Essential role for p53-mediated transcription in E1A-induced apoptosis

Peter Sabbatini, Jiayuh Lin, Arnold J. Levine, Eileen White

Research output: Contribution to journalArticlepeer-review

222 Scopus citations

Abstract

Baby rat kidney (BRK) cell lines transformed by E1A and a temperature- sensitive p53 [tsp53(val135)] undergo rapid apoptosis when p53 assumes the wild-type conformation at the permissive temperature. Wild-type p53 function is therefore required for induction of apoptosis in response to growth deregulation by E1A. BRK cells transformed by E1A and a transcriptionally defective temperature-sensitive p53 [tsp53(22-23val135)] are dramatically impaired for the ability to mediate E1A-induced apoptosis at the permissive temperature. The tsp53(22-23val135), however, still retains some ability to suppress cell growth. Thus, the activity of p53 as a transcription factor is directly correlated with the ability of E1A to induce apoptosis. In addition, there may exist at least two different mechanisms by which p53 can suppress cell-cycle progression, only one of which is dependent on p53-mediated transcription.

Original languageEnglish (US)
Pages (from-to)2184-2192
Number of pages9
JournalGenes and Development
Volume9
Issue number17
DOIs
StatePublished - Sep 1 1995

All Science Journal Classification (ASJC) codes

  • Genetics
  • Developmental Biology

Keywords

  • apoptosis
  • growth suppression
  • p53-Mediated transcription

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