Protein analysis and functional characterization of the RARG-CPSF6 gene fusion. (A) N-terminal and C-terminal anti-RARG antibodies were used to probe immunoblots prepared from NB4 cells (an APL cell line), a t(15;17) APL sample, and a sample from our patient. Both experiments were repeated independently with similar results. (B) Supervised hierarchical clustering of the top 500 dysregulated genes in t(15;17) APL (compared to all of the other non-t(15;17) AML cases included in the TCGA AML analysis) clusters the case (bright red) with other APLs (dark red). (C) A schematic of the experimental platform (top). The Gal4-RARG*395 truncation did not activate the UAS-GFP reporter when treated with either ATRA or BMS961 (a RARG agonist). Gal4-RARG and Gal4-RARA both activated the UAS-GFP reporter in response to ATRA, and this was not inhibited by coexpression of Gal4-RARG*395, indicating that the truncated RARG did not act as a dominant-negative against RARA or RARG in this assay (* and § P values calculated by ANOVA with Bonferroni correction for multiple comparisons). This experiment was repeated independently with similar results.