RELIEF OF P53-MEDIATED TRANSCRIPTIONAL REPRESSION BY THE ADENOVIRUS E1B 19-KDA PROTEIN OR THE CELLULAR BCL-2 PROTEIN

The p53 tumor suppressor gene product is a transcriptional regulatory protein. It activates transcription from promoters that contain a p53 DNA binding site but represses many promoters that lack its binding si te. High-level expression of wild-type p53 can induce apoptosis in cer tain cell types, and this activity can be blocked by the adenovirus E1 B 19-kDa oncoprotein or by the cellular Bcl-2 oncoprotein. Here we rep ort that p53-mediated repression of promoters that lack a p53 binding site is abrogated by the E1B 19-kDa protein or Bcl-2 oncoprotein. In c ontrast, transcriptional activation by p53 still occurs in the presenc e of either protein. The fact that two oncoproteins capable of prevent ing p53-mediated apoptosis also block transcriptional repression by p5 3 raises the possibility that p53 might induce apoptosis, at least in part, by repressing transcription.