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First published online October 22, 2003
doi: 10.1242/10.1242/jcs.00829
Commentary |
Departments of Medicine and Pharmacology, Comprehensive Cancer Center, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, OH 44106, USA
* Author for correspondence (e-mail: cwd{at}po.cwru.edu)
Bcl-2 has been described both as an inhibitor of programmed cell death and as an inhibitor of mitochondrial dysfunction during apoptosis. It is still not clear what biochemical activity of Bcl-2 is responsible for its function, but increasing evidence indicates that a functional activity of Bcl-2 on the endoplasmic reticulum (ER) protects mitochondria under diverse circumstances. Indeed, an emerging hypothesis is that, during apoptosis, the Bcl-2 family regulates ER-to-mitochondrion communication by BH3-only proteins and calcium ions and thereby triggers mitochondrial dysfunction and cell death.
Key words: Bcl-2, Endoplasmic reticulum, ER, Mitochondria, Bcl-Cb5, Calcium, BH3-only, Cytochrome c
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