BAK regulates catalase release from peroxisomes Journal Article


Authors: Fujiki, Y.; Miyata, N.; Mukai, S.; Okumoto, K.; Cheng, E. H.
Article Title: 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 wildtype cells permeabilizes peroxisomes in a BAK-dependent manner. Together, BAK most likely regulates peroxisomal membrane permeability.
Keywords: apoptosis; death; reactive oxygen species; oxidative stress; mitochondria; oligomerization; life; catalase; membrane permeabilization; bak; cho mutant; peroxisome; vdac2
Journal Title: Molecular & Cellular Oncology
Volume: 4
Issue: 3
ISSN: 2372-3556
Publisher: Taylor & Francis Group  
Date Published: 2017-01-01
Start Page: e1306610
Language: English
ACCESSION: WOS:000406851400004
DOI: 10.1080/23723556.2017.1306610
PROVIDER: wos
PMCID: PMC5462519
PUBMED: 28616584
Notes: Editorial Material -- Source: Wos
Altmetric
Citation Impact
BMJ Impact Analytics
MSK Authors
  1. Emily H Cheng
    78 Cheng