to DMSO-treated control. Arrowheads identify aberrantly localized VSVG molecules, whereas arrows identify normal VSVG localization. (C and D) Quantification of TSA impact on VSVG accumulation in the Golgi (C) and at the PM (D; ANOVA posthoc Tukey; n = 3). (E and F) TSA promotes GLuc flux through the secretory pathway (time = 1 h) in P4 (E) and P15 (F) dt^27J sensory neurons (ANOVA posthoc Tukey; n = 6). Error bars show means ± SEM. Cont, control; Tub, tubulin. **, P < 0.01. Bars, 10 µm.