Recruitment of the retinoblastoma protein to c-jun enhances transcription activity mediated through the AP-1 binding site

The retinoblastoma susceptibility gene product (RB) is a transcriptional mo dulator. One of the targets for this modulator effect is the AP-1 binding s ite within the c-jun and collagenase promoters. The physical interactions b etween RE and c-Jun were demonstrated by coimmunoprecipitation of these two proteins using anti-c-Jun or anti-RE antisera, glutathione S-transferase a ffinity matrix binding assays in vitro, and electrophoretic mobility shift assays. The C-terminal site of the leucine zipper of c-Jun mediated the int eraction with RB. Although the B-pocket domain of RE alone bound to c-Jun, a second c-Jun binding site in the RE was also suggested. Mammalian two-hyb rid-based assay provided corroborative evidence that transactivation of gen e expression by RE required the C-terminal region of c-Jun. me conclude tha t RE enhances transcription activity mediated through the AP-1 binding site . Adenovirus E1A or human papillomavirus E7 inhibits RE-mediated transcript ion activity. These data reveal that the interactions between these two dis tinct classes of oncoproteins RE and c-Jun may be involved in controlling c ell growth and differentiation mediated by transcriptional regulation.