Fig. 5
RBM10 and SRSF2 cooperatively controlled the splicing of ASPM. A Immunoblot analyses of RBM10 in ASPM-pulldowns derived from the WT and MUT groups transfected with ASPM-minigene constructs. B Sliver staining of ASPM-pulldowns. MS analysis was performed in WT groups. C Venn diagram of ASPM-pulldowns between positive and negative probes. D Pathway enrichment analysis of positive probe unique ASPM-pulldowns. E Potential spliceosome factors involved in ASPM ES. F Immunoblot analyses of U2AF2 and SRSF2 in ASPM-pulldowns. G, H Co-immunoprecipitation was performed to confirm the interaction between SRSF2 and RBM10/RBM10C761Y. RBM10 mutation weakened the interaction between SRSF2 and RBM10. I RNA immunoprecipitation using anti-RBM10 or anti-SRSF2 antibodies, or igG with SRSF2 knockdown. J RT-PCR was performed to detect the expression of ASPM isoforms in NC, WT, MUT, and SRSF2-knockdown groups. K Effects of RBM10 and SRSF2 on ASPM exon18 ES event were examined using minigene splicing reporter assays