We finally tested if hPIV3-C 90-195 was able, like full-length hPIV3-C, to block IFN-a/b signaling and enhance cellular response to EGF stimulation. First, cells were transfected with 36FLAG-tagged hPIV3-C, hPIV3-C 90-195 or hPIV3-C 1-89 together with the IFN-a/b reporter plasmid, and stimulated 24 h later with recombinant IFN-b. Reporter gene expression was determined 24 h post transfection and found to be inhibited exclusively by full-length hPIV3-C ( Figure 8A ). Although this may reflect the weakness of hPIV3-C interaction with STAT1 ( Figure 7B ), this also indicates that both the N-terminal and C-terminal regions of hPIV3-C are required to block IFN-a/b signaling, even if only the C-terminal region is required for the binding to STAT1. The same constructs were tested using the Elk1 activity reporter plasmids ( Figure 8B ). Again, only full-length hPIV3-C was able to enhance Elk1 activation upon EGF stimulation whereas full-length hPIV3-C and hPIV3-C 90-195 were expressed at similar levels in transfected cells ( Figure 8B , upper right panel).