Type II hexokinase is overexpressed in most neoplastic cells, and it mainly localizes on the
outer mitochondrial membrane. Hexokinase II dissociation from mitochondria triggers
apoptosis. The prevailing model postulates that hexokinase II release from its mitochondrial
interactor, the voltage-dependent anion channel, prompts outer mitochondrial membrane
permeabilization and the ensuing release of apoptogenic proteins, and that these events are
inhibited by growth factor signalling. Here we show that a hexokinase II N-terminal peptide …

Type II hexokinase (HKII) is overexpressed in the outer mitochondrial membrane of most
neoplastic cells. Current work postulates that HKII release from its mitochondrial interactor,
the voltage-dependent anion channel, prompts outer mitochondrial membrane
permeabilization and the ensuing release of apoptogenic proteins, and that these events are
inhibited by growth factors. Here we show that a HKII Nterminal peptide selectively detaches
HKII from mitochondria transduces a permeability transition pore opening signal that results …