BAK regulates catalase release from peroxisomes

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

研究成果: ジャーナルへの寄稿記事

5 引用 (Scopus)

抄録

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.
元の言語英語
記事番号e1306610
ジャーナルMolecular & Cellular Oncology
4
発行部数3
出版物ステータス出版済み - 3 17 2017

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Voltage-Dependent Anion Channel 2
Peroxisomes
Catalase
Permeability
Mitochondria
Membranes

これを引用

Fujiki, Y., Miyata, N., Mukai, S., Okumoto, K., & Cheng, E. H. (2017). BAK regulates catalase release from peroxisomes. Molecular & Cellular Oncology , 4(3), [e1306610].

BAK regulates catalase release from peroxisomes. / Fujiki, Yukio; Miyata, Non; Mukai, Satoru; Okumoto, Kanji; Cheng, Emily H.

:: Molecular & Cellular Oncology , 巻 4, 番号 3, e1306610, 17.03.2017.

研究成果: ジャーナルへの寄稿記事

Fujiki, Y, Miyata, N, Mukai, S, Okumoto, K & Cheng, EH 2017, 'BAK regulates catalase release from peroxisomes', Molecular & Cellular Oncology , 巻. 4, 番号 3, e1306610.
Fujiki, Yukio ; Miyata, Non ; Mukai, Satoru ; Okumoto, Kanji ; Cheng, Emily H. / BAK regulates catalase release from peroxisomes. :: Molecular & Cellular Oncology . 2017 ; 巻 4, 番号 3.
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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 wild-type cells permeabilizes peroxisomes in a BAK-dependent manner. Together, BAK most likely regulates peroxisomal membrane permeability.",
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AU - Cheng, Emily H.

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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.

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