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. 2014 Oct 24;6(4):2524–2538. doi: 10.18632/oncotarget.2629

Figure 4. The transforming potential of D797N Vav1 implicates a JNK-dependent pathway.

Figure 4

a-b. JNK1/2 and c-Jun phosphorylation analyses. Protein extracts from stable NIH3T3 cell lines were analysed by sequential immunoblotting with (a) anti-phospho-JNK (Thr183/Tyr185) and anti-JNK Abs; (b) anti-phospho-c-Jun (Ser63) and anti-c-Jun Abs. Fold increases of phospho-JNK1/2 and phospho-c-Jun in cells expressing wt-Vav1, onco-Vav and D797N compared to control vector were normalized to whole Jnk1/2 and c-Jun expression, respectively. Inhibition of c-Jun phosphorylation was monitored after 2h treatment (+) or not (−) with the JNK inhibitor SP600125 (10μM). c. JNK activity is required for onco-Vav and D797N-induced foci formation. Focus formation assays were performed with NIH3T3 cells transfected with the indicated constructs and 0, 5, 10 or 20 μM of SP600125. Foci formation is calculated relative to untreated cells (100%). Results are means ± SD of 3 independent experiments performed in duplicate.