Skip to main content
. Author manuscript; available in PMC: 2016 Dec 2.
Published in final edited form as: Nat Immunol. 2016 Aug 1;17(9):1016–1024. doi: 10.1038/ni.3517

Figure 2.

Figure 2

Targeting the spliceosome in myeloid neoplasms. Mutations in genes encoding spliceosomal proteins alter RNA splicing in a sequence-specific manner to drive aberrant gene expression. Mutations in the gene encoding SRSF2 result in alterations at Pro95 and result in aberrant splice-site ‘preference’ based on the nucleotide sequence of exonic splicing enhancer (ESE). In contrast, U2AF1 and SF3B1 both recognize the 3′ splice site, and mutations that affect Ser34 in U2AF1 result in altered 3′ splice-site usage based on the nucleotide sequence immediately 5′ of the canonical 3′ AG dinucleotide. In contrast, cells bearing mutations that result in the K700E substitution in SF3B1 have increased use of cryptic 3′ splice sites.