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.
本文言語 | 英語 |
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論文番号 | e1306610 |
ジャーナル | Molecular & Cellular Oncology |
巻 | 4 |
号 | 3 |
出版ステータス | 出版済み - 3月 17 2017 |