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. 2016 Apr 15;129(8):1580–1591. doi: 10.1242/jcs.182097

Fig. 2.

Fig. 2.

RSK couples FAK signaling to IKKβ activation. (A) Endothelial cells transfected with siRNA targeting RIP, both RSK1 and RSK2, TAK or NIK were treated with oxLDL and NF-κB phosphorylation (P-NF-κB) was determined by immunoblotting (n=4). (B) Endothelial cells were treated with oxLDL for the indicated times and RSK phosphorylation (P-RSK) was determined by immunoblotting (n=5). (C,D) OxLDL-induced IKKβ kinase activity was determined. (C) Cells were pretreated with BI-D1870 (BI-D, 5 μM, 1 h) or (D) transfected with RSK1 and RSK2 siRNA. Results are mean±s.e.m. (n=4). (E,F) FAK signaling in HAE cells was inhibited with (E) PF-573228 (4 μM, 1 h) or (F) FAK siRNA, and oxLDL-induced (100 μg/ml; indicated timepoints) phosphorylation of FAK and RSK was determined by immunoblotting (n=4–5). (G) Primary lung endothelial cells isolated from FAK-WT or FAK-KD transgenic mice were treated with oxLDL for 15 or 30 min, and FAK and RSK phosphorylation was assessed by immunoblotting (n=5). Results are mean±s.e.m. *P<0.05 (compared to 0 time or no treatment) or #P<0.05 (compared to respective timepoint) using either (B) one-way ANOVA or (A,C–G) two-way ANOVA with Bonferroni post-hoc test. NT, no treatment. Mock indicates mock transfection.