Hexokinase II Release from Mitochondria Triggers Apoptosis
Author Information
Author(s): Chiara Federica Castellaro, Diego Marin, Valeria Petronilli, William S. Brusilow, Magdalena Juhaszova, Steven J. Sollott, Michael Forte, Paolo Bernardi, Andrea Rasola
Primary Institution: CNR Institute of Neuroscience and Department of Biomedical Sciences, University of Padova, Padova, Italy
Hypothesis
Does hexokinase II detachment from mitochondria induce apoptosis independently of voltage-dependent anion channels?
Conclusion
Hexokinase II detachment from mitochondria activates apoptosis through a permeability transition pore that does not require voltage-dependent anion channels.
Supporting Evidence
- Hexokinase II is overexpressed in many cancer cells and is crucial for their survival.
- The study shows that hexokinase II detachment activates apoptosis through a specific mechanism.
- Insulin stimulation does not prevent cell death induced by hexokinase II detachment.
Takeaway
When a protein called hexokinase II leaves the mitochondria, it can cause the cell to die, and this process doesn't need another protein called VDAC.
Methodology
The study involved using peptides to detach hexokinase II from mitochondria and assessing the resulting apoptosis through various assays.
Limitations
The exact molecular composition of the permeability transition pore remains unresolved.
Digital Object Identifier (DOI)
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