BAK regulates catalase release from peroxisomes

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

BAK regulates catalase release from peroxisomes

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

Research output: Contribution to journal › Article › peer-review

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 language	English
Article number	e1306610
Journal	Molecular & Cellular Oncology
Volume	4
Issue number	3
Publication status	Published - Mar 17 2017

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

author = "Yukio Fujiki and Non Miyata and Satoru Mukai and Kanji Okumoto and Cheng, {Emily H.}",

year = "2017",

month = mar,

day = "17",

language = "English",

volume = "4",

journal = "Molecular & Cellular Oncology ",

publisher = "Taylor and Francis",

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TY - JOUR

T1 - BAK regulates catalase release from peroxisomes

AU - Fujiki, Yukio

AU - Miyata, Non

AU - Mukai, Satoru

AU - Okumoto, Kanji

AU - Cheng, Emily H.

PY - 2017/3/17

Y1 - 2017/3/17

N2 - 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.

AB - 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.

M3 - Article

VL - 4

JO - Molecular & Cellular Oncology

JF - Molecular & Cellular Oncology

IS - 3

M1 - e1306610

ER -

BAK regulates catalase release from peroxisomes

Abstract

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