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. 2014 Mar 19;34(12):4326–4331. doi: 10.1523/JNEUROSCI.5184-13.2014

Figure 2.

Figure 2.

Chemical ischemia induces calcineurin activity-dependent transient increase in neuronal cyclin E1 expression. Neurons were exposed to 3 mm KCN with vehicle (Veh) or FK520 (FK; 5 μm) for 90 min. Cell lysates were harvested immediately (0′) or 24 h following exposure. A, Membranes were probed with anti-PS603 Kv2.1 or anti-Kv2.1 antibody. A representative blot from one of three independent experiments is shown; phosphorylated Ser603 Kv2.1 normalized to total Kv2.1 expression is 0.18 ± 0.03 relative units (r.u.; vehicle), compared to 0.03 ± 0.02 r.u. (KCN; n = 3; p < 0.05, two-tailed paired t test). B, Membranes were probed with anti-cyclin E1 or anti-GAPDH antibody. Top, Representative immunoblots are shown. Bottom, Summaries of four (left) and five (right) independent experiments. Cyclin E1 values are normalized to loading control GAPDH (mean ± SEM). *p < 0.05 versus KCN; **p < 0.01 versus vehicle at 0′ after treatment; ***p < 0.001 versus KCN at 0′ after treatment (ANOVA/Bonferroni's test).