PML is a ROS sensor activating p53 upon oxidative stress.

ABSTRACT: Promyelocytic leukemia (PML) nuclear bodies (NBs) recruit partner proteins, including p53 and its regulators, thereby controlling their abundance or function. Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation promotes NB biogenesis. However, physiological links between PML and oxidative stress response in vivo remain unexplored. Here, we identify PML as a reactive oxygen species (ROS) sensor. Pml^-/- cells accumulate ROS, whereas PML expression decreases ROS levels. Unexpectedly, Pml^-/- embryos survive acute glutathione depletion. Moreover, Pml^-/- animals are resistant to acetaminophen hepatotoxicity or fasting-induced steatosis. Molecularly, Pml^-/- animals fail to properl

SUBMITTER: Niwa-Kawakita M 

PROVIDER: S-EPMC5679165 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature