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Stress-dependent Daxx-CHIP interaction suppresses the p53 apoptotic program.

Holly McDonough1, Peter C Charles, Eleanor G Hilliard

  • 1Carolina Cardiovascular Biology Center, University of North Carolina, Chapel Hill, North Carolina 27599-7126, USA.

The Journal of Biological Chemistry
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Carboxyl terminus of Hsp70-interacting protein (CHIP) counters stress-induced apoptosis by interacting with death domain-associated protein (Daxx). This interaction inhibits the p53 apoptotic pathway, promoting cell survival.

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Area of Science:

  • Cellular stress response
  • Apoptosis regulation
  • Protein ubiquitination

Background:

  • Carboxyl terminus of Hsp70-interacting protein (CHIP) acts as a co-chaperone and ubiquitin ligase, protecting cells from stress-induced apoptosis.
  • Death domain-associated protein (Daxx) is involved in stress-dependent cellular pathways.

Purpose of the Study:

  • To investigate the interaction between CHIP and Daxx under cellular stress.
  • To elucidate the role of this interaction in regulating p53-dependent apoptosis and cell survival pathways.

Main Methods:

  • Demonstration of stress-dependent CHIP-Daxx interaction.
  • Analysis of p53 serine 46 phosphorylation and p53-dependent gene expression via microarray.
  • In vitro ubiquitination assays of Daxx by CHIP.

Main Results:

  • CHIP-Daxx interaction inhibits stress-induced p53 phosphorylation at serine 46, blocking apoptosis.
  • Microarray analysis shows suppressed p53 transcriptional program in CHIP(+/+) cells.
  • CHIP ubiquitinates Daxx at lysines 630/631, leading to its sequestration and resistance to degradation, competing with Daxx sumoylation.

Conclusions:

  • CHIP acts as a stress-dependent regulator of Daxx, mitigating its pro-apoptotic effects.
  • CHIP integrates proteotoxic stress response with cell cycle pathways to promote cell survival by modulating Daxx ubiquitination and p53 activity.