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. 2016 May 17;291(34):17804–17815. doi: 10.1074/jbc.M115.712885

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© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 4. — Overexpressed CK2α accelerates ERK rebound or sustains ERK phosphorylation in response to RAF-MEK-ERK pathway inhibition. pERK was evaluated by Western blotting analysis of lysates from A375 cells ectopically expressing GFP, CK2α, or NRAS(Q61K) treated for 24, 48, or 72h with vemurafenib (Vem) (BRAFi; 1 μm) (A), dabrafenib (Dab) (BRAFi; 100 nm) (B), or trametinib (Tram) (MEKi; 1 nm) (C). Total ERK1/2 (tERK) served as a loading control. MEKi (trametinib)-treated cell lysates were additionally immunoblotted for phospho-MEK1/2 (pMEK) and for the ERK-specific phosphatase DUSP6. Densitometry values for pERK/total ERK are shown for each panel.