Fig. 1.

Mechanism of apoptosis induction by eIF5A-1/eIF5A-1 precursor. Over-expression of eIF5A-1 (unhypusinated precursor form) induces loss of mitochondrial transmembrane potential, translocation of Bax to the mitochondria, release of cytochrome c, caspase 9 and 3 activation. These events lead to apoptosis. On the other hand, over-expression of eIF5A-1 can also increase reactive oxygen species (ROS) generation that, creating mitochondrial dysfunction, releases cytochrome c and activates caspases leading to apoptosis. Hypusine-containing eIF5A-1 loses the ability to induce Bax translocation to mitochondria and/or ROS elevation