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Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.

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Ubiquitin-specific protease 28 (USP28) stabilizes the tumor suppressor p53 by removing ubiquitin tags, crucial for cellular stress responses. Mutations in USP28 impair this process, potentially driving cancer progression.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Cellular stress response pathways are vital for maintaining genome stability.
  • These pathways are often disrupted in cancer, leading to uncontrolled cell growth.
  • Ubiquitin-specific protease 28 (USP28) and p53-binding protein 1 (53BP1) form a complex that stabilizes p53 following mitotic stress.

Purpose of the Study:

  • To elucidate the mechanism by which USP28 stabilizes p53.
  • To investigate the role of USP28 in cellular stress responses and cancer.
  • To identify USP28 isoforms and domains critical for p53 stabilization and stress response.

Main Methods:

  • Deubiquitination assays to demonstrate USP28's mechanism.
  • Analysis of USP28 function in mitotic stress and DNA damage responses.
  • Identification and characterization of USP28 isoforms and mutation analysis.

Main Results:

  • USP28 stabilizes p53 through deubiquitination.
  • A specific USP28 isoform with a C-terminal domain is critical for p53 stabilization.
  • This domain mediates PLK1-dependent binding to 53BP1, essential for stress memory and cell cycle arrest.
  • Cancer-associated mutations in this domain disrupt 53BP1 binding and compromise p53 stabilization.

Conclusions:

  • USP28 plays a critical role in p53 stabilization and cellular stress responses.
  • A specific USP28 isoform and its interaction with 53BP1 are crucial for mitotic stress memory.
  • Mutations affecting USP28-53BP1 interaction are prevalent in cancer and may contribute to tumor progression.