FIGURE 3.
SRSF10 as a splicing activator. (A) Control of Bcl-x splicing by SRSF10. Phosphorylated SRSF10 has minimal impact on Bcl-x splicing in normal growth conditions in 293 cells. Following DNA damage by oxaliplatin, the dephosphorylation of SRSF10 increases the interaction with the repressor hnRNP K and their dissociation from the Bcl-x pre-mRNA, allowing hnRNP F/H to disrupt G-quadruplexes and favor use of the 5′ splice site of Bcl-xS. (B) Global positive and negative effects on exon inclusion can be explained by SRSF10 binding and stimulating splice site usage either on the alternative (on the right) or a constitutive (on the left) exon.
