BAK regulates catalase release from peroxisomes

Abstract

Loss of voltage-dependent anion channel 2 (VDAC2) leads to impaired peroxisome biogenesis in mammalian cells. Knockdown of BAK restores peroxisomal biogenesis in VDAC2-deficient cells, where BAK localization shifts from mitochondria to peroxisomes. Moreover, overexpression of BAK activators in wild-type cells permeabilizes peroxisomes in a BAK-dependent manner. Together, BAK most likely regulates peroxisomal membrane permeability.

Keywords

• apoptosis
• bak
• catalase
• cho mutant
• membrane permeabilization
• oligomerization
• oxidative stress
• peroxisome
• reactive oxygen species
• vdac2