| Literature DB >> 28616584 |
Yukio Fujiki1, Non Miyata2,3, Satoru Mukai2, Kanji Okumoto2, Emily H Cheng4.
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.Entities:
Keywords: Apoptosis; BAK; CHO mutant; VDAC2; catalase; membrane permeabilization; oligomerization; oxidative stress; peroxisome; reactive oxygen species
Year: 2017 PMID: 28616584 PMCID: PMC5462519 DOI: 10.1080/23723556.2017.1306610
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556