Figure 5. The isomerase activity of nuclear cyclophilins is not necessary to detect splicing inhibition.

For cyclophilins that are active isomerases against proline-containing substrates, point mutations were made at the position corresponding to Trp¹²¹ in PPIA. This mutation should abrogate proline turnover and cyclosporine binding [39]. In panels (A) and (B), it can be seen that mutation of PPIG or PPWD1 increases splicing inhibition. In panel (C), the modest effect of mutating PPIL1 is seen. In (D and E), mutation of the inhibitory PPIE PPI domain or of PPIL3 has no effect on splicing inhibition.