BAK regulates catalase release from peroxisomes

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

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

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.
Original languageEnglish
Article numbere1306610
JournalMolecular & Cellular Oncology
Volume4
Issue number3
Publication statusPublished - Mar 17 2017

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