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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: Cancer Res. 2017 May 16;77(13):3502–3512. doi: 10.1158/0008-5472.CAN-16-2745

Figure 5. BRAF fusion modularity and mutation studies.

Figure 5

(A) Schematic illustration and (B) activities in Ba/F3 of BRAF kinase domain (Exons 9–18) fused to BRAF AA100-345 with or without F247L mutation (mean luminescence, error bars denote standard deviation, N=3 respectively). GFP-BRAF-ex9 and N-BRAF-ex9 (V600E) = positive control; N-BRAF-ex9 and GFP = negative control. (C) Immunoblots of BRAF structural constructs expression and MAPK signaling activation in Ba/F3. (D) Ba/F3 cell survival assay of full-length BRAFF247L; shown mean luminescence, error bars denote standard deviation, N=3; BRAFV600E = positive control; GFP = negative control. (E) Immunoblots of expression of full-length BRAFF247L, wild-type BRAF, and BRAFV600E in Ba/F3. (F) Dose-dependent survival assays of Ba/F3 cells expressing full-length BRAFF247L treated with dabrafenib and trametinib for 72 hours (mean percentage of cell survival, error bars denote standard deviation, N=4 respectively). All p-values calculated by t-test; **, p<0.01; ****, p<0.0001.