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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The voltage-dependent anion channel-1 modulates apoptotic cell death.

The role of the voltage-dependent anion channel ( VDAC) in cell death was investigated using the expression of native and mutated murine VDAC1 in U-937 cells and VDAC inhibitors. Glutamate 72 in VDAC1, shown previously to bind dicyclohexylcarbodiimide (DCCD), which inhibits hexokinase isoform I (HK-I) binding to mitochondria, was mutated to glutamine. Binding of HK-I to mitochondria expressing E72Q-mVDAC1, as compared to native VDAC1, was decreased by approximately 70% and rendered insensitive to DCCD. HK-I and ruthenium red (RuR) reduced the VDAC1 conductance but not that of E72Q-mVDAC1. Overexpression of native or E72Q-mVDAC1 in U-937 cells induced apoptotic cell death (80%). RuR or overexpression of HK-I prevented this apoptosis in cells expressing native but not E72Q-mVDAC1. Thus, a single amino-acid mutation in VDAC prevented HK-I- or RuR-mediated protection against apoptosis, suggesting the direct VDAC regulation of the mitochondria- mediated apoptotic pathway and that the protective effects of RuR and HK-I rely on their binding to VDAC.[1]


  1. The voltage-dependent anion channel-1 modulates apoptotic cell death. Zaid, H., Abu-Hamad, S., Israelson, A., Nathan, I., Shoshan-Barmatz, V. Cell Death Differ. (2005) [Pubmed]
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