Elk1 binding sites are critical for 9E3/cCAF activation by thrombin.

The transient transfections were performed as described in Figure 1C with a reporter construct lacking Elk1 binding sites; the −534 Elk1 site was deleted and the −493 site was mutated (CAGGAT to acGcgT, pmElk1). With the mutation, both the basal and stimulated transcription levels of p495 were decreased to the p470 level of activation.