Figure 4
From: Experimental treatment of NRAS-mutated neurocutaneous melanocytosis with MEK162, a MEK-inhibitor
Pre- and posttreatment MIB-1 and pERK stains and Western Blot analysis. A and B. MIB-1 expression in the leptomeningeal melanocytosis sample before MEK162 treatment, in two hotspot regions (5% MIB-1-positive cells). C and D. The melanocytosis samples after MEK162 treatment showed lower MIB-1 expression than pre-treatment (<1% MIB-1-positive cells (arrows); compare with Figure 4 A and B. C temporobasal brain and D frontobasal brain. E. pERK protein expression in the leptomeningeal melanocytosis before MEK162 treatment. Endothelial cells serve as a positive internal control (arrow). F. pERK protein expression after MEK162 treatment showing lower pERK expression than pre-treatment (compare with 4E). G and H. Western Blots showing expression of pERK (G) and total ERK (H) in the brain sample after MEK162 treatment (lane 4), along with Rh-18 and Granta-519 as positive and negative controls in lanes 2 and 3, respectively. In the brain sample, pERK cannot be detected after MEK162 treatment (G), whereas total ERK is present (H), as indicated by the long arrows. Short arrows indicate GAPDH expression.