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. 2018 Feb 22;13(2):e0191696. doi: 10.1371/journal.pone.0191696

Fig 6. PLX4032 rescue iAβ mediated attenuation of ERK 1/2 phosphorylation.

Fig 6

(A) Immunoblot for phospho-ERK 1/2, total-ERK 1/2, and phospho-c-RAF (Ser 259) in VC or iAβ transduced HEK293 cells following pretreatment with PLX4032 (30 min) and subsequent vehicle or EGF stimulation. Loss of ERK 1/2 phosphorylation is rescued upon pre-treatment with PLX4032. Two-dimensional gel transformation of phospho-ERK 1/2 intensities performed and shown as histogram. Beta-actin used as loading control. (B) Plot of the relative densitometry analysis of phospho-ERK 1/2 intensity of biological replicates with data shown as mean ± SE (n = 3). (C) Measurement of total-ERK 1/2 intensity demonstrate unaffected levels following treatment in VC or iAβ transduced cells. (D) Histogram of the phospho-flow cytometry measurement of EGF treated VC (gray) or iAβ (black) transduced HEK293 cells for ERK 1/2 phosphorylation. Positive shift in the MFI of iAβ transduced cells reflects an EGF dependent and PLX4032 mediated increase in ERK 1/2 phosphorylation. (E) Replicate analysis shown as mean ± SE (n = 3) of the MFI with a statistically significant (*p < 0.05) 1.47-fold increase in MFI following PLX pretreatment and EGF stimulation.