CK2α-mediated maintenance of ERK phosphorylation upon pathway inhibition and resistance to BRAFi/MEKi are both kinase-independent.
A, A375 cells ectopically expressing GFP, CK2α(K68M), or CK2α(WT) were treated with BRAFi and MEKi as in Fig. 4, then lysed, and immunoblotted for pERK and total DUSP6. Total ERK (tERK) served as loading control. B, cells were treated as in A, and GI50 curves were generated after 72 h. A summary of GI50 values is shown in a table below. Results are presented as means ± S.E. (n = 4). Error bars represent S.E. Vem, vemurafenib; Dab, dabrafenib; Tram, trametinib.