Fig 2: YAP1 broadly activates receptor tyrosine kinases in an SLC35B2-dependent manner.a Phospho-RTK array of A375-EV and A375-YAP5SA cells. b Gene expression of selected RTKs and respective ligands in YAP5SA cells and EV controls as assessed by RNA-seq (LFC, log2 fold change; RNA was isolated from two biological replicates per cell line). c Phospho-RTK array of A375-YAP5SA cells treated for 24 h with 5 µM Vemurafenib or DMSO. d, e Immunoblotting of indicated antibodies using protein lysates from YAP5SA (d) or non-engineered SKMEL28R (e) melanoma cells with SLC35B2 knockout and controls treated with Vemurafenib. f Growth competition assays of SKMEL28R cells with knockout of SLC35B2 compared to non-targeting controls with and without Vemurafenib treatment (10 µM). g Immunoblotting of indicated antibodies using protein lysates from SKMEL28-YAP5SA cells treated with H2O, unfractionated heparin (UFH), and the low molecular weight heparin Nadroparin (Nadro; this experiment was performed once). h Cell viability assays to determine the effect of single treatment with the pan-ERBB inhibitor Afatinib and combination treatment with Vemurafenib in melanoma cells with acquired MAPKi resistance and different MITF/AXL expression levels (mean ± SD of three replicates is presented). Experiments in a, c–f, and h were performed at least two times independently, one representative experiment is shown.