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. 2020 Mar 1;34(5-6):413–427. doi: 10.1101/gad.332270.119

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© 2020 Rahman et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 7. — Model of oncogenic splicing factor mutation-induced altered splicing and aberrant NMD. Mutation at Pro95 of SRSF2 changes its RNA-binding preferences from a G-rich motif (GGWG) to a C-rich motif (C/GCWG) (W = A/U), causing transcriptome-wide splicing alterations. Several mRNA isoforms promoted by SRSF2 mutants harbor a premature termination codon and are therefore potential targets of NMD. In addition to altering RNA splicing, SRSF2 mutants further enhance the deposition of EJCs bound to mRNA downstream from a PTC. Specifically, mutant SRSF2 promotes the deposition of three core EJC factors (eIF4A3, MAGOH, and Y14) via RNA-mediated molecular interactions. This subsequently enhances the association of several NMD factors (UPF3B, UPF2, and UPF1), thereby enhancing mRNA decay.