Related Experiment Video

Updated: Jun 29, 2025

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

10.0K

REV7-p53 interaction inhibits ATM-mediated DNA damage signaling

Megan Biller1, Sara Kabir1, Chkylle Boado1

  • 1Department of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC, USA.

Cell Cycle (Georgetown, Tex.)
|April 1, 2024
PubMed

Insights

REV7 protein directly binds to p53, inhibiting its phosphorylation and promoting its destabilization. This reveals a new role for REV7 in DNA damage response signaling and genome stability.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Genetics

Background:

  • REV7 is a known regulator of cell cycle and DNA repair pathways like Trans-Lesion Synthesis (TLS) and Fanconi Anemia (FA).
  • A direct role for REV7 in the DNA damage response (DDR) signaling pathway remained uncharacterized.

Purpose of the Study:

  • To investigate the novel function of REV7 in DNA Double-Strand Break (DSB)-induced p53 signaling.
  • To elucidate the mechanism by which REV7 influences p53 activity and stability.

Main Methods:

  • Co-immunoprecipitation assays to demonstrate direct binding of REV7 to p53.
  • Western blotting to assess p53 phosphorylation and stability.
  • Cellular assays to evaluate the impact of REV7 on DSB-induced signaling.

Main Results:

  • REV7 directly binds to the p53 protein.
  • REV7 inhibits ATM-dependent phosphorylation of p53 at Ser15.
  • REV7 contributes to the destabilization of p53.

Conclusions:

  • REV7 plays a critical role in integrating multiple cellular processes, including cell cycle regulation and DNA repair.
  • REV7's novel function in DSB-induced p53 signaling impacts cell viability and genome stability.
  • REV7 acts as a key modulator of the DNA damage response pathway.
Keywords:
ATMDNA double-strand breaksDNA repairFanconi anemiaMAD2B/p53

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