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. 2015 Jun 3;6:119. doi: 10.3389/fphar.2015.00119

FIGURE 6.

FIGURE 6

Peptide inhibition of BVR and ERK1/2. (A) Autophosphorylation of BVR was determined in reaction mixtures that included no added peptide or either of the BVR-based peptides KKRILHC or KRNRYLSF. The products were detected by autoradiography (top) and quantified by densitometry (bottom). The peptide KRNRYLSF includes a potential IRK target site. (B) ERK2 kinase reactions with myelin basic protein as substrate were performed in the presence or absence of the BVR C-Box (FGFPAFSG) and D-Box (KKRILHCLGL) peptides, which inhibit interaction of BVR with ERK, *p < 0.01. (C) Peptide FGFPAFSG inhibits ERK-dependent signaling. Cells were transfected with Elk1 expression plasmid and an Elk1-dependent luciferase reporter, then treated with myristoylated peptide for two hours prior to inducing ERK1/2 with IGF-1. After a further 12 h, cells were harvested and luciferase activity was measured. *p < 0.01 compared to untreated control. †p < 0.01 compared to IGF-treated.