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. 2016 Nov 23;113(50):14402–14407. doi: 10.1073/pnas.1611106113

Fig. 3.

Fig. 3.

RAS-ERK signaling regulates the active chromatin state of mutant TERT promoters. (A) ChIP was performed in control or BRAF/MEK inhibitor-treated A375, UACC257, BLM, and G361 cells using antibodies specific for different histone marks and IgG as negative control. Enrichment of TERT promoter DNA fragments in ChIP DNA was normalized to DNA input. (B) ChIP was performed in si-Ctrl or si-BRAF–transfected UACC257, A375, WM793, and Malme-3M cells using antibodies specific for H3K4me3 and H3K9ac and IgG as negative control. Data shown represent at least two independent ChIP assays for all cell lines. Student’s t test (two-tailed) was used for all statistical analyses of control versus treated samples for each ChIP: *P < 0.05; **P < 0.01; ***P < 0.001.