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. 2011 Mar 7;29(22):3085–3096. doi: 10.1200/JCO.2010.33.2312

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© 2011 by American Society of Clinical Oncology

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Fig 3. — Pharmacologic and biochemical characterization of the MEK1^C121S mutation. Growth inhibition curves for (A) the RAF inhibitor PLX4720 and (B) the MEK inhibitor AZD6244 are shown for wild-type A375 (BRAF^V600E) melanoma cells (solid black) and A375 cells expressing MEK1^C121S (red), wild-type MEK1 (MEK-WT; blue), or a constitutively active MEK1 variant (MEK-DD; gold). Effect of (C) PLX4720 and (D) AZD6244 on ERK1/2 phosphorylation (pERK 1/2) in wild-type A375 cells and those expressing MEK-WT, MEK1^C121S, or MEK-DD. The levels of pERK1/2, total ERK1/2, MEK1/2, and α-tubulin are shown for A375 cells expressing MEK1 mutations after a 16-hour incubation at 0, 0.08, 0.4, 2, 5, and 10 μmol/L drug concentrations. (E) In vitro kinase assay measuring pERK in A375 cells expressing MEK1 mutations. Relative levels of pERK compared with total ERK1 and total MEK1 are shown.