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Deacetylation of p53 modulates its effect on cell growth and apoptosis

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  • Jianyuan Luo

    (College of Physicians & Surgeons, Columbia University)

  • Fei Su

    (College of Physicians & Surgeons, Columbia University)

  • Delin Chen

    (College of Physicians & Surgeons, Columbia University)

  • Ariel Shiloh

    (College of Physicians & Surgeons, Columbia University)

  • Wei Gu

    (College of Physicians & Surgeons, Columbia University)

Abstract

The p53 tumour suppressor is a transcriptional factor whose activity is modulated by protein stability and post-translational modifications including acetylation1,2,3,4. The mechanism by which acetylated p53 is maintained in vivo remains unclear. Here we show that the deacetylation of p53 is mediated by an histone deacetylase-1 (HDAC1)-containing complex. We have also purified a p53 target protein in the deacetylase complexes (designated PID; but identical to metastasis-associated protein 2 (MTA2)), which has been identified as a component of the NuRD complex5,6,7. PID specifically interacts with p53 both in vitro and in vivo, and its expression reduces significantly the steady-state levels of acetylated p53. PID expression strongly represses p53-dependent transcriptional activation, and, notably, it modulates p53-mediated cell growth arrest and apoptosis. These results show that deacetylation and functional interactions by the PID/MTA2-associated NuRD complex may represent an important pathway to regulate p53 function.

Suggested Citation

  • Jianyuan Luo & Fei Su & Delin Chen & Ariel Shiloh & Wei Gu, 2000. "Deacetylation of p53 modulates its effect on cell growth and apoptosis," Nature, Nature, vol. 408(6810), pages 377-381, November.
    • Handle: RePEc:nat:nature:v:408:y:2000:i:6810:d:10.1038_35042612
    DOI: 10.1038/35042612
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    Cited by:

    1. Jingjie Yi & Omid Tavana & Huan Li & Donglai Wang & Richard J. Baer & Wei Gu, 2023. "Targeting USP2 regulation of VPRBP-mediated degradation of p53 and PD-L1 for cancer therapy," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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