Bak Regulates Catalase Release From Peroxisomes

Yukio Fujiki,Non Miyata,Satoru Mukai,Kanji Okumoto,Emily H Cheng

MOLECULAR & CELLULAR ONCOLOGY（2017）

Cited 13|Views25

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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 wildtype cells permeabilizes peroxisomes in a BAK-dependent manner. Together, BAK most likely regulates peroxisomal membrane permeability.

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Key words

Apoptosis, BAK, catalase, CHO mutant, membrane permeabilization, oligomerization, oxidative stress, peroxisome, reactive oxygen species, VDAC2

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