Nature Communications (Nov 2018)

VDAC2 enables BAX to mediate apoptosis and limit tumor development

  • Hui San Chin,
  • Mark X. Li,
  • Iris K. L. Tan,
  • Robert L. Ninnis,
  • Boris Reljic,
  • Kristen Scicluna,
  • Laura F. Dagley,
  • Jarrod J. Sandow,
  • Gemma L. Kelly,
  • Andre L. Samson,
  • Stephane Chappaz,
  • Seong L. Khaw,
  • Catherine Chang,
  • Andrew Morokoff,
  • Kerstin Brinkmann,
  • Andrew Webb,
  • Colin Hockings,
  • Cathrine M. Hall,
  • Andrew J. Kueh,
  • Michael T. Ryan,
  • Ruth M. Kluck,
  • Philippe Bouillet,
  • Marco J. Herold,
  • Daniel H. D. Gray,
  • David C. S. Huang,
  • Mark F. van Delft,
  • Grant Dewson

DOI
https://doi.org/10.1038/s41467-018-07309-4
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 13

Abstract

Read online

BAX and BAK are pro-apoptotic proteins whose activity is essential for the action of many anti-cancer drugs and to suppress tumorigenesis. Here, the authors perform a genome-wide CRISPR/Cas9 screen and identify VDAC2 as a promoter of BAX-mediated apoptosis that is important for an efficient chemotherapeutic response and to suppress tumor formation.