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. 2013 Mar 28;8(3):e59950. doi: 10.1371/journal.pone.0059950

Figure 3. Efavirenz does not alter JNK phosphorylation status in platelets, but does induce activation of GSK3β.

Figure 3

Washed human platelets were treated as indicated for 1 h. Graphs indicate fold change in phosphorylation as compared to non-treated (NT) and determined via densitometry of immunoblots (representative blots shown above corresponding treatments), with phospho -JNK or -GSK3β quantification determined as a percentage of the total amount of each protein for each sample. (A) EFV does not induce activation of JNK, while thrombin treatment, as a positive control, induced phosphorylation of this kinase, indicating activation. This was partially reversed when treated in the presence of increasing amounts of the JNK inhibitor SP600125 (SP). Values were compared using an one-way ANOVA followed by Bonferroni’s test for multiple comparisons, which indicated statistical significance as *p<0.05 and **p<0.01 compared to all other conditions. N.S. indicates not significant; D indicates DMSO as a vehicle control. (B) EFV treatment resulted in dephosphorylation of GSK3β at the inhibitory phosphorylation site (Ser9), indicating activation of this molecule in platelets. One-way ANOVA followed by Bonferroni’s test for multiple comparisons indicated statistical significance as *p<0.05, **p<0.01, and ***p<0.001.