FIGURE 4.

Strategies for targeting splicing alterations in cancers. A, The U2 snRNP inhibitor disrupts U2 snRNP’s ability to recognize the branchpoint region of the intron. B, Sulfonamide compounds physically link RBM39 to the CUL4‐DCAF15 ubiquitin ligase, resulting in ubiquitination of RBM39 and subsequent proteasomal degradation. C, CLK, SRPK, and PRMT inhibitors are promising because the function, cellular localization, and assembly of a variety of splicing proteins depend on post–translational modifications. D, Antisense oligonucleotides modify splicing of specific transcripts by blocking the RNA‐RNA base pairing or protein‐RNA binding interactions