We tested these mutants regarding their ability to interfere with IFN induction. For this purpose, cells were transfected with L1-169 or the catalytic mutants C40A, H151A or Q16R, along with the reporter plasmids pIFNb-luc and pJATLacZ ( fig. 8c) . The IFNb promoter was activated by infection of cells with Sendai virus (SV) for eight hours. Interestingly all three mutants lost their ability to block SV-induced IFNb promoter activity when compared to the wildtype. These results showed that the catalytic activity of the OTU is necessary to counteract IFN induction. The results with the Q16R mutant were interesting, as it retained its deubiquitinating and deISG15ylation activity but, despite that, was not able to block IFN induction.