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. 2017 Jun 6;8:15729. doi: 10.1038/ncomms15728

Figure 8. Increased ROS induce EphA2 phosphorylation via PTP1B inactivation.

Figure 8

(a) Intracellular ROS levels were measured by DCF fluorescence in RPE-1 cells treated with or without DXR and NAC. NAC was added to the medium 6 h before analysis at a concentration of 2 mM. (b) Oxidized-PTP1B was immunoprecipitated by scFvs45 antibody from RPE-1 cells treated with or without DXR and NAC. Inputs and immunoprecipitates were immunoblotted with anti-PTP1B antibody. Dot plot represents the relative density of oxidized-PTP1B/PTP1B analysed by ImageJ. (c) Relative PTP1B activity in RPE-1 cells treated with or without DXR and NAC. (d) EphA2 immunoprecipitates prepared from RPE-1 cells treated with or without DXR and NAC were immunoblotted with anti-phosphotyrosine and anti-EphA2 antibody. Dot plot represents the relative density of phospho-EphA2/EphA2 analysed by ImageJ. (e) Schematic model of the regulation and function of sEV-associated EphA2 in senescent cells. Replicates are biological replicates (n=3 for a,b,d and n=4 for c). Error bars indicate s.d. *P<0.05 (one-way ANOVA with the post-hoc Dunnett's two-tailed test for a–c) and two-tailed t-test for d).