Nature Communications (Aug 2021)

ZNF768 links oncogenic RAS to cellular senescence

  • Romain Villot,
  • Audrey Poirier,
  • Inan Bakan,
  • Karine Boulay,
  • Erlinda Fernández,
  • Romain Devillers,
  • Luciano Gama-Braga,
  • Laura Tribouillard,
  • Andréanne Gagné,
  • Éma Duchesne,
  • Danielle Caron,
  • Jean-Sébastien Bérubé,
  • Jean-Christophe Bérubé,
  • Yan Coulombe,
  • Michèle Orain,
  • Yves Gélinas,
  • Stéphane Gobeil,
  • Yohan Bossé,
  • Jean-Yves Masson,
  • Sabine Elowe,
  • Steve Bilodeau,
  • Venkata Manem,
  • Philippe Joubert,
  • Frédérick A. Mallette,
  • Mathieu Laplante

DOI
https://doi.org/10.1038/s41467-021-24932-w
Journal volume & issue
Vol. 12, no. 1
pp. 1 – 15

Abstract

Read online

KEY FINDINGS ZNF768 is phosphorylated and degraded upon RAS activation ZNF768 depletion impairs proliferation and causes cellular senescence ZNF768 binds and represses p53 and its overexpression suffices to bypass senescence Elevated ZNF768 levels in human tumors may serve to avoid cellular senescence and support proliferation