SIRT2 controls the pentose phosphate switch

EMBO J. 2014 Jun 17;33(12):1287-8. doi: 10.15252/embj.201488713. Epub 2014 May 13.


The most common enzyme defect in humans is glucose-6-phosphate dehydrogenase (G6PD) deficiency, which affects more than 400 million people. G6PD shunts glucose into the pentose phosphate pathway (PPP) to generate nucleotides and reducing potential in the form of NADPH. In this issue, Wang et al (2014) show that G6PD activity is post-translationally regulated by SIRT2, a cytoplasmic NAD+-dependent deacetylase, thereby linking NAD+ levels to DNA repair and oxidative defences, and identifying potential new approaches to treating this common genetic disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Animals
  • Cell Survival / physiology*
  • Glucosephosphate Dehydrogenase / metabolism*
  • Histone Acetyltransferases / metabolism*
  • Homeostasis / physiology*
  • Humans
  • NADP / metabolism*
  • Nerve Tissue Proteins / metabolism*
  • Oxidative Stress / physiology*
  • Sirtuin 2 / metabolism*


  • Nerve Tissue Proteins
  • NADP
  • Glucosephosphate Dehydrogenase
  • ELP3 protein, human
  • Histone Acetyltransferases
  • Sirt2 protein, mouse
  • Sirtuin 2