Fig. 1

Active RSK signaling in MAPK pathway-hyperactivated melanoma cells is effectively blocked by RSK-specific inhibitors. A Western blot analysis of the MAPK/RSK signaling axis in whole cell protein lysates of MAPK pathway-hyperactivated melanoma cells of different genomic subgroups (NRAS^Mut, NF-1^LOF, BRAF^Mut) and of primary melanocytes (NHM, normal human melanocytes) as benign control cells. GAPDH and Vinculin were used as loading controls. B, C Immunoblot analysis of RSK activity in whole cell protein lysates of 451LU (BRAF^Mut, B) or a panel of MAPK pathway-hyperactivated melanoma cell lines (BRAF^Mut, NRAS^Mut, NF-1^LOF) and patient-derived short-term cultures (C) after treatment with increasing doses of RSK inhibitors (PMD-026, BI-D1870) or solvent control treatment with DMSO for 6 h (B) or 72 h (C), respectively. GAPDH served as loading control