hADA3 is required for p53 activity

Ting Wang, Takahiko Kobayashi, Rishu Takimoto, Alec E. Denes, Eric L. Snyder, Wafik S. El-Deiry, Rainer K. Brachmann

Research output: Contribution to journalArticle

69 Scopus citations

Abstract

The tumor suppressor protein p53 is a transcription factor that is frequently mutated in human cancers. In response to DNA damage, p53 protein is stabilized and activated by post-translational modifications that enable it to induce either apoptosis or cell cycle arrest. Using a novel yeast p53 dissociator assay, we identify hADA3, a part of histone acetyltransferase complexes, as an important cofactor for p53 activity. p53 and hADA3 physically interact in human cells. This interaction is enhanced dramatically after DNA damage due to phosphorylation event(s) in the p53 N-terminus. Proper hADA3 function is essential for full transcriptional activity of p53 and p53-mediated apoptosis.

Original languageEnglish (US)
Pages (from-to)6404-6413
Number of pages10
JournalEMBO Journal
Volume20
Issue number22
DOIs
StatePublished - Nov 15 2001

Keywords

  • Apoptosis
  • DNA damage
  • Histone acetyltransferase
  • hADA3
  • p53

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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    Wang, T., Kobayashi, T., Takimoto, R., Denes, A. E., Snyder, E. L., El-Deiry, W. S., & Brachmann, R. K. (2001). hADA3 is required for p53 activity. EMBO Journal, 20(22), 6404-6413. https://doi.org/10.1093/emboj/20.22.6404