Abstract
Within the mitochondrial pathway of apoptosis, VDAC2 controls both the localization and proapoptotic activity of BAK. In this issue, Hosoi et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201605002) find that loss of VDAC2 diverts BAK into peroxisome membranes, revealing the ability of BAK to control peroxisome membrane integrity and the release of soluble peroxisomal matrix proteins.
© 2017 Chipuk and Luna-Vargas.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / physiology
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Humans
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Membrane Proteins / metabolism
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Mitochondria / metabolism
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Mitochondrial Membranes / metabolism
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Peroxisomes / metabolism*
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
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Voltage-Dependent Anion Channel 2 / metabolism
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bcl-2 Homologous Antagonist-Killer Protein / metabolism*
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bcl-2-Associated X Protein / metabolism
Substances
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Membrane Proteins
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Proto-Oncogene Proteins c-bcl-2
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Voltage-Dependent Anion Channel 2
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bcl-2 Homologous Antagonist-Killer Protein
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bcl-2-Associated X Protein